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1.
J Biomed Mater Res A ; 2021 Apr 06.
Artigo em Inglês | MEDLINE | ID: mdl-33822474

RESUMO

Native decellularized extracellular matrix provides an adequate platform for tissues and organs and promotes the development of organogenesis and tissue remodeling. However, thrombosis poses a great challenge that hinders the transplantation for a substantial organ in vivo. Therefore, anticoagulation and re-reendothelialization of organ biological scaffolds are the primary concerns to be addressed before orthotopic transplantation. Herein, a heparinized decellularized kidney scaffold (HEP-DKSs) was prepared using end-point attachment technology, followed by binding the vascular endothelial growth factor (VEGF) to greatly improve the hemocompatibility and angiogenesis of DKSs. Based on the anticoagulant, co-culture of human umbilical vein endothelial cells, and subcapsular transplantation of kidney experiments, HEP-VEGF-DKSs are shown to reduce platelet adhesion, which is crucial for subsequent vascularization and slow release of heparin and VEGF, suggesting its ability of improve neovascularization. Taken together, these data indicated an optimal anticoagulation function of HEP-VEGF-DKSs and the potential of vascularization for regeneration of whole decellularized kidney.

2.
mBio ; 12(2)2021 03 30.
Artigo em Inglês | MEDLINE | ID: mdl-33785628

RESUMO

The ketogenic diet (KD), which can induce changes in gut microbiota, has shown benefits for epilepsy and several neurodegenerative diseases. However, the effects of a KD on glucose and lipid metabolism remain inconclusive. Using two formulas of ketogenic diets (KDR with 89.5% fat and KDH with 91.3% fat), which are commonly used in mouse trials, we found that KDR but not KDH induced insulin resistance and damaged glucose homeostasis, while KDH induced more fat accumulation in mice. Further study showed that KD impacted glucose metabolism, which was related to the sources of fat, while both the sources and proportions of fat affected lipid metabolism. And the KD widely used in human studies still induced insulin resistance and fat accumulation in mice. Moreover, KDs changed the gut microbiota and metabolites in mice, and the sources and proportions of fat in the diets respectively changed the abundance of specific bacteria and metabolites which were correlated with parameters related to glucose intolerance and lipid accumulation. Overall, our study demonstrated that the metabolic disorders induced by KDs are closely related to the source and proportion of fat in the diet, which may be associated with the changes of the gut microbiota and metabolites.IMPORTANCE The ketogenic diet with extremely high fat and very low carbohydrate levels is very popular in society today. Although it has beneficial effects on epilepsy and neurodegenerative diseases, how ketogenic diets impact host glucose and lipid metabolism and gut microbiota still needs further investigation. Here, we surveyed the effects of two ketogenic diets which are commonly used in mouse trials on metabolic phenotypes, gut microbiota, and metabolites in mice. We found that both ketogenic diets impaired glucose and lipid metabolism in mice, and this may be due to the sources and proportions of fat in the diets. This work highlights the potential risk of glucose and lipid metabolism disorders and the importance of evaluating the sources and proportions of fat in the diets, when using ketogenic diets for weight loss and the treatment of diseases.

3.
Biomed Eng Online ; 20(1): 18, 2021 Feb 09.
Artigo em Inglês | MEDLINE | ID: mdl-33563294

RESUMO

BACKGROUND: Advances in regenerative medicine technologies have been strongly proposed in the management of thyroid diseases. Mechanistically, the adoption of thyroid bioengineering requires a scaffold that shares a similar three-dimensional (3D) space structure, biomechanical properties, protein component, and cytokines to the native extracellular matrix (ECM). METHODS: 24 male New Zealand white rabbits were used in this experimental study. The rabbit thyroid glands were decellularized by immersion/agitation decellularization protocol. The 3D thyroid decellularization scaffolds were tested with histological and immunostaining analyses, scanning electron microscopy, DNA quantification, mechanical properties test, cytokine assay and cytotoxicity assays. Meanwhile, the decellularization scaffold were seeded with human thyroid follicular cells, cell proliferation and thyroid peroxidase were determined to explore the biocompatibility in vitro. RESULTS: Notably, through the imaging studies, it was distinctly evident that our protocol intervention minimized cellular materials and maintained the 3D spatial structure, biomechanical properties, ECM composition, and biologic cytokine. Consequently, the decellularization scaffold was seeded with human thyroid follicular cells, thus strongly revealing its potential in reinforcing cell adhesion, proliferation, and preserve important protein expression. CONCLUSIONS: The adoption of our protocol to generate a decellularized thyroid scaffold can potentially be utilized in transplantation to manage thyroid diseases through thyroid bioengineering.

