scholarly journals Chemically Modified Heparin Inhibits Mesangial Cell Proliferation Induced by High Glucose through Interfering with the Cell Cycle

2007 ◽  
Vol 30 (12) ◽  
pp. 2274-2278 ◽  
Author(s):  
Deng-Ke Yin ◽  
Wen-Bing Yao ◽  
Xiang-Dong Gao
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
High Glucose ◽  
Mesangial Cell ◽  
Chemically Modified ◽  
Mesangial Cell Proliferation

scholarly journals Alpha Lipoic Acid Modulated High Glucose-Induced Rat Mesangial Cell Dysfunction via mTOR/p70S6K/4E-BP1 Pathway

2014 ◽  
Vol 2014 ◽  
pp. 1-14 ◽  
Author(s):  
Chuan Lv ◽  
Can Wu ◽  
Yue-hong Zhou ◽  
Ying Shao ◽  
Guan Wang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Extracellular Matrix ◽  
Cell Proliferation ◽  
Lipoic Acid ◽  
High Glucose ◽  
Mesangial Cell ◽  
Mesangial Cells ◽  
S Phase ◽  
Alpha Lipoic Acid ◽  
Mesangial Cell Proliferation

The aim of this study was to investigate whether alpha lipoic acid (LA) regulates high glucose-induced mesangial cell proliferation and extracellular matrix production via mTOR/p70S6K/4E-BP1 signaling. The effect of LA on high glucose-induced cell proliferation, fibronectin (FN), and collagen type I (collagen-I) expression and its mechanisms were examined in cultured rat mesangial cells by methylthiazol tetrazolium (MTT) assay, flow cytometry, ELISA assay, and western blot, respectively. LA at a relatively low concentration (0.25 mmol/L) acted as a growth factor in rat mesangial cells, promoted entry of cell cycle into S phase, extracellular matrix formation, and phosphorylated AKT, mTOR, p70S6K, and 4E-BP1. These effects disappeared when AKT expression was downregulated with PI3K/AKT inhibitor LY294002. Conversely, LA at a higher concentration (1.0 mmol/L) inhibited high glucose-induced rat mesangial cell proliferation, entry of cell cycle into S phase, and extracellular matrix exertion, as well as phosphorylation of mTOR, p70S6K, and 4E-BP1 but enhanced the activity of AMPK. However, these effects disappeared when AMPK activity was inhibited with CaMKK inhibitor STO-609. These results suggest that LA dose-dependently regulates mesangial cell proliferation and matrix protein secretion by mTOR/p70S6K/4E-BP1 signaling pathway under high glucose conditions.

Carnosine inhibits high glucose-induced mesangial cell proliferation through mediating cell cycle progression

2009 ◽  
Vol 154 (1-3) ◽  
pp. 69-76 ◽  
Author(s):  
Huijie Jia ◽  
Xiaodan Qi ◽  
Shaohong Fang ◽  
Yuhong Jin ◽  
Xiaoying Han ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
High Glucose ◽  
Cell Cycle Progression ◽  
Mesangial Cell ◽  
Cycle Progression ◽  
Mesangial Cell Proliferation

scholarly journals Inhibitory effect of Poria cocos on high glucose‐induced rat mesangial cell proliferation

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Jung Joo Yoon ◽  
Yun Jung Lee ◽  
So Min Lee ◽  
Yong Pyo Lee ◽  
Jin Sook Kim ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
High Glucose ◽  
Mesangial Cell ◽  
Inhibitory Effect ◽  
Poria Cocos ◽  
Mesangial Cell Proliferation

Poria cocosInhibits High Glucose-Induced Proliferation of Rat Mesangial Cells

2013 ◽  
Vol 41 (01) ◽  
pp. 71-83 ◽  
Author(s):  
Jung Joo Yoon ◽  
Yun Jung Lee ◽  
So Min Lee ◽  
Song Nan Jin ◽  
Dae Gill Kang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
High Glucose ◽  
Mesangial Cell ◽  
Mesangial Cells ◽  
Water Extract ◽  
Mitogen Activated Protein Kinase ◽  
Dependent Manner ◽  
Proliferative Effect ◽  
Mesangial Cell Proliferation ◽  
Mitogen Activated Protein

