A5101942631- Chromatin Remodeling and Cancer
- Epigenetics and DNA Methylation
- RNA modifications and cancer
- MicroRNA in disease regulation
- Cancer-related gene regulation
- Cancer, Hypoxia, and Metabolism
- Histone Deacetylase Inhibitors Research
- Signaling Pathways in Disease
- Advanced Radiotherapy Techniques
- Radiation Dose and Imaging
- Advanced X-ray and CT Imaging
- Nuclear Receptors and Signaling
- Medical Imaging Techniques and Applications
- Immune cells in cancer
- Kruppel-like factors research
- Cancer Mechanisms and Therapy
- Circular RNAs in diseases
- Endoplasmic Reticulum Stress and Disease
- Neuroinflammation and Neurodegeneration Mechanisms
- Immune Cell Function and Interaction
- Adenosine and Purinergic Signaling
- RNA Interference and Gene Delivery
- Cardiac Fibrosis and Remodeling
- RNA regulation and disease
- interferon and immune responses
Jiangsu Vocational College of Medicine
2013-2024
Liaocheng University
2019-2021
Soochow University
2014-2021
Nanjing Medical University
2008-2018
Jiangsu Provincial Hospital of Traditional Chinese Medicine
2017
Jiangsu Province Hospital
2015-2017
Nanjing University of Chinese Medicine
2017
China Pharmaceutical University
2014-2017
State Key Laboratory of Reproductive Medicine
2016
Army Medical University
2013-2015
Background: Excessive accumulation of reactive oxygen species (ROS), catalyzed by the NADPH oxidases (NOX), is involved in pathogenesis ischemia-reperfusion (IR) injury. The underlying epigenetic mechanism remains elusive. Methods: We evaluated potential role megakaryocytic leukemia 1 (MKL1), as a bridge linking activation NOX to ROS production and cardiac Results: Following IR injury, MKL1-deficient (knockout) mice exhibited smaller myocardial infarction along with improved heart function...
Macrophage-dependent inflammatory response is considered a pivotal biological process that contributes to host of diseases when aberrantly activated. The underlying epigenetic mechanism not completely understood. We report here MKL1 was both sufficient and necessary for p65-dependent pro-inflammatory transcriptional program in immortalized macrophages, primary human mouse an animal model systemic inflammation (endotoxic shock). Extensive chromatin immunoprecipitation (ChIP) profiling...
Abstract Malignant lung cancer cells are characterized by uncontrolled proliferation and migration. Aberrant cell migration programmed altered transcriptome. The underlying epigenetic mechanism is unclear. Here we report that expression levels of BRG1, a chromatin remodeling protein, were significantly up-regulated in human biopsy specimens higher malignancy grades compared to those lower grades. Small interfering RNA mediated depletion or pharmaceutical inhibition BRG1 suppressed cells. was...
Increased synthesis of endothelin-1 (ET-1) by human vascular endothelial cells (HVECs) in response to hypoxia underscores persistent vasoconstriction observed patients with pulmonary hypertension. The molecular mechanism whereby stimulates ET-1 gene transcription is not well understood. Here we report that megakaryocytic leukemia 1 (MKL1) potentiated hypoxia-induced transactivation HVECs. Disruption MKL1 activity either a dominant negative mutant or small interfering RNA mediated knockdown...
Enhanced interaction between vascular endothelial cells and circulating leukocytes, as a result of transcriptional activation cell adhesion molecules (CAM), helps establish proinflammatory milieu contributing to the pathogenesis chronic hypoxia-induced pulmonary hypertension. The molecular switch that dictates CAM transactivation is not clearly defined. Our goal was determine involvement modulator megakaryocytic leukemia 1 (MKL1), also known myocardin-related transcription factor A (MRTF-A),...
