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The advancement demands of high-speed wireless data link ask for higher requirements on visible light communication (VLC), where wide coverage stands as a critical criterion. Here, we present the design and implementation of a transmitter structure capable of emitting a high-power wide-coverage white light laser. This laser source exhibits excellent stability, with an irradiation range extending to a half-angle of 20°. Its high brightness satisfies the needs of indoor illumination while maintaining excellent communication performance. Utilizing bit-loading discrete multi-tone modulation, a peak data transmission rate of 3.24â Gbps has been achieved, spanning 1 to 5â m. Remarkably, the data rates exceed 2.5â Gbps within a 40° range at a distance of 5â m, enabling a long-distance, wide coverage, high-speed VLC link for future mobile network applications.
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OBJECTIVE: This system review and meta-analysis was aim to evaluate the accuracy of prenatal ultrasound in diagnosing cleft palates (CPs) during first trimester. DATA SOURCE: We systematically searched the databases of PubMed, Embase, and Cochrane Library for the articles, which assessed the accuracy of CPs diagnosed by ultrasound during first trimester. REVIEW METHOD: The characteristics of the included studies were recorded. The quality of included studies was assessed by QUADAS-2. The pooled sensitivity, specificity, positive likelihood ratio (PLR), negative likelihood ratio (NLR), diagnostic odds ratio (DOR), and the area under the curve (AUC) were calculated using Meta-Disc software version 1.4. The publication bias was assessed by Stata software version 12.0. RESULTS: This meta-analysis included 13 studies with 39 806 fetuses. The pooled sensitivity, specificity, PLR, NLR were 0.874, 0.999, 689.84, and 0.161, respectively. The DOR and AUC were 6651.3 and 0.9084, respectively. CONCLUSION: The overall detection rate was 0.874, which indicated high value of first trimester ultrasound in diagnosing CPs.
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Fisura del Paladar , Embarazo , Femenino , Humanos , Primer Trimestre del Embarazo , Sensibilidad y Especificidad , Fisura del Paladar/diagnóstico por imagen , Ultrasonografía , FetoRESUMEN
BACKGROUND: The treatment and prevention of perinatal venous thromboembolism (VTE) are challenging because of the potential for both fetal and maternal complications. METHODS: This study developed a rapid assessment scale for VTE and evaluate its validity based on Delphi-AHP (Analytic Hierarchy Process) method in China. The research was conducted by literature retrieval and two rounds of Delphi expert consultation. The item pools of the scale were developed and a questionnaire was designed according to literature retrieval published between 2010 and 2020. A survey was conducted among experts from 25 level A hospitals in China, and data of experts' opinions were collected and analyzed by the Delphi method. RESULTS: A perinatal VTE risk assessment scale was formed, including 5 first-level items, 20 s-level items and 40 third-level items. The response rates in the two rounds of expert consultation were 97.4% and 98.0%, and the authoritative coefficients were 0.89 and 0.92. The coefficients of variation ranged from 0.04 to 0.28. CONCLUSIONS: The scale is significantly valid and reliable with a high authority and coordination degree, and it can be used to assess the risk of perinatal VTE and initiate appropriate thrombophylactic interventions in China.
