Objective. To investigate the clinical features of dermatomyositis (DM) and clinically amyopathic DM (CADM) patients
The varied rate of morbidity (both general and PTSD-specific) could be attributed to the relative impact of the earthquake as represented by epicenter proximity and as measured by the rate of property damage and loss in the three earthquake-affected areas.
Backgrounds: The NuRD (Nucleosome Remodeling and Deacetylation) complex is a repressive complex in gene transcription by modulating chromatin accessibility of target genes to transcription factors and RNA polymerase II. Although individual subunits of the complex have been implicated in many other cancer types, the complex's role in human hepatocellular carcinoma (HCC) is not fully understood. More importantly, the NuRD complex has not yet been investigated as a whole in cancers. Methods: We analyzed the expression of the NuRD complex in HCC and evaluated the prognostic value of NuRD complex expression in HCC using the RNA-seq data obtained from the TCGA project. We examined the effect of CHD4 knockdown on HCC cell proliferation, apoptosis, migration, invasion, epithelial-mesenchymal transition, colony-forming ability, and on complement gene expression. We also performed bioinformatic analyses to investigate the correlation between the NuRD complex expression and immune infiltration. Results: We found that nine subunits, out of 14 subunits of the NuRD complex examined, were significantly overexpressed in HCC, and their expression levels were positively correlated with cancer progression. More importantly, our data also demonstrated that these subunits tended to be overexpressed as a whole in HCC. Subsequent studies demonstrated that knockdown of CHD4 in HCC cells inhibits cell proliferation, migration, invasion, and colony-forming ability and promotes apoptosis of HCC cells, indicating that the CHD4/NuRD complex plays oncogenic roles in HCC. Further analysis revealed that the CHD4/NuRD complex regulates complement gene expression in HCC. Intriguingly, we found that the CHD4/NuRD complex expression was inversely correlated with CD8 T cell infiltration in HCC. Conclusions: Our data demonstrate that the CHD4/NuRD complex plays an oncogenic role in human HCC and regulates complement gene expression in HCC cells. The results of inverse correlation between the CHD4/NuRD complex and CD8 T cell and DC cell infiltration in HCC suggest that the CHD4/NuRD complex not only plays direct regulatory roles in HCC cells, but also has an impact on the immune microenvironment of HCC.
Background/Aims: Cardiac fibrosis after myocardial infarction (MI) has been identified as a key factor in the development of heart failure, but the mechanisms undelying cardiac fibrosis remained unknown. microRNAs (miRNAs) are novel mechanisms leading to fibrotic diseases, including cardiac fibrosis. Previous studies revealed that miR-22 might be a potential target. However, the roles and mechanisms of miR-22 in cardiac fibrosis remained ill defined. The present study thus addressed the impact of miR-22 in cardiac fibrosis. Methods: After seven days following coronary artery occlusion in mice, tissues used for histology were collected and processed for Masson's Trichrome staining. In addition, cardiac fibroblasts were transfected with mimics and inhibitors of miR-22 using Lipofectamin 2000, and luciferase activity was measured in cell lysates using a luciferase assay kit. Western blotting was used to detect the expression of collagen1, α-SMA and TGFβRI proteins levels, and real time-PCR was employed to measure the Col1α1, Col3α1, miR-22 and TGFβRI mRNA levels. Results: In this study, we found that miR-22 was dynamically downregulated following MI induced by permanent ligation of the left anterior descending coronary artery for 7 days, an effect paralleled by significant collagen deposition. Inhibition of miR-22 with AMO-22 resulted in increased expression of Col1α1, Col3α1 and fibrogenesis in cultured cardiac fibroblasts. Conversely, overexpression of miR-22 in cultured cardiac fibroblasts significantly abrogated angiotensin II-induced collagen formation and fibrogenesis. Furthermore, we found that TGFβRI is a direct target for miR-22, and downregulation of TGFβR may have mediated the antifibrotic effect of miR-22. Conclusion: Our data clearly demonstrate that miR-22 acts as a novel negative regulator of angiotensin II-induced cardiac fibrosis by suppressing the expression of TGFβRI in the heart and may represent a new potential therapeutic target for treating cardiac fibrosis.
Deficiency of certain elements can cause leaf chlorosis in Areca catechu L. trees, which causes considerable production loss. The linkage between nutrient deficiency and chlorosis phenomenon and physiological defect in A. catechu remains unclear. Here, we found that low iron supply is a determinant for chlorosis of A. catechu seedling, and excessive iron supply resulted in dark green leaves. We also observed morphological characters of A. catechu seedlings under different iron levels and compared their fresh weight, chlorophyll contents, chloroplast structures and photosynthetic activities. Results showed that iron deficiency directly caused chloroplast degeneration and reduced chlorophyll synthesis in chlorosis leaves, while excessive iron treatment can increase chlorophyll contents, chloroplasts sizes, and inflated starch granules. However, both excessive and deficient of iron decreases fresh weight and photosynthetic rate in A. catechu seedlings. Therefore, we applied transcriptomic and metabolomic approaches to understand the effect of different iron supply to A. catechu seedlings. The genes involved in nitrogen assimilation pathway, such as NR (nitrate reductase) and GOGAT (glutamate synthase), were significantly down-regulated under both iron deficiency and excessive iron. Moreover, the accumulation of organic acids and flavonoids indicated a potential way for A. catechu to endure iron deficiency. On the other hand, the up-regulation of POD-related genes was assumed to be a defense strategy against the excessive iron toxicity. Our data demonstrated that A. catechu is an iron-sensitive species, therefore the precise control of iron level is believed to be the key point for A. catechu cultivation.
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