Collagen type I enhances cell growth and insulin biosynthesis in rat pancreatic cells

Author:

Zhu Yingying1,Liu Weiwei1,Chen Shuaigao1,Xu Fanxing1,Zhang Luxin1,Hayashi Toshihiko123,Mizuno Kazunori3,Hattori Shunji3,Fujisaki Hitomi3,Ikejima Takashi14

Affiliation:

1. 1Wuya College of Innovation, Shenyang Pharmaceutical University, Shenyang, Liaoning, China

2. 2Department of Chemistry and Life Science, School of Advanced Engineering Kogakuin University, Tokyo, Japan

3. 3Nippi Research Institute of Biomatrix, Toride, Ibaraki, Japan

4. 4Key Laboratory of Computational Chemistry-Based Natural Antitumor Drug Research and Development, Liaoning, China

Abstract

Type I collagen (collagen I) is the most abundant component of the extracellular matrix (ECM) in the pancreas. We previously reported that collagen I-coated culture dishes enhanced proliferation of rat pancreatic β cell line, INS-1 cells, via up-regulation of β-catenin nuclear translocation. In this study, we further investigated the effects of collagen I on insulin production of INS-1 cells. The results indicate that insulin synthesis as well as cell proliferation is increased in the INS-1 cells cultured on the dishes coated with collagen I. Up-regulation of insulin-like growth factor 1 receptor (IGF-1R) on the INS-1 cells cultured on the collagen-coated dishes is involved in up-regulation of cell proliferation and increase of insulin biosynthesis; however, up-regulation of insulin secretion in the INS-1 cells on collagen I-coated dishes was further enhanced by inhibition of IGF-1R. Autophagy of INS-1 cells on collagen I-coated dishes was repressed via IGF-1R upregulation, and inhibition of autophagy with 3MA further enhanced cell proliferation and insulin biosynthesis but did not affect insulin secretion. E-cadherin/β-catenin adherent junction complexes are stabilized by autophagy. That is, autophagy negatively regulates the nuclear translocation of β-catenin that leads to insulin biosynthesis and cell proliferation. In conclusion, IGF-1R/downregulation of autophagy/nuclear translocation of β-catenin is involved in collagen I-induced INS-1 cell proliferation and insulin synthesis.

Publisher

Bioscientifica

Subject

Endocrinology,Molecular Biology

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