MAPK pathway mediates the induction of visfatin in neonatal SD rat cardiomyocytes pretreated with glucose

Yang,Rong; Chang,Liang; Wang,Mei; Zhang,Hui; Liu,Jinming; Wang,Yaling; Jin,Xin; Xu,Lu; Li,Yongjun

doi:10.3892/br.2014.221

March-April 2014 Volume 2 Issue 2

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March-April 2014 Volume 2 Issue 2

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Article

MAPK pathway mediates the induction of visfatin in neonatal SD rat cardiomyocytes pretreated with glucose

Authors:
- Rong Yang
- Liang Chang
- Mei Wang
- Hui Zhang
- Jinming Liu
- Yaling Wang
- Xin Jin
- Lu Xu
- Yongjun Li
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Affiliations: Department of Cardiology, Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, P.R. China
Pages: 282-286
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Published online on: January 15, 2014

https://doi.org/10.3892/br.2014.221
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Abstract

The protein visfatin is an insulin mimetic that has been shown to reduce plasma glucose levels, increase cytokine production and induce angiogenesis. However, few studies have focused on visfatin expression in cardiomyocytes at the cellular level. Therefore, the aim of the present study was to investigate visfatin expression and its potential mechanisms in cultured neonatal rat cardiomyocytes exposed to high‑glucose concentrations. Primary cultures of 2-to 3‑day-old Sprague Dawley (SD) rat cardiomyocytes were pretreated with increasing concentrations of glucose. P38 mitogen‑activated protein kinase (MAPK) pathway inhibitor SB203580, extra cellular signal-regulated kinase (ERK1/2) pathway inhibitor PD098059 and c-Jun NH 2-terminal kinase (JNK) pathway inhibitor SP600125 were used to block the effect of glucose on visfatin expression. Cell viability following each glucose treatment was determined using the MTT assay. Expression of visfatin was detected using RT-PCR and western blot analysis. Increased glucose concentration directly correlated with an increased expression of visfatin mRNA and protein in neonatal rat cardiomyocytes. Following high doses of glucose, visfatin mRNA and protein expression peaked after 24 h with no significant change thereafter. Increased visfatin expression was blocked by the P38 MAPK inhibitor SB203580, suggesting a potential mechanism not yet identified. Expression of visfatin in cardiomyocytes was increased through the P38 MAPK pathway in the presence of high-glucose concentrations.

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Journals

International Journal of Molecular Medicine

International Journal of Oncology

Molecular Medicine Reports

Oncology Reports

Experimental and Therapeutic Medicine

Oncology Letters

Biomedical Reports

Molecular and Clinical Oncology

World Academy of Sciences Journal

International Journal of Functional Nutrition

International Journal of Epigenetics

Medicine International

MAPK pathway mediates the induction of visfatin in neonatal SD rat cardiomyocytes pretreated with glucose

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