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Tromboembolia Venosa , China/epidemiología , Técnica Delphi , Femenino , Humanos , Embarazo , Medición de Riesgo , Encuestas y Cuestionarios , Tromboembolia Venosa/diagnóstico , Tromboembolia Venosa/epidemiología , Tromboembolia Venosa/prevención & controlRESUMEN
Our previous studies have shown that the Adipose-derived mesenchymal stem cells (ADSCs) can regulate metastasis and development of ovarian cancer. However, its specific mechanism has yet to be fully revealed. In this study, an RNA-seq approach was adopted to compare the differences in mRNA levels in ovarian cancer cells being given or not given ADSCs. The mRNA level of paired box 8 (PAX8) changed significantly and was confirmed as an important factor in tumour-inducing effect of ADSCs. In comparison with the ovarian cancer cells cultured in the common growth medium, those cultured in the medium supplemented with ADSCs showed a significant increase of the PAX8 level. Moreover, the cancer cell growth could be restricted, even in the ADSC-treated group (P < .05), by inhibiting PAX8. In addition, an overexpression of PAX8 could elevate the proliferation of ovarian cancer cells. Moreover, Co-IP assays in ovarian cancer cells revealed that an interaction existed between endogenous PAX8 and TAZ. And the PAX8 levels regulated the degradation of TAZ. The bioluminescence images captured in vivo manifested that the proliferation and the PAX8 expression level in ovarian cancers increased in the ADMSC-treated group, and the effect of ADSCs in promoting tumours was weakened through inhibiting PAX8. Our findings indicate that the PAX8 expression increment could contribute a role in promoting the ADSC-induced ovarian cancer cell proliferation through TAZ stability regulation.
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Biomarcadores de Tumor/metabolismo , Regulación Neoplásica de la Expresión Génica , Péptidos y Proteínas de Señalización Intracelular/química , Células Madre Mesenquimatosas/citología , Neoplasias Ováricas/patología , Factor de Transcripción PAX8/metabolismo , Animales , Apoptosis , Biomarcadores de Tumor/genética , Movimiento Celular , Proliferación Celular , Femenino , Humanos , Péptidos y Proteínas de Señalización Intracelular/genética , Péptidos y Proteínas de Señalización Intracelular/metabolismo , Ratones , Ratones Endogámicos BALB C , Ratones Desnudos , Neoplasias Ováricas/genética , Neoplasias Ováricas/metabolismo , Factor de Transcripción PAX8/genética , Proteínas Coactivadoras Transcripcionales con Motivo de Unión a PDZ , Células Tumorales Cultivadas , Ensayos Antitumor por Modelo de XenoinjertoRESUMEN
Endometrial cancer is the most common gynaecological cancer, and its incidence is increasing. Obesity is a well-recognized risk factor for endometrial cancer, and the mechanisms by which adipose tissue influences tumour development remain controversial. In this study, we examined the high IL-6 level in the ADSCs supernatant following treatment of endometrial cancer cell CM. Then, the activation of STAT3, a major tumourigenic IL-6 effector, was examined in ADSCs CM treated endometrial cancer cells. Conditioned ADSC medium was used to stimulate endometrial cancer cell growth in vitro. Similar to IL-6, ADSC-conditioned medium significantly promoted endometrial cancer growth and invasion. Furthermore, siRNA-mediated STAT3 inhibition in endometrial cancer cells decreased the ADSC-mediated promotion of cell proliferation and invasion. In addition, a subcutaneous nude mouse model of endometrial cancer was established to monitor the tumour-promoting effect of ADSCs. ADSC-conditioned medium promoted tumour growth, and STAT3 inhibition attenuated this effect. Based on these data, ADSCs promote endometrial cancer progression by the STAT3 signalling pathway.
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Tejido Adiposo/citología , Neoplasias Endometriales/patología , Interleucina-6/metabolismo , Factor de Transcripción STAT3/metabolismo , Células Madre/citología , Animales , Línea Celular Tumoral , Proliferación Celular , Femenino , Humanos , Ratones Endogámicos BALB C , Ratones Desnudos , Invasividad Neoplásica , Metástasis de la NeoplasiaRESUMEN
Deer antlers are amazing appendages with the fastest growth rate among mammalian organs. Antler growth is driven by the growth center through a modified endochondral ossification process. Thus, identification of signaling pathways functioning in antler growth center would help us to uncover the underlying molecular mechanism of rapid antler growth. Furthermore, exploring and dissecting the molecular mechanism that regulates antler growth is extremely important and helpful for identifying methods to enhance long bone growth and treat cartilage- and bone-related diseases. In this study, we build a comprehensive intercellular signaling network in antler growth centers from both the slow growth stage and rapid growth stage using a state-of-art RNA-Seq approach. This network includes differentially expressed genes that regulate the activation of multiple signaling pathways, including the regulation of actin cytoskeleton, calcium signaling, and adherens junction. These signaling pathways coordinately control multiple biological processes, including chondrocyte proliferation and differentiation, matrix homeostasis, mechanobiology, and aging processes, during antler growth in a comprehensive and efficient manner. Therefore, our study provides novel insights into the molecular mechanisms regulating antler growth and provides valuable and powerful insight for medical research on therapeutic strategies targeting skeletal disorders and related cartilage and bone diseases.
