RESUMO
Centromeres in eukaryotes are composed of highly repetitive DNAs, which evolve rapidly and are thought to achieve a favorable structure in mature centromeres. However, how the centromeric repeat evolves into an adaptive structure is largely unknown. We characterized the centromeric sequences of Gossypium anomalum through chromatin immunoprecipitation against CENH3 antibodies. We revealed that the G. anomalum centromeres contained only retrotransposon-like repeats but were depleted in long arrays of satellites. These retrotransposon-like centromeric repeats were present in the African-Asian and Australian lineage species, suggesting that they might have arisen in the common ancestor of these diploid species. Intriguingly, we observed a substantial increase and decrease in copy numbers among African-Asian and Australian lineages, respectively, for the retrotransposon-derived centromeric repeats without apparent structure or sequence variation in cotton. This result indicates that the sequence content is not a decisive aspect of the adaptive evolution of centromeric repeats or at least retrotransposon-like centromeric repeats. In addition, two active genes with potential roles in gametogenesis or flowering were identified in CENH3 nucleosome-binding regions. Our results provide new insights into the constitution of centromeric repetitive DNA and the adaptive evolution of centromeric repeats in plants.
Assuntos
Gossypium , Retroelementos , Gossypium/genética , Austrália , Centrômero/genéticaRESUMO
A metal-free environmentally benign, simple, and efficient transfer hydrogenation process of quinoxaline has been developed using the HBpin reagent as a hydrogen source. This reaction is compatible with a variety of quinoxalines offering the desired tetrahydroquinoxalines in moderate-to-excellent yields with Bu4NBr as a noncorrosive and low-cost catalyst.
Assuntos
Hidrogênio , Quinoxalinas , Catálise , Hidrogenação , Compostos de Amônio QuaternárioRESUMO
An efficient, catalyst/photocatalyst-free, and cost-effective methodology for the decarboxylative alkylation of α,ß-unsaturated carboxylic acids to synthesize ß,γ-unsaturated nitriles has been developed. The reaction proceeded in an environmentally benign atmosphere of blue light-emitting diode irradiation with K2CO3 and water at room temperature. The methodology worked for a wide range of substrates (22 examples) with up to 83% yield. The protocol is also compatible for gram-scale synthesis.
RESUMO
A palladium-catalyzed asymmetric hydrogenation of levulinic acid has been successful developed by using Zn(OTf)2 as co-catalyst. The present method not only has provided a strategy in the palladium-catalyzed asymmetric hydrogenation of ketone, but also allowed the preparation of a wide range of chiral γ-valerolactones in good yields with excellent enantioselectivities.
RESUMO
An efficient method for the dehydrogenative coupling of silanes with alcohols under photocatalysis was developed. The reaction proceeded in the presence of Ru(bpy)3Cl2 (0.5 mol%) under visible light irradiation in acetonitrile at room temperature. The developed methodology was also applicable for the synthesis of silanols using water as a coupling partner.
RESUMO
BACKGROUND: Emerging evidence show that long noncoding RNAs (lncRNAs) are crucial regulators in pathophysiology of acute lung injury (ALI). Small nucleolar RNA host gene 14 (SNHG14) is a novel oncogenic lncRNA, and has been associated with inflammation-related cell injuries. Thus, we wondered the role and mechanism of SNHG14 in lipopolysaccharides (LPS)-induced ALI cell model. METHODS: Expression of SNHG14, miRNA (miR)-124-3p, and transforming growth factor ß type 2 receptor (TGFBR2) was detected by RT-qPCR and western blotting. Cell apoptosis was determined by methyl thiazolyl tetrazolium assay, flow cytometry, western blotting, and lactate dehydrogenase activity kit. Inflammation was measured by enzyme-linked immunosorbent assay. The interaction among SNHG14, miR-124-3p, and TGFBR2 was validated by dual-luciferase reporter assay and RNA immunoprecipitation. RESULTS: LPS administration attenuated human lung epithelial cell viability and B-cell lymphoma-2 expression, but augmented apoptosis rate, cleaved-caspase-3 expression, lactate dehydrogenase activity, and secretions of tumor necrosis factor-α, interleukin-1ß, and IL-6 in A549 cells. Thus, LPS induced A549 cells apoptosis and inflammation, wherein SNHG14 was upregulated and miR-124-3p was downregulated. However, silencing SNHG14 could suppress LPS-induced apoptosis and inflammation depending on upregulating miR-124-3p via target binding. Similarly, overexpressing miR-124-3p attenuated LPS-induced A549 cells injury through inhibiting its downstream target TGFBR2. Furthermore, SNHG14 knockdown could also affect TGFBR2 expression via miR-124-3p. CONCLUSIONS: SNHG14 knockdown prevents A549 cells from LPS-induced apoptosis and inflammation through regulating miR-124-3p and TGFBR2, suggesting a novel SNHG14/miR-124-3p/TGFBR2 circuit in alveolar epithelial cells on the set of ALI.