4.
Int J Oncol ; 58(2): 278-279, 2021 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-33491746

RESUMO

Subsequently to the publication of the above article, an interested reader drew to the attention of the Editorial Office that, in Fig. 1C on p. 1242, the flow cytometric images contained what appeared to be regular and repeating groups of cells. The office consequently asked the authors to provide the raw data for these images, as they would have been generated from the printouts, and the authors were able to demonstrate that these apparent anomalies were not contained in the original data. It is possible that the anomalous appearance of the data in this Figure may have resulted either from low resolution of the images, or the Figure itself may have been compressed. We are reprinting Fig. 1C opposite, highlighting the data of interest in greater detail. We trust that this satisfies the concerns of the reader in this instance, and thank them for their enquiry to the Editorial Office. The authors also requested that, after having provided the raw data of the original image in order to clarify the concerns of the reader, they may republish Fig. 1 featuring alternative data for Fig. 1C. The revised version of Fig. 1 is consequently shown on the next page. In this figure, flow cytometric analysis demonstrated that treatment with 10 µM gemcitabine induced the death of 66.5% of the BxPC­3 cells, 29.54% of the Panc­1 cells, and 34.52% of the MIApaca­2 cells (Fig. 1C). The authors confirm that these data support the main conclusions presented in their paper, and are grateful to the Editor of International Journal of Oncology for allowing them this opportunity to publish a Corrigendum. They also apologise to the readership for any inconvenience caused. [the original article was published in International Journal of Oncology 51: 1239­1248, 2017; DOI: 10.3892/ijo.2017.4099].

5.
JAMA ; 325(3): 234-243, 2021 01 19.
Artigo em Inglês | MEDLINE | ID: mdl-33464335

RESUMO

Importance: For patients with large vessel occlusion strokes, it is unknown whether endovascular treatment alone compared with intravenous thrombolysis plus endovascular treatment (standard treatment) can achieve similar functional outcomes. Objective: To investigate whether endovascular thrombectomy alone is noninferior to intravenous alteplase followed by endovascular thrombectomy for achieving functional independence at 90 days among patients with large vessel occlusion stroke. Design, Setting, and Participants: Multicenter, randomized, noninferiority trial conducted at 33 stroke centers in China. Patients (n = 234) were 18 years or older with proximal anterior circulation intracranial occlusion strokes within 4.5 hours from symptoms onset and eligible for intravenous thrombolysis. Enrollment took place from May 20, 2018, to May 2, 2020. Patients were enrolled and followed up for 90 days (final follow-up was July 22, 2020). Interventions: A total of 116 patients were randomized to the endovascular thrombectomy alone group and 118 patients to combined intravenous thrombolysis and endovascular thrombectomy group. Main Outcomes and Measures: The primary end point was the proportion of patients achieving functional independence at 90 days (defined as score 0-2 on the modified Rankin Scale; range, 0 [no symptoms] to 6 [death]). The noninferiority margin was -10%. Safety outcomes included the incidence of symptomatic intracerebral hemorrhage within 48 hours and 90-day mortality. Results: The trial was stopped early because of efficacy when 234 of a planned 970 patients had undergone randomization. All 234 patients who were randomized (mean age, 68 years; 102 women [43.6%]) completed the trial. At the 90-day follow-up, 63 patients (54.3%) in the endovascular thrombectomy alone group vs 55 (46.6%) in the combined treatment group achieved functional independence at the 90-day follow-up (difference, 7.7%, 1-sided 97.5% CI, -5.1% to ∞)P for noninferiority = .003). No significant between-group differences were detected in symptomatic intracerebral hemorrhage (6.1% vs 6.8%; difference, -0.8%; 95% CI, -7.1% to 5.6%) and 90-day mortality (17.2% vs 17.8%; difference, -0.5%; 95% CI, -10.3% to 9.2%). Conclusions and Relevance: Among patients with ischemic stroke due to proximal anterior circulation occlusion within 4.5 hours from onset, endovascular treatment alone, compared with intravenous alteplase plus endovascular treatment, met the prespecified statistical threshold for noninferiority for the outcome of 90-day functional independence. These findings should be interpreted in the context of the clinical acceptability of the selected noninferiority threshold. Trial Registration: Chinese Clinical Trial Registry: ChiCTR-IOR-17013568.