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Cuernos de Venado/crecimiento & desarrollo , Ciervos/crecimiento & desarrollo , Ciervos/genética , Transducción de Señal/genética , Animales , Cuernos de Venado/metabolismo , Perfilación de la Expresión Génica , Análisis de Secuencia de ARN , TranscriptomaRESUMEN
BACKGROUND: The study aimed to investigate the clinical value of velocity vector imaging (VVI) in assessing heart function in fetuses of pregnant women with thyroid dysfunction. The inter-observer and intra-observer variability was assessed for all VVI parameters observed. MATERIAL AND METHODS: The participants were enrolled from singleton pregnant women with gestational ages ranging 24+0 to 40+1 weeks who visited the Department of Obstetrics and Gynecology at the Affiliated Hospital of Qingdao University, China, for prenatal care from July 2011 to February 2014. Digital 2-dimensional (2D) dynamic 4-chamber images of the heart were collected. A total of qualified 226 images from 125 fetuses of pregnant women with normal thyroid (control group), 64 fetuses of pregnant women with hypothyroidism (hypothyroidism group), and 37 fetuses of pregnant women with hyperthyroidism (hyperthyroidism group) were interrogated offline using VVI software. The echocardiographic parameters including the myocardium peak systolic velocity (Vs), peak diastolic velocity (Vd), peak systolic strain (S), peak systolic strain rate (SRs), peak diastolic strain rate (SRd) of RV and LV, were obtained from the velocity curves of 2D myocardial motion. The heart rate was measured using a virtual M-mode algorithm built into the software. RESULTS: The study found that the longitudinal Vs and Vd of both ventricles in the control group gradually decreased from basal segments to apical segments and significantly increased over the gestation. S, SRs, and SRd of both ventricles remained stable after middle gestation. Compared with the control group, the hypothyroidism and hyperthyroidism groups exhibited significantly reduced S, SRs, and SRd, even for fetuses at 24-weeks gestation. There were no significant differences in global Vs and global Vd between the control group and the hyperthyroidism or hypothyroidism groups. CONCLUSIONS: The thyroid dysfunction of pregnant women may damage fetal heart function, and VVI could be a sensitive technique to measure the variation of fetal heart function.
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Ecocardiografía , Corazón Fetal/diagnóstico por imagen , Ventrículos Cardíacos/embriología , Corazón/embriología , Hipertiroidismo/diagnóstico por imagen , Hipotiroidismo/diagnóstico por imagen , Ultrasonografía Prenatal , Algoritmos , Estudios de Casos y Controles , Femenino , Edad Gestacional , Ventrículos Cardíacos/diagnóstico por imagen , Humanos , Hipertiroidismo/complicaciones , Hipotiroidismo/complicaciones , Procesamiento de Imagen Asistido por Computador , Madres , Variaciones Dependientes del Observador , Embarazo , Complicaciones del Embarazo , Segundo Trimestre del Embarazo , Tercer Trimestre del Embarazo , Programas Informáticos , Glándula Tiroides/diagnóstico por imagenRESUMEN
INTRODUCTION: Necroptosis triggered by H2O2 is hypothesized to be a critical factor in the rupture of atherosclerotic plaques, which may precipitate acute cardiovascular events. Nevertheless, the specific regulatory molecules of this development remain unclear. We aims to elucidate a mechanism from the perspective of circular RNA. OBJECTIVES: There are few studies on circRNA in VSMCs necroptosis. The objective of our research is to shed light on the intricate roles that circHIPK3 plays in the process of necroptosis in VSMCs and the development of atherosclerotic plaques that are prone to rupture. Our study elucidates the specific molecular mechanisms by which circHIPK3 regulates necroptosis and atherosclerotic vulnerable plaque formation through targeted proteins. Identifying this mechanism at the cellular level offers a molecular framework for understanding plaque progression and stability regulation, as well as a potential biomarker for the prognosis of susceptible atherosclerotic plaques. METHODS: We collected clinical vascular tissue for HE staining and Masson staining to determine the presence and stability of plaques. Then, NCBI database was used to screen out circRNA with elevated expression level in plaque tissue, and the up-regulated