Mesangial cell proliferation is correlated with the progression of renal failure. The purpose of this study was to determine whether a water extract of Poria cocos Wolf (WPC), a well-known medicinal plant, regulates rat mesangial cell proliferation in the presence of high glucose (HG). HG significantly accelerated [3H]-thymidine incorporation, which was inhibited by WPC (1–50 μg/mL) in a dose-dependent manner. Cell migration and fibronectin mRNA expression data also supported the anti-proliferative effect of WPC. Western blot analysis revealed that pretreatment with WPC decreased the expression of cyclins and cyclin-dependent kinases (CDKs) and promoted the expression of p21waf1/cip1and p27kip1. WPC also suppressed HG-induced p38 mitogen-activated protein kinase (p38 MAPK) and extracellular-signal-regulated kinase 1/2 (ERK 1/2) phosphorylation. Furthermore, WPC inhibited HG-induced production of dichlorofluorescein (DCF)-sensitive intracellular reactive oxygen species (ROS). In conclusion, HG promoted mesangial cell proliferation, and WPC inhibited this activity, at least in part, via induction of cell cycle arrest and activation of anti-oxidant properties. Taken together, these results suggest that P. cocos may be a potent regulator of HG-induced proliferation.

scholarly journals Rosiglitazone Inhibits Angiotensin II-Induced Proliferation of Glomerular Mesangial Cells via the Gαq/Plcβ4/TRPC Signaling Pathway

2017 ◽  
Vol 44 (6) ◽  
pp. 2228-2242 ◽  
Author(s):  
Linting Wei ◽  
Jiarong Mao ◽  
Jiamei Lu ◽  
Jie Gao ◽  
Dan Zhu ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Signaling Pathway ◽  
Mesangial Cell ◽  
Mesangial Cells ◽  
Glomerular Mesangial Cells ◽  
Expression Levels ◽  
Qrt Pcr ◽  
Ppar Γ ◽  
Mesangial Cell Proliferation

Background/Aims: Mesangial cell proliferation and extracellular matrix accumulation (ECM) deposition play an important role in the pathogenesis of glomerulosclerosis. TRPC and PPAR-γ can regulate cell proliferation. Angiotensin II (AngII) can induce mesangial cell proliferation and affect TRPC expression. However, the mechanism has not been fully elucidated. This study was designed to investigate the role of TRPC and the effect of rosiglitazone (RSG) in the proliferation of rat glomerular mesangial cells (HBZY-1) that were stimulated by AngII and the underlying mechanisms. Methods: Immunofluorescence staining and qRT-PCR were performed to examine the expression levels of TRPCs in HBZY-1. Gene expression levels of TRPC, PPAR-γ, RGS4 (regulators of G protein signaling), the GPCR/Gαq/PLCβ4/TRPC signaling pathway and major downstream molecules (PCNA, SKP2, P21 and P27) were detected by qRT-PCR and western blotting. Additionally, changes in intracellular Ca2+ levels were determined through Fluo-4 Ca2+ imaging, and the cell cycle was analyzed by flow cytometry. Results: Our results found that TRPC1 and 6 were at higher expression levels in HBZY-1 cells. Following AngII stimulation, there were increased levels of TRPC1 and 6, Ca2+ entry, PCNA and SKP2, decreased expression levels of P21 and P27 and a reduced G0/G1 percentage. Silencing TRPC1 and 6 by siRNAs led to decrease in Ca2+ influx, G0/G1 cell cycle arrest and cell proliferation. Notably, PPAR-γ activation by RSG upregulated RGS4 expression, which can interact with the Gαq family to inhibit the Gαq-mediated signaling cascade. The results were similar to silencing TRPC1 and 6 by siRNAs. Conclusion: All these results indicate that RSG could inhibit HBZY-1 cell proliferation via the Gαq/PLCβ4/TRPC signaling pathway.

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