Assuntos
Fibrinolíticos/administração & dosagem , /cirurgia , Trombectomia , Ativador de Plasminogênio Tecidual/administração & dosagem , Doença Aguda , Idoso , Hemorragia Cerebral/etiologia , Terapia Combinada , Procedimentos Endovasculares , Feminino , Fibrinolíticos/efeitos adversos , Humanos , Infusões Intravenosas , Masculino , Pessoa de Meia-Idade , Trombectomia/efeitos adversos , Ativador de Plasminogênio Tecidual/efeitos adversos
6.
Am J Clin Nutr ; 113(2): 338-347, 2021 02 02.
Artigo em Inglês | MEDLINE | ID: mdl-33330917

RESUMO

BACKGROUND: Single measurements of waist circumference (WC) predict the incident cardiovascular disease (CVD); however, long-term patterns of WC and their association with the incidence of CVD are poorly characterized. OBJECTIVE: We aimed to identify WC trajectories and determine their association with incident CVD (stroke and myocardial infarction) and examine whether the association persisted among individuals without obesity. METHODS: We included 75,535 participants from a community-based cohort in China who were aged >18 y and free of stroke, coronary artery disease, and cancer in 2010 (the baseline). WC and other covariates were repeatedly measured in 2006, 2008, and 2010. WC trajectories were identified by latent mixture modeling. A Cox proportional hazards model was used to examine the association between WC trajectories and incident CVD, after adjustment for age, sex, income, education, systolic blood pressure, lipid profiles, plasma concentrations of glucose, C-reactive protein, smoking, and alcohol drinking. RESULTS: We identified 4 WC trajectories based on 2006 WC measurement and change patterns during 2006-2010: low stable (n = 12,072; mean WC 74.1-75.1 cm), moderate stable (n = 41,750; mean WC 85.1-86.6 cm), moderate-high stable (n = 19,914; mean WC 95.6-97.2 cm), and high stable (n = 1,799; mean WC 106.3-110.9 cm). During 2010-2016, we documented 2819 incident CVD events. Compared with the low-stable group, groups with elevated WC trajectories had a higher risk of CVD events during 6 y of follow-up (2010-2016). Adjusted HRs (95% CIs) were 1.49 (1.21, 1.83) for the moderate stable group, 1.71(1.38, 2.12) for the moderate-high stable group, and 1.45 (1.06, 2.00) for the high stable group. After further adjusting for BMI or excluding obese participants, we observed similar results. The positive association between WC and incident CVD was higher in individuals who were aged <60 y (P-interaction < 0.0001). CONCLUSIONS: WC trajectory patterns were associated with altered risk of CVD among Chinese adults, even among people without BMI-defined obesity. When stratifying by age, the association was observed to be higher in younger adults.