circRNA, circHIPK3, was verified by qRT-PCR and FISH. Further, we synthesized circHIPK3's small interference sequence and overexpressed plasmid in vitro, and verified its regulation effect on necroptosis of VSMCs under physiological and pathological conditions by WB, qRT-PCR and PI staining. Through RNA pull down, mass spectrometry and RNA immunoprecipitation, DRP1 was identified as circHIPK3 binding protein and was positively regulated by circHIPK3. Meanwhile, on the basis of silencing of DRP1, the regulation of circHIPK3 on necroptosis is verified to be mediated by DRP1. Finally, we validated the regulation of circHIPK3 on vulnerable plaque formation in ApoE-/- mice. RESULTS: We investigated that circHIPK3 was highly expressed in vulnerable plaques, and the increase in expression level promoted H2O2 induced necroptosis of VSMCs. CircHIPK3 targeted the protein DRP1, leading to an elevation in mitochondrial division rate, resulting in increased reactive oxygen species and impaired mitochondrial function, ultimately leading to necroptosis of VSMCs and vulnerable plaque formation. CONCLUSION: CircHIPK3 interact with DRP1 involve in H2O2 induced Mitochondrial damage and necroptosis of VSMCs, and Silencing circHIPK3 in vivo can reduce atherosclerotic vulnerable plaque formation. Our research findings may have applications in providing diagnostic biomarkers for vulnerable plaques.
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While the home is an important place for individuals to act pro-environmentally, researchers have rarely explored the pro-environmental behavior of hotel customers in terms of their home away from home experiences during their travels. This study uses a combination of qualitative (interviews) and quantitative (questionnaires) methods to explore customer experiences of home spaces in the hotel context and the relationship between people's experience in hotels and their pro-environmental behavior. The study shows that (1) customers' experience of home spaces in hotels occurs through three dimensions: the function of home, the emotion of home, and the imagination of home. (2) Both the function of home and the emotion of home exert a significantly positive impact on hotel customers pro-environmental behavior. (3) The imagination of home exerts a significant positive effect on pro-environmental behavior both inside and outside of the hotel. (4) The pro-environmental behavior of customers in their own homes has a positive moderating effect on the relationship between the home experience and pro-environmental behavior in the hotel context. By combining the concepts of home spaces and pro-environmental behavior, this study, on the one hand, bridges the research gap between place experience and pro-environmental behavior in the hotel context; on the other hand, the study transcends the limitations engendered by studying pro-environmental behavior in the hotel and home space from a binary perspective.
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Emociones , Humanos , Encuestas y CuestionariosRESUMEN
Clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (Cas9) gene-editing technology is the ideal tool of the future for treating diseases by permanently correcting deleterious base mutations or disrupting disease-causing genes with great precision and efficiency. A variety of efficient Cas9 variants and derivatives have been developed to cope with the complex genomic changes that occur during diseases. However, strategies to effectively deliver the CRISPR system to diseased cells in vivo are currently lacking, and nonviral vectors with target recognition functions may be the focus of future research. Pathological and physiological changes resulting from disease onset are expected to serve as identifying factors for targeted delivery or targets for gene editing. Diseases are both varied and complex, and the choice of appropriate gene-editing methods and delivery vectors for different diseases is important. Meanwhile, there are still many potential challenges identified when targeting delivery of CRISPR/Cas9 technology for disease treatment. This paper reviews the current developments in three aspects, namely, gene-editing type, delivery vector, and disease characteristics. Additionally, this paper summarizes successful examples of clinical trials and finally describes possible problems associated with current CRISPR applications.
