Jiangsu Jiankang Vocational College

Nanjing, China

Jiangsu Jiankang Vocational College

Nanjing, China
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Song M.,Jiangsu Jiankang Vocational College | Fang F.,Nanjing Medical University | Dai X.,Nanjing Medical University | Yu L.,Nanjing Medical University | And 2 more authors.
FEBS Letters | Year: 2017

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 is obscure. We show here that megakaryocytic leukemia 1 (MKL1) is an epigenetic mediator of TNF-α-induced proinflammatory transcription. Overexpression of a dominant negative form of MKL1 abrogates TNF-α-induced transactivation of proinflammatory genes. Proteomic analysis identifies the histone H3K4 trimethyltransferase ASH2 as a potential cofactor for MKL1. In response to TNF-α stimulation, ASH2 is recruited by MKL1 and interacts with MKL1 to catalyze H3K4 di- and trimethylation. ASH2 modulates proinflammatory transcription at least in part by altering the affinity of p65 for target promoters. Together, our data support an interplay between MKL1 and ASH2 to promote TNF-α-induced proinflammatory transcription in macrophages. © 2017 Federation of European Biochemical Societies

Lei M.,Jiangsu Jiankang Vocational College | Zhu Z.,Jiangsu Jiankang Vocational College | Wen Z.,Nanjing Medical University | Ke S.,Jiangsu Jiankang Vocational College
NeuroReport | Year: 2013

Impairments of tight junctions are implicated in the course of various age-related neurodegenerative disorders. Chronic injection of D-galactose can cause a progressive deterioration in learning and memory capacity and serve as an animal model of aging. To investigate the involvement of tight junctions in this model, oxidative stress biomarkers, expression and ultrastructure of tight junctions, and the permeability of blood-brain barrier were examined in the hippocampus of the mice, which received an injection of D-galactose for 6 weeks. D-Galactose-injected mice showed impaired antioxidant systems, decreased levels of tight junction proteins, and ultrastructural pathological changes of tight junctions, accompanied by increased blood-brain barrier permeability in the hippocampus. These results show that impairments in tight junctions are involved in D-galactose-induced brain aging. © 2013 Wolters Kluwer Health | Lippincott Williams & Wilkins.

Xu W.,Jiangsu Jiankang Vocational College | Xu H.,Nanjing Medical University | Fang M.,Jiangsu Jiankang Vocational College | Wu X.,Nanjing Medical University | Xu Y.,Nanjing Medical University
Biochemical and Biophysical Research Communications | Year: 2017

Responding to pro-metastatic cues such as low oxygen tension, cancer cells develop several different strategies to facilitate migration and invasion. During this process, expression levels of matrix metalloproteinases (MMPs) are up-regulated so that cancer cells can more easily enter or exit the circulation. In this report we show that message levels of the transcriptional modulator MKL1 were elevated in malignant forms of ovarian cancer tissues in humans when compared to more benign forms accompanying a similar change in MMP2 expression. MKL1 silencing blocked hypoxia-induced migration and invasion of ovarian cancer cells (SKOV-3) in vitro. Over-expression of MKL1 activated while MKL1 depletion repressed MMP2 transcription in SKOV-3 cells. MKL1 was recruited to the MMP2 promoter by NF-κB in response to hypoxia. Mechanistically, MKL1 recruited a histone methyltransferase, SET1, and a chromatin remodeling protein, BRG1, and coordinated their interaction to alter the chromatin structure surrounding the MMP2 promoter leading to transcriptional activation. Both BRG1 and SET1 were essential for hypoxia-induced MMP2 trans-activation. Finally, expression levels of SET1 and BRG1 were positively correlated with ovarian cancer malignancies in humans. Together, our data suggest that MKL1 promotes ovarian cancer cell migration and invasion by epigenetically activating MMP2 transcription. © 2017 Elsevier Inc.

Yu L.,Nanjing Medical University | Li Z.,Nanjing Medical University | Fang M.,Jiangsu Jiankang Vocational College | Xu Y.,Nanjing Medical University
Biochimica et Biophysica Acta - Gene Regulatory Mechanisms | Year: 2017

Inflammation is considered a fundamental host defense mechanism and, when aberrantly activated, contributes to a host of human diseases. Previously we have reported that the transcriptional regulator megakaryocytic leukemia 1 (MKL1) plays a role programming cellular inflammatory response by modulating NF-κB activity. Here we report that MKL1 was acetylated in vivo and pro-inflammatory stimuli (TNF-α and LPS) augmented MKL1 acetylation accompanying increased MKL1 binding to NF-κB target promoters. Further analysis revealed that the lysine acetyltransferase PCAF mediated MKL1 acetylation: TNF-α and LPS promoted the interaction between MKL1 and PCAF whereas depletion of PCAF abrogated the induction of MKL1 acetylation by TNF-α and LPS. Acetylation of MKL1 was necessary for MKL1 to activate the transcription of pro-inflammatory genes because mutation of four conserved lysine residues in MKL1 attenuated its capacity as a trans-activator of NF-κB target genes. Mechanistically, MKL1 acetylation served to promote MKL1 nuclear enrichment, to enhance the MKL1-NF-κB interaction, and to stabilize the binding of MKL1 on target promoters. In conclusion, our data unveil an important pathway that contributes to the transcriptional regulation of inflammatory response. © 2017 Elsevier B.V.