Endothelin (ET-1) was initially identified as a potent vasoconstrictor contributing to the maintenance of vascular rhythm. Later studies have implicated ET-1, when aberrantly up-regulated within vasculature, in range human pathologies associated with disruption homeostasis. ET-1 has been shown invoke strong pro-inflammatory response smooth muscle cells (VSMCs); underlying mechanism, however, remains elusive. Here, we report that transcriptional modulator MRTF-A mediates activation mediators...
Cardiac ischemia-reperfusion injury (IRI) represents a major pathophysiological event associated with permanent loss of heart function. Several inter-dependent processes contribute to cardiac IRI that include accumulation reactive oxygen species (ROS), aberrant inflammatory response, and depletion energy supply. Inducible nitric oxide synthase (iNOS) is pro-inflammatory mediator catalyst ROS generation. In the present study we investigated epigenetic mechanism whereby iNOS transcription...
Brain damage following cerebral ischemia-reperfusion (I/R) is a complicated pathophysiological course, in which inflammation and oxidative stress have been suggested to serve an important role. Toll‑like receptor 4 (TLR4) has be involved secondary inflammatory process ischemia. Nuclear factor erythroid 2-related 2 (Nrf2), regulator of the antioxidant host defense, maintains cellular redox homeostasis. Tissue kallikrein (TK) proven elicit variety biological effects ischemic stroke through its...
Abstract Interstitial fibrosis represents a key pathological process in non-alcoholic steatohepatitis (NASH). In the liver, fibrogenesis is primarily mediated by activated hepatic stellate cells (HSCs) transitioning from quiescent state response to host of stimuli. The molecular mechanism underlying HSC activation not completely understood. Here we report that there was simultaneous up-regulation PIAS4 expression and down-regulation SIRT1 accompanying increased an MCD-diet induced mouse...
The matricellular protein SPON2 plays diverse roles in the development of cardiovascular diseases. is expressed endothelial cells, but its transcription regulation context atherogenesis remains incompletely appreciated. Here we report that expression was up-regulated by pro-atherogenic stimuli (oxLDL and TNF-α) vascular endothelia cells. In addition, elevated Apoe –/– mice fed on a Western diet compared to control mice. Induction cells mediated BRG1, chromatin remodeling protein, both vitro...
Phenotypic modulation of vascular smooth muscle cells represents a hallmark event in injury. The underlying mechanism is not completely sorted out. We investigated the involvement angiogenic factor with G patch and FHA domains 1 (Aggf1) injury focusing on transcriptional regulation cell signature genes.We report here that Aggf1 expression was downregulated several different models phenotypic vitro vessels after carotid artery ligation mice. Adenovirus-mediated overexpression dampened...
Tumor necrosis factor alpha (TNF-α) is a prototypical proinflammatory cytokine that can elicit strong inflammation in macrophages by activating NF-κB. The underlying epigenetic mechanism obscure. We show here megakaryocytic leukemia 1 (MKL1) an mediator of TNF-α-induced transcription. Overexpression dominant negative form MKL1 abrogates transactivation genes. Proteomic analysis identifies the histone H3K4 trimethyltransferase ASH2 as potential cofactor for MKL1. In response to TNF-α...
Accumulating evidences suggest that microRNAs (miRNAs) play key roles in mediating glioblastoma progression. Decreased expression of miR-152-3p was reported several cancer types including glioblastoma.The sensitivity cells to cisplatin assessed by the cell counting kit-8 assay and flow cytometry analysis. The determined RT-qPCR method. Bioinformatic analysis, dual luciferase reporter Western blot were used explore target gene miR-152-3p. association between SOS1 confirmed tissues Pearson...
Efficient antigen presentation by major histocompatibility complex (MHC) molecules represents a critical process in adaptive immunity. Class II transactivator (CIITA) is considered the master regulator of MHC class (MHC II) transcription. Previously, we have shown that CIITA expression upregulated smooth muscle cells deficient A2b adenosine receptor. Here, report treatment with receptor agonist adenosine-5'N-ethylcarboxamide (NECA) attenuated transcription lung fibro-blast as result...