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Sistemas CRISPR-Cas , Edición Génica , Sistemas CRISPR-Cas/genética , Terapia Genética/métodosRESUMEN
Many previous studies have underestimated the role of magnetic components in improving photocatalytic performance. It is significance to explore the migration mechanism of photoinduced carriers in magnetic heterojunction. Here, a magnetic heterojunction, BiOI/BaFe12O19, was synthesized by a simple preparation method. The optimal synthesis conditions and photocatalytic reaction conditions were explored. The growth mechanism of bismuth iodide oxide (BiOI) was elaborated by introducing a micromagnetic field stemming from barium ferrite (BaFe12O19). The electrochemical impedance spectroscopy (EIS), Mott-Schottky curve (MS), transient fluorescence spectrometer (PL), and photocurrent response plot (i ~ t) tests indicated that the BiOI/BaFe12O19 possessed a higher transfer capacity of electrons, higher separation efficiency of photoinduced carriers, stronger photocurrent response, and higher carriers density, compared with pure BiOI. The ultraviolet-visible diffuse reflectance spectrophotometer (UV-vis DRS), electron paramagnetic resonance spectrometer (EPR), MS, and quenching experiments revealed band structure configuration and migration mechanism of photoinduced carriers. The enhancement mechanism of photocatalysis and photocatalytic reaction mechanism was clearly proclaimed in BiOI/BaFe12O19 catalytic system.
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Bismuto , Óxidos , Bismuto/química , LuzRESUMEN
Purpose: To explore the therapeutic mechanism of bone marrow mesenchymal stem cells derived exosomes (BMSC-Exos) for doxorubicin (DOX)-induced cardiotoxicity (DIC) and identify the long noncoding RNAs' (lncRNAs') anti-inflammation function derived by BMSC-Exos. Materials and Methods: High-throughput sequencing and transcriptome bioinformatics analysis of lncRNA were performed between DOX group and BEC (bone marrow mesenchymal stem cells derived exosomes coculture) group. Elevated lncRNA (ElncRNA) in the cardiomyocytes of BEC group compared with DOX group were confirmed. Based on the location and co-expression relationship between ElncRNA and its target genes, we predicted two target genes of ElncRNA, named cis_targets and trans_targets. The target genes were analyzed by enrichment analyses. Then, we identified the key cellular biological pathways regulating DIC. Experiments were performed to verify the therapeutic effects of exosomes and the origin of lncRNAs in vitro and in vivo. Results: Three hundred and one lncRNAs were differentially expressed between DOX and BEC groups (fold change >1.5 and p < 0.05), of which 169 lncRNAs were elevated in the BEC group compared with the DOX group. GO enrichment analysis of target genes of ElncRNAs showed that they were predominantly involved in inflammation-associated processes. KEGG analysis indicated that their regulatory pathways were mainly involved in oxidative stress-induced inflammation and proliferation of cardiomyocyte. The verification experiments in vitro showed that the oxidative stress and cell deaths were decreased in BEC groups. Moreover, from the top 10 ElncRNAs identified in the sequencing results, MSTRG.98097.4 and MSTRG.58791.2 were both decreased in the DOX group and elevated in BEC group. While in verification experiments in vivo, only the expression of MSTRG.58791.2 is consistent with the result in vitro. Conclusion: Our results show that ElncRNA, MSTRG.58791.2, is possibly secreted by the BMSC-Exos and able to alleviate DIC by suppressing inflammatory response and inflammation-related cell death.