Assuntos
Doenças Cardiovasculares/epidemiologia , Circunferência da Cintura , Adulto , China/epidemiologia , Estudos de Coortes , Feminino , Humanos , Masculino , Pessoa de Meia-Idade
7.
Sci Adv ; 6(48)2020 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-33246959

RESUMO

Nanozymes as artificial enzymes that mimicked natural enzyme-like activities have received great attention in cancer therapy. However, it remains a great challenge to design nanozymes that precisely exert its activity in tumor without producing off-target toxicity to surrounding normal tissues. Here, we report a synergetic enhancement strategy through the combination between nanozyme and tumor vascular normalization to destruct tumors, which was based on tumor microenvironment (TME) "unlocking." This nanozyme that we developed not only has photothermal properties but also can produce reactive oxygen species efficiently under the stimulation of TME. Moreover, this nanozyme also showed remarkable imaging performance in fluorescence imaging in the second near-infrared region and magnetic resonance imaging for visualization tracing in vivo. The process of combination therapy showed remarkable therapeutic effect for breast cancer. This study provides a therapeutic strategy by the cooperation between multifunctional nanozyme and tumor vascular normalization for intensive combination therapy of breast cancer.

8.
Dalton Trans ; 49(43): 15433-15442, 2020 Nov 10.
Artigo em Inglês | MEDLINE | ID: mdl-33140784

RESUMO

Octahedral [CaY]F2 crystals with an average particle size of 1 µm were synthesized via a mild one-step hydrothermal route without employing any surfactants. Various morphologies, including cubes, truncated cubes, truncated octahedrons, and spheres, were achieved via manipulating the amount of EDTA used, and a possible growth mechanism was proposed based on the surface energies of different crystal planes and the influence of the surfactant. XRD, SEM, EDS, TEM, HRTEM, and PL analysis were used to characterize the products. The effects of the morphologies and Li+ doping concentrations on the luminescence intensities of the [CaY]F2:Ce3+/Tb3+ phosphors were explored, and the strongest luminescence intensity is obtained when the sample is cubic with (100) crystal faces and the doping concentration of Li+ is 0.25 mol%. Additionally, multicolor emission (blue → aquamarine blue → green) was obtained from [CaY]F2:Ce3+/Tb3+ phosphors via adjusting the doping concentration of Tb3+, which resulted from the Ce3+ → Tb3+ energy transfer behavior; the energy transfer here happened through a dipole-dipole mechanism. This work may result in the as-synthesized phosphors having great application potential in many optoelectronic device fields, such as in displays and multicolor lighting.

9.
Biomed Pharmacother ; 132: 110898, 2020 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-33113432

RESUMO

Nasopharyngeal carcinoma (NPC) is a malignant tumor originating from the superior mucosal epithelium of the nasopharynx. However, effective therapies for NPC are still required. Reducing Hedgehog signaling pathway has been shown to suppress tumor growth. In this study, we attempted to explore whether Jervine (JV), an inhibitor of Hedgehog signaling, had anti-cancer effects on NPC, and the underlying mechanisms. Our findings showed that JV treatments markedly reduced the proliferation of NPC cells in a dose- and time-dependent manner. Cell cycle arrest in G2/M phase was significantly enhanced by JV, along with evident DNA damage. Moreover, JV treatment effectively induced apoptosis in NPC cells through improving Caspase-3 activation. Furthermore, ROS production and mitochondrial impairments were detected in JV-incubated NPC cells with elevated releases of Cyto-c from mitochondria. JV also dramatically triggered autophagy through blocking AKT/mTOR and increasing AMPK signaling pathways. Intriguingly, we showed that JV-induced apoptosis was mainly via an autophagy-dependent manner. In addition, the expression levels of SHH, PTCH1, SMO and GLI1 were markedly suppressed in NPC cells, demonstrating the hindered Hedgehog signaling. Importantly, we found that JV-induced apoptosis and autophagy were closely associated with the blockage of Hedgehog signaling. Our in vivo studies confirmed the anti-cancer effects of JV on NPC through inducing autophagy, as evidenced by the markedly reduced tumor growth rate and weight without side effects and toxicity. Taken together, JV may be a promising and effective agent for human NPC treatment through repressing Hedgehog signaling pathway and inducing autophagic cell death.

