Open Access

KATP channels in high glucose-induced rat mesangial cell proliferation and release of MMP-2 and fibronectin

  • Authors:
    • Bei Zhang
    • Yongquan Shi
    • Junjie Zou
    • Xiangfang Chen
    • Wei Tang
    • Fei Ye
    • Zhimin Liu
  • View Affiliations

  • Published online on: May 17, 2017     https://doi.org/10.3892/etm.2017.4458
  • Pages: 135-140
  • Copyright: © Zhang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

ATP-sensitive potassium (KATP) channels are well characterized in cardiac, pancreatic and many other muscle cells. The purpose of this study was to determine if KATP channels play a role in diabetic nephropathy (DN). In the present study, functional expression of the KATP channel was examined in rat mesangial cells with or without high glucose (HG) stimulation. The mesangial cell proliferation and the release of matrix metalloproteinase (MMP)-2 and fibronectin in response to high glucose with a selective opener of KATP (diazoxide, DZX), or with a selective inhibitor of KATP (5-hydroxydecanoate, 5-HD) were also measured. The cell proliferation was observed using Cell Counting Kit-8 assay, and the mRNA expressions of KATP subunit, including Kir6.1, Kir6.2, sulfonylurea receptor 1 (SUR1), SUR2A and SUR2B, were assessed using quantitative real-time PCR. MMP-2 and fibronectin release was measured by ELISA. The present study clarified expression of SUR subunit of KATP in plasma. HG treatment could cause increased cell proliferation and release of MMP-2 and fibronectin in a dose-dependent manner. HG also significantly decreased the expression of Kir6.1, SUR2A and SUR2B. Pretreatment of DZX markedly decreased the expression of SUR1, SUR2A and SUR2B, but had no effect on Kir6.1 expression compared with HG alone, while these changes were inhibited by 5-HD pretreatment. Moreover, DZX also inhibited cell proliferation and release of MMP-2 and fibronectin in HG-induced rat mesangial cells, and that was corrected by 5-HD. These data suggest that HG stimulates mesangial cell proliferation and cellular matrix release via inhibiting KATP channel activity, leading us to propose that KATP channel dysfunction may be involved in the development of DN.
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July-2017
Volume 14 Issue 1

Print ISSN: 1792-0981
Online ISSN:1792-1015

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Spandidos Publications style
Zhang B, Shi Y, Zou J, Chen X, Tang W, Ye F and Liu Z: KATP channels in high glucose-induced rat mesangial cell proliferation and release of MMP-2 and fibronectin. Exp Ther Med 14: 135-140, 2017.
APA
Zhang, B., Shi, Y., Zou, J., Chen, X., Tang, W., Ye, F., & Liu, Z. (2017). KATP channels in high glucose-induced rat mesangial cell proliferation and release of MMP-2 and fibronectin. Experimental and Therapeutic Medicine, 14, 135-140. https://doi.org/10.3892/etm.2017.4458
MLA
Zhang, B., Shi, Y., Zou, J., Chen, X., Tang, W., Ye, F., Liu, Z."KATP channels in high glucose-induced rat mesangial cell proliferation and release of MMP-2 and fibronectin". Experimental and Therapeutic Medicine 14.1 (2017): 135-140.
Chicago
Zhang, B., Shi, Y., Zou, J., Chen, X., Tang, W., Ye, F., Liu, Z."KATP channels in high glucose-induced rat mesangial cell proliferation and release of MMP-2 and fibronectin". Experimental and Therapeutic Medicine 14, no. 1 (2017): 135-140. https://doi.org/10.3892/etm.2017.4458