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Aminoacyl-tRNA synthetases (ARSs) are widely found in organisms, which can activate amino acids and make them bind to tRNA through ester bond to form the corresponding aminoyl-tRNA. The classic function of ARS is to provide raw materials for protein biosynthesis. Recently, emerging evidence demonstrates that ARSs play critical roles in controlling inflammation, immune responses, and tumorigenesis as well as other important physiological and pathological processes. With the recent development of genome and exon sequencing technology, as well as the discovery of new clinical cases, ARSs have been reported to be closely associated with a variety of cardiovascular diseases (CVDs), particularly angiogenesis and cardiomyopathy. Intriguingly, aminoacylation was newly identified and reported to modify substrate proteins, thereby regulating protein activity and functions. Sensing the availability of intracellular amino acids is closely related to the regulation of a variety of cell physiology. In this review, we summarize the research progress on the mechanism of CVDs caused by abnormal ARS function and introduce the clinical phenotypes and characteristics of CVDs related to ARS dysfunction. We also highlight the potential roles of aminoacylation in CVDs. Finally, we discuss some of the limitations and challenges of present research. The current findings suggest the significant roles of ARSs involved in the progress of CVDs, which present the potential clinical values as novel diagnostic and therapeutic targets in CVD treatment.
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Doxorubicin (DOX) is a kind of representative anthracyclines. It has greatly prolonged lifespan of cancer patients. However, a long course of DOX chemotherapy could induce various forms of deaths of cardiomyocytes, such as apoptosis, pyroptosis and ferroptosis, contributing to varieties of cardiac complications called cardiotoxicity. It has become a major concern considering the large number of cancer patients' worldwide and increased survival rates after chemotherapy. Exosomes, a subgroup of extracellular vesicles (EVs), are secreted by nearly all cells and consist of lipid bilayers, nucleic acids and proteins. They can serve as mediators between intercellular communication via the transfer of bioactive molecules from secretory to recipient cells, modulating multiple pathophysiological processes. It has been proven that exosomes in body fluids can serve as biomarkers for doxorubicin-induced cardiotoxicity (DIC). Moreover, exosomes have attracted considerable attention because of their capacity as carriers of certain proteins, genetic materials (miRNA and lncRNA), and chemotherapeutic drugs to decrease the dosage of DOX and alleviate cardiotoxicity. This review briefly describes the characteristics of exosomes and highlights their clinical application potential as diagnostic biomarkers and drug delivery vehicles for DIC, thus providing a strategy for addressing it based on exosomes.
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Cardiotoxicidad , Doxorrubicina , Portadores de Fármacos/metabolismo , Exosomas/metabolismo , Antineoplásicos/farmacología , Biomarcadores/metabolismo , Cardiotoxicidad/etiología , Cardiotoxicidad/metabolismo , Cardiotoxicidad/prevención & control , Comunicación Celular , Doxorrubicina/farmacología , Doxorrubicina/toxicidad , Humanos , Miocitos Cardíacos/efectos de los fármacos , Miocitos Cardíacos/metabolismoRESUMEN
As a potent chemotherapeutic agent, doxorubicin (DOX) is widely used for the treatment of a variety of cancers However, its clinical utility is limited by dose-dependent cardiotoxicity, and pathogenesis has traditionally been attributed to the formation of reactive oxygen species (ROS). Accordingly, the prevention of DOX-induced cardiotoxicity is an indispensable goal to optimize therapeutic regimens and reduce morbidity. Acetylation is an emerging and important epigenetic modification regulated by histone deacetylases (HDACs) and histone acetyltransferases (HATs). Despite extensive studies of the molecular basis and biological functions of acetylation, the application of acetylation as a therapeutic target for cardiotoxicity is in the initial stage, and further studies are required to clarify the complex acetylation network and improve the clinical management of cardiotoxicity. In this review, we summarize the pivotal functions of HDACs and HATs in DOX-induced oxidative stress, the underlying mechanisms, the contributions of noncoding RNAs (ncRNAs) and exercise-mediated deacetylases to cardiotoxicity. Furthermore, we describe research progress related to several important SIRT activators and HDAC inhibitors with potential clinical value for chemotherapy and cardiotoxicity. Collectively, a comprehensive understanding of specific roles and recent developments of acetylation in doxorubicin-induced cardiotoxicity will provide a basis for improved treatment outcomes in cancer and cardiovascular diseases.