10.
Mol Med Rep ; 22(3): 1976-1984, 2020 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-32705248

RESUMO

Nephrotic syndrome (NS) is one of the most common causes of chronic kidney disease in the pediatric population. Hyperlipidemia is one of the main features of NS. The present study investigated the role of CXC motif chemokine ligand 16 (CXCL16) and ADAM metallopeptidase domain 10 (ADAM10) in oxidized low­density lipoprotein (oxLDL)­stimualted podocytes and the underlying mechanisms. CXCL16 and ADAM10 expression levels in oxLDL­treated podocytes were measured via reverse transcription­quantitative PCR and western blotting. Cell migration assays were conducted to assess the migration of oxLDL­treated podocytes. CXCL16 or ADAM10 overexpression and knockdown assays were conducted. The results indicated that oxLDL stimulation increased ADAM10 and CXCL16 expression levels, and enhanced podocyte migration compared with the control group. Moreover, CXCL16 and ADAM10 overexpression significantly increased podocyte migration and the expression of actinin­α4 (ACTN4) compared with the control groups. By contrast, CXCL16 and ADAM10 knockdown significantly reduced podocyte migration and the expression of ACTN4 compared with the control groups. The results suggested that oxLDL promoted podocyte migration by regulating CXCL16 and ADAM10 expression, as well as by modulating the actin cytoskeleton. Therefore, CXCL16 and ADAM10 may serve as novel therapeutic targets for primary nephrotic syndrome in children.

12.
Chin Med J (Engl) ; 133(10): 1192-1202, 2020 May 20.
Artigo em Inglês | MEDLINE | ID: mdl-32433051

RESUMO

BACKGROUND: Pulmonary fibrosis is a respiratory disease caused by the proliferation of fibroblasts and accumulation of the extracellular matrix (ECM). It is known that the lung ECM is mainly composed of a three-dimensional fiber mesh filled with various high-molecular-weight proteins. However, the small-molecular-weight proteins in the lung ECM and their differences between normal and fibrotic lung ECM are largely unknown. METHODS: Healthy adult male Sprague-Dawley rats (Rattus norvegicus) weighing about 150 to 200 g were randomly divided into three groups using random number table: A, B, and C and each group contained five rats. The rats in Group A were administered a single intragastric (i.g.) dose of 500 µL of saline as control, and those in Groups B and C were administered a single i.g. dose of paraquat (PQ) dissolved in 500 µL of saline (20 mg/kg). After 2 weeks, the lungs of rats in Group B were harvested for histological observation, preparation of de-cellularized lung scaffolds, and proteomic analysis for small-molecular-weight proteins, and similar procedures were performed on Group C and A after 4 weeks. The differentially expressed small-molecular-weight proteins (DESMPs) between different groups and the subcellular locations were analyzed. RESULTS: Of the 1626 small-molecular-weight proteins identified, 1047 were quantifiable. There were 97 up-regulated and 45 down-regulated proteins in B vs. A, 274 up-regulated and 31 down-regulated proteins in C vs. A, and 237 up-regulated and 28 down-regulated proteins identified in C vs. B. Both the up-regulated and down-regulated proteins in the three comparisons were mainly distributed in single-organism processes and cellular processes within biological process, cell and organelle within cellular component, and binding within molecular function. Further, more up-regulated than down-regulated proteins were identified in most sub-cellular locations. The interactions of DESMPs identified in extracellular location in all comparisons showed that serum albumin (Alb) harbored the highest degree of node (25), followed by prolyl 4-hydroxylase beta polypeptide (12), integrin ß1 (10), apolipoprotein A1 (9), and fibrinogen gamma chain (9). CONCLUSIONS: Numerous PQ-induced DESMPs were identified in de-cellularized lungs of rats by high throughput proteomics analysis. The DESMPs between the control and treatment groups showed diversity in molecular functions, biological processes, and pathways. In addition, the interactions of extracellular DESMPs suggested that the extracellular proteins Alb, Itgb1, Apoa1, P4hb, and Fgg in ECM could be potentially used as biomarker candidates for pulmonary fibrosis. These results provided useful information and new insights regarding pulmonary fibrosis.

