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Fibronectin synthesis by high glucose level mediated proliferation of mouse embryonic stem cells: Involvement of ANG II and TGF-beta1.
J Cell Physiol. 2010 May; 223(2):397-407.JC

Abstract

The role of individual supplements necessary for the long-term self-renewal of embryonic stem (ES) cells is poorly characterized in feeder/serum-free culture systems. This study sought to characterize the relationship between the effects of glucose on ES cell proliferation and fibronectin (FN) synthesis, and to assess the mechanisms responsible for these cellular effects of glucose. Treatment of the two ES cells (ES-E14TG2a and ES-R1) with 25 mM glucose (high glucose) increased the expression levels of FN mRNA and protein. In addition, high glucose and ANG II synergistically increased FN expression level, which coincident with data showing that high glucose increased the mRNA expression of angiotensin II (ANG II) type 1 receptor (AT(1)R), angiotensinogen, and FN, but not ANG II type 2 receptor. High glucose also increased the intracellular calcium (Ca(2+)) concentration and pan-protein kinase C (PKC) phosphorylation. Inhibition of the Ca(2+)/PKC pathway blocked high glucose-induced FN expression. High glucose or ANG II also synergistically increased transforming growth factor-beta1 (TGF-beta(1)) expression, while pretreatment with losartan abolished the high glucose-induced increase in TGF-beta(1) production. Moreover, TGF-beta(1)-specific small interfering RNA inhibited high glucose-induced FN expression and c-Jun N-terminal kinase (JNK) activation. The JNK inhibitor SP600125 blocked high glucose-induced FN expression and inhibited cell cycle regulatory protein expression induced by high glucose or TGF-beta(1). In this study, inhibition of AT(1)R, Ca(2+)/PKC, TGF-beta(1), JNK, FN receptor blocked the high glucose-induced DNA synthesis, increased the cell population in S phase, and the number of cells. It is concluded that high glucose increases FN synthesis through the ANG II or TGF-beta1 pathways, which in part mediates proliferation of mouse ES cells.

Authors+Show Affiliations

Department of Veterinary Physiology, Biotherapy Human Resources Center (BK 21), College of Veterinary Medicine, Chonnam National University, Gwangju 500-757, Korea.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

20112290

Citation

Kim, Yun Hee, et al. "Fibronectin Synthesis By High Glucose Level Mediated Proliferation of Mouse Embryonic Stem Cells: Involvement of ANG II and TGF-beta1." Journal of Cellular Physiology, vol. 223, no. 2, 2010, pp. 397-407.
Kim YH, Ryu JM, Lee YJ, et al. Fibronectin synthesis by high glucose level mediated proliferation of mouse embryonic stem cells: Involvement of ANG II and TGF-beta1. J Cell Physiol. 2010;223(2):397-407.
Kim, Y. H., Ryu, J. M., Lee, Y. J., & Han, H. J. (2010). Fibronectin synthesis by high glucose level mediated proliferation of mouse embryonic stem cells: Involvement of ANG II and TGF-beta1. Journal of Cellular Physiology, 223(2), 397-407. https://doi.org/10.1002/jcp.22048
Kim YH, et al. Fibronectin Synthesis By High Glucose Level Mediated Proliferation of Mouse Embryonic Stem Cells: Involvement of ANG II and TGF-beta1. J Cell Physiol. 2010;223(2):397-407. PubMed PMID: 20112290.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Fibronectin synthesis by high glucose level mediated proliferation of mouse embryonic stem cells: Involvement of ANG II and TGF-beta1. AU - Kim,Yun Hee, AU - Ryu,Jung Min, AU - Lee,Yu Jin, AU - Han,Ho Jae, PY - 2010/1/30/entrez PY - 2010/1/30/pubmed PY - 2010/5/7/medline SP - 397 EP - 407 JF - Journal of cellular physiology JO - J. Cell. Physiol. VL - 223 IS - 2 N2 - The role of individual supplements necessary for the long-term self-renewal of embryonic stem (ES) cells is poorly characterized in feeder/serum-free culture systems. This study sought to characterize the relationship between the effects of glucose on ES cell proliferation and fibronectin (FN) synthesis, and to assess the mechanisms responsible for these cellular effects of glucose. Treatment of the two ES cells (ES-E14TG2a and ES-R1) with 25 mM glucose (high glucose) increased the expression levels of FN mRNA and protein. In addition, high glucose and ANG II synergistically increased FN expression level, which coincident with data showing that high glucose increased the mRNA expression of angiotensin II (ANG II) type 1 receptor (AT(1)R), angiotensinogen, and FN, but not ANG II type 2 receptor. High glucose also increased the intracellular calcium (Ca(2+)) concentration and pan-protein kinase C (PKC) phosphorylation. Inhibition of the Ca(2+)/PKC pathway blocked high glucose-induced FN expression. High glucose or ANG II also synergistically increased transforming growth factor-beta1 (TGF-beta(1)) expression, while pretreatment with losartan abolished the high glucose-induced increase in TGF-beta(1) production. Moreover, TGF-beta(1)-specific small interfering RNA inhibited high glucose-induced FN expression and c-Jun N-terminal kinase (JNK) activation. The JNK inhibitor SP600125 blocked high glucose-induced FN expression and inhibited cell cycle regulatory protein expression induced by high glucose or TGF-beta(1). In this study, inhibition of AT(1)R, Ca(2+)/PKC, TGF-beta(1), JNK, FN receptor blocked the high glucose-induced DNA synthesis, increased the cell population in S phase, and the number of cells. It is concluded that high glucose increases FN synthesis through the ANG II or TGF-beta1 pathways, which in part mediates proliferation of mouse ES cells. SN - 1097-4652 UR - https://www.unboundmedicine.com/medline/citation/20112290/Fibronectin_synthesis_by_high_glucose_level_mediated_proliferation_of_mouse_embryonic_stem_cells:_Involvement_of_ANG_II_and_TGF_beta1_ L2 - https://doi.org/10.1002/jcp.22048 DB - PRIME DP - Unbound Medicine ER -