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Cardiotoxicidad , Miocitos Cardíacos , Acetilación , Cardiotoxicidad/etiología , Cardiotoxicidad/metabolismo , Doxorrubicina/efectos adversos , Humanos , Miocitos Cardíacos/metabolismo , Estrés Oxidativo , Especies Reactivas de Oxígeno/metabolismoRESUMEN
Accumulating evidence shows that tRNA-derived fragments are a novel class of functional small non-coding RNA; however, their roles in aortic dissection (AD) are still unknown. In this study, we found that 5'-tiRNA-Cys-GCA was significantly downregulated in human and mouse models of aortic dissection. The abnormal proliferation, migration, and phenotypic transition of vascular smooth muscle cells (VSMCs) played a crucial role in the initiation and progression of aortic dissection, with 5'-tiRNA-Cys-GCA as a potential phenotypic switching regulator, because its overexpression inhibited the proliferation and migration of VSMCs and increased the expression of contractile markers. In addition, we verified that signal transducer and activator of transcription 4 (STAT4) was a direct downstream target of 5'-tiRNA-Cys-GCA. We found that the STAT4 upregulation in oxidized low-density lipoprotein (ox-LDL)-treated VSMCs, which promoted cell proliferation, migration, and phenotypic transformation, was reversed by 5'-tiRNA-Cys-GCA. Furthermore, 5'-tiRNA-Cys-GCA treatment reduced the incidence and prevented the malignant process of angiotensin II- and ß-aminopropionitrile-induced AD in mice. In conclusion, our findings reveal that 5'-tiRNA-Cys-GCA is a potential regulator of the AD pathological process via the STAT4 signaling pathway, providing a novel clinical target for the development of future treatment strategies for aortic dissection.
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tsRNAs are small fragments of RNAs with specific lengths that are generated by particular ribonucleases, such as dicer and angiogenin (ANG), clipping on the rings of transfer RNAs (tRNAs) in specific cells and tissues under specific conditions. Depending on where the splicing site is, tsRNAs can be segmented into two main types, tRNA-derived stress-induced RNAs (tiRNAs) and tRNA-derived fragments (tRFs). Many studies have shown that tsRNAs are functional molecules, not the random degradative products of tRNAs. Notably, due to their regulatory mechanism in regulating mRNA stability, transcription, ribosomal RNA (rRNA) synthesis and RNA reverse transcription, tsRNAs are significantly involved in the cell function, such as cell proliferation, migration, cycle and apoptosis, as well as the occurrence and development of a variety of diseases. In addition, tsRNAs may represent a new generation of clinical biomarkers or therapeutic targets because of their stable structures, high conservation and widely distribution, particularly in the peripheral tissues, bodily fluids and exosomes. In this review, we describe the generation, function and mechanism of tsRNAs and illustrate the current research progress of tsRNAs in various diseases, highlight their potentials as biomarkers and therapeutic targets in clinical application. Although our understanding of tsRNAs is still in infancy, the application prospects shown in this field deserve further exploration.