13.
J Exp Clin Cancer Res ; 39(1): 61, 2020 Apr 09.
Artigo em Inglês | MEDLINE | ID: mdl-32272940

RESUMO

BACKGROUND: Revealing the mechanical role of long non-coding RNAs (lncRNAs) in tumorigenesis can contribute to novel therapeutic target for cancers. The regulatory role of linc01134 in hepatocellular carcinoma (HCC) has not been studied yet. MATERIALS AND METHODS: qRT-PCR and western blot were conducted to measure relevant RNA and protein expressions. CCK-8, colony formation, EdU, flow cytometry, wound-healing, transwell assays and xenograft experiments were performed to determine the role of linc01134 in HCC. ChIP and luciferase reporter assays were performed to analyze the effects of Yin Yang-1 (YY1) on linc01134 transcription activity. Relevant mechanical experiments were performed to verify interaction between relative genes. RESULTS: YY1 enhanced linc01134 transcription by interacting with linc01134 promoter. Knockdown of linc01134 inhibited proliferation, migration and epithelial-mesenchymal transition (EMT), yet promoting apoptosis in HCC cells. Mechanically, linc01134 acted as miR-324-5p sponge and interacted with insulin-like growth factor 2 mRNA binding protein 1 (IGF2BP1) to increase the stability of YY1 mRNA expression. Up-regulated YY1 continuously stimulated linc01134 expression by enhancing linc01134 promoter activity, forming a positive feedback loop. CONCLUSION: Linc01134/miR-324-5p/IGF2BP1/YY1 feedback loop mediates HCC progression, which possibly provide prognosis and treatment target of HCC.

14.
Cancer Med ; 9(10): 3437-3444, 2020 May.
Artigo em Inglês | MEDLINE | ID: mdl-32207253

RESUMO

There were no ideal markers to predict the development of radiation pneumonitis (RP). We want to investigate the value of variations of lymphocytes and T lymphocyte subsets in predicting RP after radiotherapy (RT) of lung cancer based on previous clinical findings. A total of 182 lung cancer patients who received RT were retrospectively analyzed. Circulating lymphocytes and T lymphocyte subsets were measured before, during, and after RT. Patients were evaluated from the start of RT to 6 months post-RT. A mice model with acute radiation-induced lung injury was established and circulating lymphocytes were measured weekly until 8 weeks after irradiation. Univariate and multivariate analyses were adopted to identify risk factors of RP. Lymphocyte levels significantly decreased (P < .001) in patients before RP symptoms developed that also was able to be seen in the mice model and the values recovered during remission of symptoms. The decrease in lymphocyte count reflected the severity of RP. Meanwhile, CD4+  T lymphocyte count was significantly lower during the occurrence of symptoms in patients with RP than in those without RP (P < .001), and it improved along with RP recovery. Levels of lymphocytes and CD4+  T lymphocyte subsets proved as independent predictors of RP. Here we showed that lower peripheral blood levels of lymphocytes and CD4+  T lymphocyte were associated with an increased risk of RP, which was validated by this mice model, and thus are associated with differences in radiation-induced lung toxicity among individuals and help identify those who are susceptible to developing RP after RT.

15.
J Cell Physiol ; 235(7-8): 5711-5721, 2020 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-31975384

RESUMO

Dysregulation of microRNAs (miRNAs) expression has been demonstrated in gastrointestinal stromal tumor (GIST). In this study, we aimed to determine the differential miRNAs expression in GISTs and explore the functional mechanism of differential miRNAs in GIST cells. We measured differential miRNAs in six pairs of GIST tissues and matched adjacent tissues through a high-throughput sequencing, which was confirmed in 64 pairs of GIST tissues and adjacent tissues by real-time polymerase chain reaction. We found that miR-4510 expression was significantly downregulated in GIST tissues compared to matched control tissues. Luciferase reporter assay identified apolipoprotein C-II (APOC2) as a direct target of miR-4510. Overexpression of miR-4510 inhibited the mRNA and protein expression of APOC2. In addition, overexpression of miR-4510 suppressed GIST cell proliferation, migration, and invasion. Overexpression of miR-4510 also inhibited the phosphorylation of AKT and ERK1/2, reduced the expression of matrix metallopeptidase 2 (MMP2) and MMP9. APOC2 knockdown mimicked the effect of miR-4510 overexpression. Further investigation confirmed that APOC2 was notably upregulated in GIST tissues compared to adjacent control tissues. These results suggested that miR-4510 downregulation could promote GIST progression, including growth, invasion, and metastasis, through increasing APOC2 expression.

