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Role of receptor for advanced glycation end-product (RAGE) and the JAK/STAT-signaling pathway in AGE-induced collagen production in NRK-49F cells

2001; Wiley; Volume: 81; Issue: 1 Linguagem: Inglês

10.1002/1097-4644(20010401)81

1097-4644

Jau‐Shyang Huang, Jinn‐Yuh Guh, Hung‐Chun Chen, Wen‐Chun Hung, Yung‐Hsiung Lai, Lea‐Yea Chuang,

Apelin-related biomedical research

Journal of Cellular BiochemistryVolume 81, Issue 1 p. 102-113 Articles Role of receptor for advanced glycation end-product (RAGE) and the JAK/STAT-signaling pathway in AGE-induced collagen production in NRK-49F cells Jau-Shyang Huang, Jau-Shyang Huang Department of Biochemistry, Kaohsiung Medical University, Kaohsiung, Taiwan, Republic of ChinaSearch for more papers by this authorJinn-Yuh Guh, Jinn-Yuh Guh Department of Internal Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan, Republic of ChinaSearch for more papers by this authorHung-Chun Chen, Hung-Chun Chen Department of Internal Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan, Republic of ChinaSearch for more papers by this authorWen-Chun Hung, Wen-Chun Hung School of Technology for Medical Science, Kaohsiung Medical University, Kaohsiung, Taiwan, Republic of ChinaSearch for more papers by this authorYung-Hsiung Lai, Yung-Hsiung Lai Department of Internal Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan, Republic of ChinaSearch for more papers by this authorLea-Yea Chuang, Corresponding Author Lea-Yea Chuang jiyugu@cc.kmu.edu.tw Department of Biochemistry, Kaohsiung Medical University, Kaohsiung, Taiwan, Republic of ChinaDepartment of Biochemistry, Kaohsiung Medical University, Kaohsiung 80708, Taiwan, Republic of China.Search for more papers by this author Jau-Shyang Huang, Jau-Shyang Huang Department of Biochemistry, Kaohsiung Medical University, Kaohsiung, Taiwan, Republic of ChinaSearch for more papers by this authorJinn-Yuh Guh, Jinn-Yuh Guh Department of Internal Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan, Republic of ChinaSearch for more papers by this authorHung-Chun Chen, Hung-Chun Chen Department of Internal Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan, Republic of ChinaSearch for more papers by this authorWen-Chun Hung, Wen-Chun Hung School of Technology for Medical Science, Kaohsiung Medical University, Kaohsiung, Taiwan, Republic of ChinaSearch for more papers by this authorYung-Hsiung Lai, Yung-Hsiung Lai Department of Internal Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan, Republic of ChinaSearch for more papers by this authorLea-Yea Chuang, Corresponding Author Lea-Yea Chuang jiyugu@cc.kmu.edu.tw Department of Biochemistry, Kaohsiung Medical University, Kaohsiung, Taiwan, Republic of ChinaDepartment of Biochemistry, Kaohsiung Medical University, Kaohsiung 80708, Taiwan, Republic of China.Search for more papers by this author First published: 06 February 2001 https://doi.org/10.1002/1097-4644(20010401)81:1 3.0.CO;2-YCitations: 146Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Abstract Advanced glycation end-product (AGE) is important in the pathogenesis of diabetic nephropathy (DN), and captopril (an angiotensin converting enzyme inhibitor) is effective in treating this disorder. We have shown that the Janus kinase (JAK)/signal transducers and activators of transcription (STAT) cascade is responsible for AGE-induced mitogenesis in NRK-49F (normal rat kidney fibroblast) cells, but its role in renal fibrosis in DN remains unknown. Therefore, we have sought to determine whether JAK/STAT is involved in AGE-regulated collagen production in NRK-49F cells. We found that AGE time (1–7 days) and dose (10–200 μg/ml)-dependently increased collagen production in these cells. Additionally, AGE increased RAGE (receptor for AGE) protein expression. AGE-induced RAGE expression was dose-dependently inhibited by antisense RAGE oligodeoxynucleotide (ODN) and captopril. AGE-induced type I collagen production and JAK2-STAT1/STAT3 activation were decreased by AG-490 (a specific JAK2 inhibitor), antisense RAGE ODN and captopril. Meanwhile, STAT1 and STAT3 decoy ODNs also suppressed the induction of collagen by AGE. We concluded that RAGE and the JAK2-STAT1/STAT3 pathway were involved in AGE-induced collagen production in NRK-49F cells. Furthermore, captopril was found to reverse AGE-induced collagen production, probably by attenuating RAGE expression and JAK2-STAT1/STAT3 activities. J. Cell. Biochem. 81:102–113, 2001. © 2001 Wiley-Liss, Inc. Citing Literature Volume81, Issue11 April 2001Pages 102-113 RelatedInformation