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Exosomas/metabolismo , ARN de Transferencia/genética , ARN de Transferencia/metabolismo , Animales , Biomarcadores/análisis , Proliferación Celular/fisiología , Humanos , ARN/genética , Ribonucleasa Pancreática/genéticaRESUMEN
BACKGROUND: Our previous study showed that human omental adipose-derived stem cells (ADSCs) promote ovarian cancer growth and metastasis. In this study, the role of autophagy in the ovarian cancer-promoting effects of omental ADSCs was further determined. METHODS: The growth and invasion of ovarian cancer cells were detected by CCK-8 and Transwell assays, respectively. The autophagy of ovarian cancer cells transfected with MRFP-GFP-LC3 adenoviral vectors was evaluated by confocal microscopy and western blot assay. Transfection of STAT3 siRNA was used to inhibit the expression of STAT3. RESULTS: Our results show that autophagy plays a vital role in ovarian cancer and is promoted by ADSCs. Specifically, we show that proliferation and invasion are correlated with autophagy induction by ADSCs in two ovarian cancer cell lines under hypoxic conditions. Mechanistically, ADSCs activate the STAT3 signalling pathway, thereby promoting autophagy. Knockdown of STAT3 expression using siRNA decreased hypoxia-induced autophagy and decreased the proliferation and metastasis of ovarian cancer cells. CONCLUSION: Taken together, our data indicate that STAT3-mediated autophagy induced by ADSCs promotes ovarian cancer growth and metastasis.
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Autofagia , Células Madre Mesenquimatosas , Neoplasias Ováricas , Factor de Transcripción STAT3/metabolismo , Línea Celular Tumoral , Movimiento Celular , Proliferación Celular , Femenino , Humanos , Células Madre Mesenquimatosas/metabolismo , Células Madre Mesenquimatosas/patología , Epiplón/citología , Neoplasias Ováricas/metabolismo , Neoplasias Ováricas/patología , Transducción de SeñalRESUMEN
Antler growth is a unique event compared to other growth and development processes in mammals. Antlers grow extremely fast during the rapid growth stage when growth rate peaks at 2 cm per day. Antler growth is driven by a specific endochondral ossification process in the growth center that is in the distal region of the antler tip. In this study, we used state-of-art RNA-seq technology to analyze the expression profiles of mRNAs and miRNAs during antler growth. Our results indicated that the expression levels of multiple genes involved in chondrogenesis and endochondral ossification, including Fn1, Sox9, Col2a1, Acan, Col9a1, Col11a1, Hapln1, Wwp2, Fgfr3, Comp, Sp7 and Ihh, were significantly increased at the rapid growth stage. Our results also indicated that there were multiple differentially expressed miRNAs interacting with differentially expressed genes with opposite expression patterns. Furthermore, some of the miRNAs, including miR-3072-5p, miR-1600, miR-34-5p, miR-6889-5p and miR-6729-5p, simultaneously interacted with and controlled multiple genes involved in the process of chondrogenesis and endochondral ossification. Therefore, we established a miRNA-mRNA regulatory network by identifying miRNAs and their target genes that were differentially expressed in the antler growth centers by comparing the rapid growth stage and the initial growth stage.
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Cuernos de Venado/crecimiento & desarrollo , Ciervos/genética , MicroARNs/genética , ARN Mensajero/genética , Animales , Cuernos de Venado/metabolismo , Condrogénesis/genética , Ciervos/crecimiento & desarrollo , Regulación del Desarrollo de la Expresión Génica , Secuenciación de Nucleótidos de Alto Rendimiento , Osteogénesis/genéticaRESUMEN
Deer antlers are amazing natural appendages that grow faster than any other known mammalian bone. Antler growth occurs at the tip and is initially cartilage, which is later replaced by bone tissue. However, little is known regarding the precise role of cooperation between cell lineages and functional genes in regulating antler growth, and molecular mechanisms responsible for rapid growth remain elusive. In this study, we use an RNA-Seq approach to elucidate the full spectrum of cell lineages, functional genes, and their cooperative interactions during antler growth. We identify Sox9 as a pivotal transcription factor during chondrogenesis and skeletal development expressed in the chondrocyte lineage from the multipotent mesenchymal precursor stage through most subsequent cell differentiation stages with a particularly strong activity in proliferating and prehypertrophic chondrocytes. Furthermore, we analyze the miRNA expression patterns at initial growth stage and rapid growth stage and identify several miRNAs that involve in regulating antler chondrogenesis and rapid growth. Among these miRNAs, miR-140 plays pivotal role during antler growth by targeting Sox9 and vice versa.