16.
Plant Dis ; 104(2): 521-526, 2020 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-31801036

RESUMO

Rice orange leaf disease (ROLD), caused by rice orange leaf phytoplasma (ROLP), is transmitted by leafhopper vectors Recilia dorsalis and Nephotettix cinticeps. ROLD severely devastates rice production in Asia. Accurate detection of the pathogen is important for disease management. Current nested polymerase chain reaction (nested PCR) method using phytoplasma universal primers is widely used to detect phytoplasmas; however, it has shortcoming of inconvenience and inaccuracy, for it needs two round of PCR reactions and could produce false positive results due to nontarget amplification. In this study, we developed a PCR assay using a set of primers designed based on the ROLP genome sequence to amplify house-keeping gene FtsH-1 in rice and leafhopper vector samples. This method is simple and rapid, and its sensitivity up to 10 pg/µl of total ROLP DNA. It also minimizes the false positive problem produced by nested PCR. This method was used to survey the geographic distribution of ROLD in southern China from 2016 to 2018. The results showed that the distribution areas and vector carrying rate of ROLD had gradually increased.


Assuntos
Oryza , Phytoplasma , Animais , China , Doenças das Plantas , Reação em Cadeia da Polimerase
17.
Exp Cell Res ; 386(1): 111713, 2020 01 01.
Artigo em Inglês | MEDLINE | ID: mdl-31705846

RESUMO

Reprogrammed glucose metabolism is essential for tumor initiation and development, especially for pancreatic ductal adenocarcinoma (PDAC). Most cancer cells rely on aerobic glycolysis, a phenomenon termed "the Warburg effect", to support uncontrolled proliferation and evade apoptosis. However, the direct regulators of the Warburg effect remain areas of active investigation. In this study, we found that the highly conserved transcription factor, TWIST1, is a crucial regulator of aerobic glycolysis in PDAC. Genetic silencing of TWIST1 significantly inhibited the glycolytic phenotypes of PDAC cells as revealed by reduced glucose uptake, lactate production, and extracellular acidification rate, which can be restored by re-expression of siRNA-resistant TWIST1. Moreover, tamoxifen-inducible expression of TWIST1 promoted the Warburg metabolism of PDAC cells. Mechanistically, by luciferase reporter assay and chromatin immunoprecipitation experiment, we showed that TWIST1 can directly increase the expression of several glycolytic genes, including SLC2A1, HK2, ENO1, and PKM2. Of note, the transcriptional regulation by TWIST1 was not dependent on HIF1α or c-Myc. In The Cancer Genome Atlas and Gene Expression Omnibus accession GSE15471, we confirmed that TWIST1 was closely associated with the glycolysis pathway. Collectively, our findings indicate that TWIST1 is likely to act as important regulator of the Warburg effect in PDAC.


Assuntos
Adenocarcinoma/metabolismo , Regulação Neoplásica da Expressão Gênica , Glicólise , Proteínas Nucleares/genética , Neoplasias Pancreáticas/metabolismo , Proteína 1 Relacionada a Twist/genética , Adenocarcinoma/genética , Adenocarcinoma/patologia , Biomarcadores Tumorais/genética , Biomarcadores Tumorais/metabolismo , Proteínas de Transporte/genética , Proteínas de Transporte/metabolismo , Linhagem Celular Tumoral , Proteínas de Ligação a DNA/genética , Proteínas de Ligação a DNA/metabolismo , Transportador de Glucose Tipo 1/genética , Transportador de Glucose Tipo 1/metabolismo , Hexoquinase/genética , Hexoquinase/metabolismo , Humanos , Proteínas de Membrana/genética , Proteínas de Membrana/metabolismo , Neoplasias Pancreáticas/genética , Neoplasias Pancreáticas/patologia , Fosfopiruvato Hidratase/genética , Fosfopiruvato Hidratase/metabolismo , Hormônios Tireóideos/genética , Hormônios Tireóideos/metabolismo , Proteínas Supressoras de Tumor/genética , Proteínas Supressoras de Tumor/metabolismo
18.
Drug Chem Toxicol ; 43(4): 415-422, 2020 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-30192650

