MeCP2 triggers diabetic cardiomyopathy and cardiac fibroblast proliferation by inhibiting RASSF1A.

Diabetes causes cardiomyopathy and increases the risk of heart failure independent of hypertension and cardiac fibrosis disease. However, the molecular mechanism of cardiomyopathy caused by diabetic (DCM) is currently unknown. Here we explore the role of the Methyl CpG binding protein 2 (MeCP2) in DCM patients and a type 1 DM (T1DM) rat model.

[Content Levels and Compositions Characteristics of Volatile Organic Compounds(VOCs) Emission from Architectural Coatings Based on Actual Measurement].

The content levels and composition characteristics of Volatile Organic Compounds (VOCs) from architectural coatings including interior wall coatings, exterior wall coatings, waterproofing coatings, anticorrosive coatings and floor coatings were investigated in this study. Architectural coating samples were obtained from manufacturers and retail outlets and the associated VOC contents and compositions were determined based on the domestic standard methods for measurement of VOCs in architectural coatings.The results showed that the VOC contents were 0-145 g·L and 0-171 g·L for interior and exterior wall coatings respectively.

[Research and Application of the Technical Method for the Compilation of VOCs Emission Inventories from Architectural Coatings in Beijing].

VOCs(volatile organic compounds) are important precursors of ozone and secondary organic aerosols in the atmosphere, which increase atmospheric oxidation, creating pollutants such as photochemical smog, fine particulate matter and so on. This study documented information about architectural coating VOC emission characteristics to facilitate formulation of control strategies by environmental management departments. This research was based on measured data for architectural wall and waterproof coatings to identify localized emission factors, used industry research to compile additional information, and was combined with the Beijing completed building inventory, to develop a compilation method for VOC emissions from architectural coatings.

Pathological bases and clinical impact of long noncoding RNAs in prostate cancer: a new budding star.

Long non-coding RNAs (lncRNAs) are functional RNAs longer than 200 nucleotides. Recent advances in the non-protein coding part of human genome analysis have discovered extensive transcription of large RNA transcripts that lack coding protein function, termed non-coding RNA (ncRNA). It is becoming evident that lncRNAs may be an important class of pervasive genes involved in carcinogenesis and metastasis.

LncRNA GAS5 controls cardiac fibroblast activation and fibrosis by targeting miR-21 via PTEN/MMP-2 signaling pathway.

Long noncoding RNAs (LncRNAs) are aberrantly expressed in many diseases including cardiac fibrosis. LncRNA growth arrest-specific 5 (GAS5) is reported as a significant mediator in the control of cell proliferation and growth; however, the role and function in cardiac fibrosis remain unknown. In this study, we confirmed that GAS5 was lowly expressed in cardiac fibrosis tissues as well as activated cardiac fibroblast.

miR-200a controls hepatic stellate cell activation and fibrosis via SIRT1/Notch1 signal pathway.

Objectives: miR-200a has been established as a key regulator of HSC activation processes in liver fibrosis. Epigenetic silencing of miR-200a contributing to SIRT1 over-expression has been discussed in breast cancer; however, whether miR-200a controls SIRT1 gene expression in hepatic fibrosis is still unknown.

Methods And Materials: We analyzed miR-200a regulation of SIRT1 expression in CCl-induced liver fibrosis and TGF-β1-mediated activation of HSC.

MeCP2 silencing of LncRNA H19 controls hepatic stellate cell proliferation by targeting IGF1R.

Methyl-CpG-binding protein 2 (MeCP2) plays a key role in liver fibrosis. However, the potential mechanism of MeCP2 in liver fibrosis remains unclear. Early reports suggest that LncRNA H19 is important epigenetic regulator with critical roles in cell proliferation, but its role in hepatic fibrosis remains elusive.

Noncoding RNA as regulators of cardiac fibrosis: current insight and the road ahead.

Cardiac fibrosis is an important pathological feature of cardiac remodeling in heart diseases. The molecular mechanisms of cardiac fibrosis are unknown. Genomic analyses estimated that many noncoding DNA regions generate noncoding RNAs (ncRNAs).

Emerging role of long noncoding RNAs in lung cancer: Current status and future prospects.

Lung cancer is the leading cause of cancer-related death worldwide with a 5-year survival rate of less than 15%, despite significant advances in both diagnostic and therapeutic approaches. Combined genomic and transcriptomic sequencing studies have identified numerous genetic driver mutations that are responsible for the development of lung cancer. Importantly, these approaches have also uncovered the widespread expression of "noncoding RNAs" including long noncoding RNAs (LncRNAs), which impact biologic responses through the regulation of mRNA transcription or translation.

MeCP2 regulation of cardiac fibroblast proliferation and fibrosis by down-regulation of DUSP5.

Cardiac fibrosis is a complex pathological process that includes the abnormal proliferation of cardiac fibroblasts and deposition of the extracellular matrix (ECM) proteins and collagens. Methyl-CpG-binding protein 2 (MeCP2) is a multifunctional nuclear protein, and plays a key role in the fibrotic diseases. However, the potential role of MeCP2 in cardiac fibrosis remains unclear.

Non-coding RNA-mediated epigenetic regulation of liver fibrosis.

Hepatic stellate cells (HSC) activation plays a key role in liver fibrosis. Numerous studies have indicated that non-coding RNAs (ncRNAs) control liver fibrosis and fibroblasts proliferation. Greater knowledge of the role of the ncRNAs-mediated epigenetic mechanism in liver fibrosis could improve understanding of the liver fibrosis pathogenesis.

MicroRNA-200a controls Nrf2 activation by target Keap1 in hepatic stellate cell proliferation and fibrosis.

Hepatic fibrosis is a common final pathological process in the progression of liver disease, which is primarily due to oxidative stress. Nrf2 is known to coordinate induction of genes that encode antioxidant enzymes. Moreover, Nrf2 expression is largely regulated through the association of Nrf2 with Keap1, which results in cytoplasmic Nrf2 degradation.

DNA methylation in cardiac fibrosis: new advances and perspectives.

Cardiac fibrosis is characterized by net accumulation of extracellular matrix (ECM) proteins in the cardiac interstitium, and contributes to both systolic and diastolic dysfunction in many cardiac pathophysiologic conditions. More specifically, cardiac fibroblasts are activated by a variety of pathological stimuli, thereby undergoing proliferation, differentiation to myofibroblasts, and production of various cytokines and ECM proteins. Thus, understanding the biological processes of cardiac fibroblasts will provide novel insights into the underlying mechanisms of cardiac fibrosis.

Effect of oxymatrine on the p38 mitogen-activated protein kinases signalling pathway in rats with CCl4 induced hepatic fibrosis.

Background: Recent studies have suggested that p38 mitogen-activated protein kinases (MAPK) signalling pathway plays an important role in hepatic fibrosis. This study explored the antifibrotic effect of oxymatrine on tetrachloromethane induced liver fibrosis in rats and its modulation on the p38 MAPK signalling pathway.

Methods: One hundred and twenty healthy male Sprague-Dawley rats were randomly assigned to six groups: normal (n = 20), induced fibrosis (n = 20), colchicine (n = 20) and three treatment groups of oxymatrine (n = 20 x 3).