Assuntos
Lesão Pulmonar Aguda/genética , MicroRNAs/metabolismo , RNA Longo não Codificante/metabolismo , Receptor do Fator de Crescimento Transformador beta Tipo II/genética , Células A549 , Lesão Pulmonar Aguda/imunologia , Apoptose/genética , Apoptose/imunologia , Sobrevivência Celular/genética , Sobrevivência Celular/imunologia , Regulação para Baixo/imunologia , Perfilação da Expressão Gênica , Técnicas de Silenciamento de Genes , Humanos , Lipopolissacarídeos/imunologia , MicroRNAs/agonistas , MicroRNAs/genética , RNA Longo não Codificante/genética , Regulação para Cima/imunologiaRESUMO
AIM: The present study explored the clinical significance of microRNA-22 (miR-22) expression in lung squamous cell carcinoma and to explore the targeting relationship with vascular endothelial growth factor receptor 3 (VEGFR3). METHODS: A total of 49 patients with lung squamous cell carcinoma who underwent surgical treatment were selected. The expression of miR-22 was detected by fluorescence quantitative realtime PCR (qPCR), the expression of VEGFR3 was detected by Western blotting assays, and D240 labeled microlymphatic vessels density (MLVD) was detected by immunohistochemistry (IHC). Lung squamous cell carcinoma cell line SK-MES-1 was selected and the targeting relationship between miR-22 and VEGFR3 was analyzed by double luciferase reporter gene assay. Western blotting assays were used to detect the expression of vascular endothelial growth factor-D (VEGFD) and D240 in the blank control group, empty vector transfection group, miR-22 transfection group, miR-22 and VEGFR3 co-transfection group. RESULTS: The expression range of miR-22 in lung squamous cell carcinoma was 0.8-3.5. The expression of miR-22 in lung squamous cell carcinoma was significantly different by tumor maximum diameter, lymph node metastasis, vascular invasion and TNM stage. The expression of miR-22 was linked to survival time. There was a negative correlation between miR-22 and VEGFR3, miR-22 and MLVD. Double luciferase reporter gene assays showed that miR-22 reduced the luciferase activity of pGL3-VEGFR3-WT transfected cells. Compared with the control group, the expression of VEGF-D and D2-40 in the miR-22 transfection group was significantly decreased. However, VEGF-D and D240 in the miR-22 and VEGFR3 co-transfection group reversed the changes. CONCLUSION: We assumed that the abnormal expression of miR-22 in lung squamous cell carcinoma may be involved in the development and progression of lung squamous cell carcinoma. MiR-22 negatively regulated the target gene VEGFR3 to mediate lymphangiogenesis. The expression of miR-22 may also be linked to the prognosis of the disease.
Assuntos
Carcinoma de Células Escamosas/metabolismo , Neoplasias Pulmonares/metabolismo , MicroRNAs/metabolismo , Receptor 3 de Fatores de Crescimento do Endotélio Vascular/metabolismo , Linhagem Celular Tumoral , Proliferação de Células/efeitos dos fármacos , Feminino , Regulação Neoplásica da Expressão Gênica , Humanos , Pulmão , Metástase Linfática , Masculino , Prognóstico , Fator D de Crescimento do Endotélio Vascular/genética , Fator D de Crescimento do Endotélio Vascular/metabolismoRESUMO
Cigarette smoking plays an important role in increased incidence of chronic obstructive pulmonary disease (COPD). The underlying mechanism in which cigarette smoking induced impairment of lung epithelial cells is still unknown. SIRT5 is a nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylase, which has been implicated in the regulation of metabolism, stress responses, and aging. Forkhead box O3 (FOXO3) belongs to the O subclass of the forkhead family of transcription factors. It is also involved in protection from oxidative stress by upregulating antioxidants in epithelial cells. Here, we show that cigarette smoke extract (CSE) induces SIRT5 to deacetylate FOXO3 at K271 and K290. Deacetylation of FOXO3 promotes its nuclear localization. Notably, transfection with FOXO3 K271R- or K290R-attenuated CSE-induced apoptosis in SIRT5 knocked down cells, suggesting the protective effects of SIRT5, is mediated by FOXO3. In contrast, CSE stress upregulates SIRT5, which activates FOXO3α leading to rescuing apoptosis. Thus, SIRT5 constitutes a determinant of apoptosis by CSE in lung epithelial cells.