RESUMO

Amiodarone is a high effectiveness anti-arrhythmia agent which is able to induce pulmonary fibrosis. Many studies have shown that the epithelial-mesenchymal transition (EMT) was a significant process in pulmonary fibrosis. So far, there are no studies about whether EMT was associated with amiodarone-induced pulmonary fibrosis, which was therefore explored in this study. In addition, the underlying mechanisms of amiodarone-induced pulmonary fibrosis were examined in vitro. We found the EMT marker (α-SMA) was significantly increased, while the E-cadherin was significantly decreased in adenocarcinomic human alveolar basal epithelial cells (A549) after amiodarone treatment, suggesting that the epithelial cells were an important source of mesenchymal cells. Transforming growth factor beta1 (TGF-ß1) was also increased significantly after amiodarone treatment. In conclusion, this study suggested amiodarone could induce pulmonary fibrosis via EMT, and the TGF-ß1 may be a key profibrotic cytokine in mechanisms of amiodarone-induced pulmonary fibrosis.

20.
Biomed Pharmacother ; 120: 109483, 2019 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-31629252

RESUMO

Lung cancer is the leading cause of cancer-related deaths. Ginsenoside Rg3 is the main ingredient of Ginseng which is used to treat non-small cell lung cancer (NSCLC). It has been found to enhance the efficiency of chemotherapy thereby reducing its side effects. Previous studies found that ginsenoside Rg3 can reduce the occurrence of NSCLC by inducing DNA damage. Yet, its anti-DNA damaging effects and mechanisms in tumor cells are still not fully understood. This study explored the effect of ginsenoside Rg3 on DNA repair and VRK1/P53BP1 signaling pathway. Ginsenoside Rg3 treatment significantly decreased the incidence and invasionin a mouse model of lung cancer induced by urethane. The results of cell survival assay and single cell gel electrophoresis showed that ginsenoside Rg3 protected lung adenocarcinoma cells from DNA damage as well as inhibited the proliferation of tumor cells. Ginsenoside Rg3 increased the mRNA and protein expression of VRK1 in NSCLC cells as measured by RT-qPCR and western blot, respectively. These findings suggests that ginsenoside Rg3 regulates VRK1 signaling. Immunofluorescence assays showed that P53BP1 and VRK1 protein level increased, and the VRK1 protein translocated between the nuclei and cytoplasm. Finally, this conclusion was confirmed by the reverse validation in VRK1-knockdown cells. Taken together, these results show that ginsenoside Rg3 upregulate VRK1 expression and P53BP1 foci formation in response to DNA damage thereby inhibiting the tumorigenesis and viability of cancer cells. These findings reveal the role of Rg3 in lung cancer and provides therapeutic targets for developing new drugs in the prevention and treatment of lung cancer.


Assuntos
Carcinoma Pulmonar de Células não Pequenas/tratamento farmacológico , Dano ao DNA/efeitos dos fármacos , Ginsenosídeos/farmacologia , Neoplasias Pulmonares/tratamento farmacológico , Proteínas Serina-Treonina Quinases/metabolismo , Transdução de Sinais/efeitos dos fármacos , Proteína 1 de Ligação à Proteína Supressora de Tumor p53/metabolismo , Células A549 , Animais , Apoptose/efeitos dos fármacos , Carcinogênese/efeitos dos fármacos , Carcinogênese/metabolismo , Carcinoma Pulmonar de Células não Pequenas/metabolismo , Linhagem Celular Tumoral , Núcleo Celular/efeitos dos fármacos , Núcleo Celular/metabolismo , Sobrevivência Celular/efeitos dos fármacos , Citoplasma/efeitos dos fármacos , Citoplasma/metabolismo , Humanos , Neoplasias Pulmonares/metabolismo , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Panax/química , RNA Mensageiro/metabolismo , Regulação para Cima/efeitos dos fármacos
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