Glibenclamide Elicits Endoplasmic Reticulum Stress and Myokine Expression in the L6 Skeletal Muscle Cells-Reference-Cited by-同舟云学术

Glibenclamide Elicits Endoplasmic Reticulum Stress and Myokine Expression in the L6 Skeletal Muscle Cells

Published:2022-01-18 Issue: Volume:16 Page:161-167
ISSN:1998-4510
Container-title:International Journal of Biology and Biomedical Engineering
language:en
Short-container-title:

Author:

Kwon Kisang¹,Ko Younghwa²,Park Hyewon²,Kim Junghae²,Kang Kyung-Hee³,Kim Seung-Whan⁴,Kwon O-Yu²

Affiliation:

1. Department of Clinical Laboratory Science, Wonkwang Health Science University, Iksan 54538, Korea

2. Department of Anatomy & Cell Biology, College of Medicine, Chungnam National University, Daejeon 35015, Korea

3. Department of Dental Hygiene, College of Medical Science, Konyang University, Daejeon 35365, Korea

4. Department of Emergency Medicine, College of Medicine, Chungnam National University, Daejeon 35015, Korea

Abstract

Although glibenclamide is an oral hypoglycemic agent used in type 2 diabetes, skeletal muscle wasting has been reported as a side effect. To understand how to reduce this side effect, we determined whether glibenclamide induces endoplasmic reticulum (ER) stress in skeletal muscle cells and which myokine expression changes at this time. The ER chaperone genes do not show a significant change by glibenclamide, but the ER stress sensor genes are upexpressed approximately twice, and those downstream [ATF6 (activating transcription factor 6) fragmentation, eIF2α (eukaryotic initiation factor-2α) phosphorylation, and XBP1 (Xbox DNA-binding protein) mRNA splicing] are activated. Additionally, the myokine gene expression was up- or downregulated by glibenclamide. These results will serve as useful data for overcoming the side effects of sarcopenia caused by glibenclamide.

Publisher

North Atlantic University Union (NAUN)

Subject

General Biochemistry, Genetics and Molecular Biology,Biomedical Engineering,General Medicine,Bioengineering

Reference22 articles.

1. D. Sola, L. Rossi, G. P. Carnevale Schianca, P. Maffioli, M. Bigliocca, R. Mella, et al. Sulfonylureas and their use in clinical practice. Arch Med Sci. 11(4): 840-848. 2015.

2. S. Seino. ATP-sensitive potassium channels: a model of heteromultimeric potassium channel/receptor assemblies. Annu Rev Physiol. 61: 337-362. 1999.

3. T. G. Skillman, J. M. Feldman. The pharmacology of sulfonylureas. Am J Med. 70(2): 361-372. 1981.

4. G. Giannico, P. Cortes, M. H. Baccora, C. Hassett, D. W. Taube, J. Yee. Glibenclamide prevents increased extracellular matrix formation induced by high glucose concentration in mesangial cells. Am J Physiol Renal Physiol. 292(1): F57-65. 2007.

5. F. Sawada, T. Inoguchi, H. Tsubouchi, S. Sasaki, M. Fujii, Y. Maeda, et al. Differential effect of sulfonylureas on production of reactive oxygen species and apoptosis in cultured pancreatic beta-cell line, MIN6. Metabolism 57(8): 1038-1045. 2008.