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Exendin-4 induction of Egr-1 expression in INS-1 beta-cells: interaction of SRF, not YY1, with SRE site of rat Egr-1 promoter.
J Cell Biochem 2008; 104(6):2261-71JC

Abstract

Glucagon-like peptide-1 (GLP-1) induces several immediate early response genes such as c-fos, c-jun, and early growth response-1 (Egr-1), which are involved in cell proliferation and differentiation. We recently reported that exendin-4 (EX-4), a potent GLP-1 agonist, upregulated Egr-1 expression via phosphorylation of CREB, a transcription factor in INS-1 beta-cells. This study was designed to investigate the role of another transcription factors, serum response factor (SRF) and Yin Yang-1 (YY1), in EX-4-induced Egr-1 expression. EX-4 significantly increased Egr-1 mRNA and subsequently its protein level. EX-4-induced Egr-1 expression was inhibited by pretreatment with a PKA inhibitor, H-89, and an MEK inhibitor, PD 98059. The siRNA-mediated inhibition of PKA and ERK1 resulted in significant reduction of EX-4-induced Egr-1 expression. Promoter analyses showed that SRE clusters were essential for Egr-1 transcription, and YY1 overexpression did not affect Egr-1 promoter activity. EMSA results demonstrated that EX-4-induced transient increase in DNA-protein complex on SRE site, and that both SRF and phospho-SRF were bound to this site. Treatment of either YY1 consensus oligonucleotide or YY1 antibody did not effect the change of density or migration of the DNA-protein complex. Collectively, EX-4-induced Egr-1 expression is largely dependent on cAMP-mediated extracellular signal-regulated kinase activation, and EX-4 induces Egr-1 transcription via the interaction of SRF and phospho-SRF to SRE sites.

Authors+Show Affiliations

Department of Physiology, College of Medicine, The Catholic University of Korea, Seoul 137-701, South Korea.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo 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

18446785

Citation

Kim, Myung-Jun, et al. "Exendin-4 Induction of Egr-1 Expression in INS-1 Beta-cells: Interaction of SRF, Not YY1, With SRE Site of Rat Egr-1 Promoter." Journal of Cellular Biochemistry, vol. 104, no. 6, 2008, pp. 2261-71.
Kim MJ, Kang JH, Chang SY, et al. Exendin-4 induction of Egr-1 expression in INS-1 beta-cells: interaction of SRF, not YY1, with SRE site of rat Egr-1 promoter. J Cell Biochem. 2008;104(6):2261-71.
Kim, M. J., Kang, J. H., Chang, S. Y., Jang, H. J., Ryu, G. R., Ko, S. H., ... Jo, Y. H. (2008). Exendin-4 induction of Egr-1 expression in INS-1 beta-cells: interaction of SRF, not YY1, with SRE site of rat Egr-1 promoter. Journal of Cellular Biochemistry, 104(6), pp. 2261-71. doi:10.1002/jcb.21783.
Kim MJ, et al. Exendin-4 Induction of Egr-1 Expression in INS-1 Beta-cells: Interaction of SRF, Not YY1, With SRE Site of Rat Egr-1 Promoter. J Cell Biochem. 2008 Aug 15;104(6):2261-71. PubMed PMID: 18446785.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Exendin-4 induction of Egr-1 expression in INS-1 beta-cells: interaction of SRF, not YY1, with SRE site of rat Egr-1 promoter. AU - Kim,Myung-Jun, AU - Kang,Jung-Hoon, AU - Chang,Seo-Yoon, AU - Jang,Hyun-Jong, AU - Ryu,Gyeong Ryul, AU - Ko,Seung Hyun, AU - Jeong,In-Kyung, AU - Kim,Myung-Suk, AU - Jo,Yang-Hyeok, PY - 2008/5/1/pubmed PY - 2008/10/16/medline PY - 2008/5/1/entrez SP - 2261 EP - 71 JF - Journal of cellular biochemistry JO - J. Cell. Biochem. VL - 104 IS - 6 N2 - Glucagon-like peptide-1 (GLP-1) induces several immediate early response genes such as c-fos, c-jun, and early growth response-1 (Egr-1), which are involved in cell proliferation and differentiation. We recently reported that exendin-4 (EX-4), a potent GLP-1 agonist, upregulated Egr-1 expression via phosphorylation of CREB, a transcription factor in INS-1 beta-cells. This study was designed to investigate the role of another transcription factors, serum response factor (SRF) and Yin Yang-1 (YY1), in EX-4-induced Egr-1 expression. EX-4 significantly increased Egr-1 mRNA and subsequently its protein level. EX-4-induced Egr-1 expression was inhibited by pretreatment with a PKA inhibitor, H-89, and an MEK inhibitor, PD 98059. The siRNA-mediated inhibition of PKA and ERK1 resulted in significant reduction of EX-4-induced Egr-1 expression. Promoter analyses showed that SRE clusters were essential for Egr-1 transcription, and YY1 overexpression did not affect Egr-1 promoter activity. EMSA results demonstrated that EX-4-induced transient increase in DNA-protein complex on SRE site, and that both SRF and phospho-SRF were bound to this site. Treatment of either YY1 consensus oligonucleotide or YY1 antibody did not effect the change of density or migration of the DNA-protein complex. Collectively, EX-4-induced Egr-1 expression is largely dependent on cAMP-mediated extracellular signal-regulated kinase activation, and EX-4 induces Egr-1 transcription via the interaction of SRF and phospho-SRF to SRE sites. SN - 1097-4644 UR - https://www.unboundmedicine.com/medline/citation/18446785/Exendin_4_induction_of_Egr_1_expression_in_INS_1_beta_cells:_interaction_of_SRF_not_YY1_with_SRE_site_of_rat_Egr_1_promoter_ L2 - https://doi.org/10.1002/jcb.21783 DB - PRIME DP - Unbound Medicine ER -