Chang L.,Nanjing Southeast University | Tian X.,Nanjing Southeast University | Lu Y.,Nanjing General Hospital of Nanjing Military Command | Jia M.,Nanjing Southeast University | And 2 more authors.
PLoS ONE | Year: 2014

AZGP1 is a multifaceted protein associated with lipid mobilization, a process that is regulated by FASN and other metabolic pathways such as mTOR signaling. The active mTOR signaling pathway has been found to be involved in a variety of tumors. However, it remains unclear whether it is involved in the regulation of AZGP1 and FASN. An AZGP1-expressing plasmid was transfected into a human colorectal cancer cell line (LoVo) with a low expression of AZGP1. The expression of AZGP1, FASN, eIF4E, p-mTOR, p-S6,and S6K1 were measured by Western blot analysis, and target genes were detected by RT-PCR. Cell proliferation was studied using the MTT and colony formation assays. The analysis of apoptosis and the cell cycle phase were assessed by flow cytometry. The capacity of cell migration was investigated using the transwell migration assay. We found that the expression of AZGP1 was up-regulated while the expression of FASN, eIF4E, p-mTOR, p-S6, and S6K1 were down-regulated in LoVo cells after AZGP1 was expressed. The proliferation of malignant cells was reduced in AZGP1-overexpression cells, which is consistent with an increased in the G2-arrest and apoptosis rate. Furthermore, the migration of AZGP1-overexpression cells was decreased. The overexpression of AZGP1 suppressed the activation of the mTOR pathway and endogenous FASN-regulated fatty acid synthesis, mitigating the malignant phenotype of LoVo cells. Herein, we provide evidence that AZGP1 may constitute a novel tumor suppressor for LoVo colorectal cancer cells. © 2014 Chang et al.

PubMed | Jiangsu Province Hospital of Traditional Chinese Medicine, The Second Peoples Hospital of Huaian, Jiangsu University, Nanjing Maternity and Child Health Care Hospital and 2 more.
Type: Journal Article | Journal: Bioscience reports | Year: 2016

Stress-activated protein kinase (SAPK) interacting protein 1 (SIN1) is an essential TORC2 component and a key regulator of Akt pathway that plays an important role in various pathological conditions including cancer. Whereas its functional role in breast cancer has not been well characterized. In the present study, SIN1 is associated with the progression and survival of breast cancer patients, as well as human breast cancer cell proliferation and migration. SIN1 mRNA level was significantly up-regulated in human breast cancer samples compared with their corresponding paracancerous histological normal tissues. Furthermore, the expression levels of SIN1 were also increased in three human breast cancer cell lines compared with human breast epithelial cell MCF10A. Overexpression of SIN1 promoted cell proliferation, colony formation and migration of breast cancer cells. Knockdown of SIN1in MDA-MB-468 cells inhibited cell proliferation, colony formation and migration. In addition, SIN1 overexpression increased phosphorylation of Akt and knockdown of SIN1 inhibited phosphorylation of Akt in MDA-MB-468 cells. In a tumour xenograft model, overexpression of SIN1 promoted tumour growth of MDA-MB-468 cells invivo, whereas SIN1 knockdown inhibits the tumour growth. Taken together, our results reveal that SIN1 plays an important role in breast cancer and SIN1 is a potential biomarker and a promising target in the treatment of breast cancer.

PubMed | Jiangsu Jiankang Vocational College and Nanjing University
Type: Review | Journal: The world journal of men's health | Year: 2017

Premature ejaculation (PE) is a common male sexual dysfunction that can have significant effects on a couples relationship. Behavioral therapy and psychotherapy are both safe and effective methods of treating PE. Ancient Chinese

PubMed | Nanjing Medical University and Jiangsu Jiankang Vocational College
Type: | Journal: Biochemical and biophysical research communications | Year: 2016

The regeneration of injured tubular cell occurs primarily from intrinsic renal stem/progenitor cells (RSCs) labeled with CD24 and CD133 after acute tubular necrosis (ATN). Bmi-1 plays a crucial role in regulating self-renewal, differentiation and aging of multiple adult stem cells and progenitor cells. Bmi-1 was rapidly elevated in the induction of adult kidney regeneration by renal injury. To determine whether Bmi-1 maintained mobilization of RSCs in the protection from ATN, glycerol-rhabdomyolysis-induced ATN were performed in wild type (WT) and Bmi-1-deficient (Bmi-1

PubMed | Nanjing Medical University and Jiangsu Jiankang Vocational College
Type: Journal Article | Journal: Cell death & disease | Year: 2016

Impaired apoptosis of fibroblast-like synoviocytes (FLSs) causes synovial hyperplasia, facilitating destruction of cartilage and bone in rheumatoid arthritis (RA). Tumor necrosis factor (TNF)-, a dominant inflammatory mediator in RA pathogenesis, promotes progression of RA symptoms. Prevalence of 1, 25-dihydroxy-vitamin D

PubMed | Jiangsu Jiankang Vocational College and China Pharmaceutical University
Type: Journal Article | Journal: Chinese journal of natural medicines | Year: 2016

TRPA1 channels are non-selective cation channels that could be activated by plant-derived pungent products, including gingerol, a main active constituent of ginger. Ginger could improve the digestive function; however whether ginger improves the digestive function through activating TRPA1 receptor in gastrointestinal tract has not been investigated. In the present study, gingerol was used to stimulate cell lines (RIN14B or STC-1) while depletion of extracellular calcium. TRPA1 inhibitor (rethenium red) and TRPA1 gene silencing via TRPA1-specific siRNA were also used for mechanistic studies. The intracellular calcium and secretion of serotonin or cholecystokinin were measured by fura-2/AM and ELISA. Stimulation of those cells with gingerol increased intracellular calcium levels and the serotonin or cholecystokinin secretion. The gingerol-induced intracellular calcium increase and secretion (serotonin or cholecystokinin) release were completely blocked by ruthenium red, EGTA, and TRPA1-specific siRNA. In summary, our results suggested that gingerol derived from ginger might improve the digestive function through secretion releasing from endocrine cells of the gut by inducing TRPA1-mediated calcium influx.

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