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Effect of ER stress in Collagen 6A3 and ATF3 expression in adipocytes
Author(s) -
Saraf Manish Kumar,
Choudhary Sanjeev,
Chandalia Manisha,
Abate Nicola
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1169.18
Subject(s) - atf3 , chemistry , adipose tissue , endoplasmic reticulum , transcriptional regulation , microbiology and biotechnology , gene expression , endocrinology , biology , promoter , gene , biochemistry
Although increased expression of Collagen 6A3 (Col6A3) has been linked with elevated adipose tissue inflammation, mechanisms of Col6A3 regulation have not yet been identified. We identified ATF3 binding site in the promoter region of Col6A3. ATF3, a marker endoplasmic reticulum (ER) stress, is transcriptional repressor protein that binds to the promoter region and represses expression of adiponectin receptor‐1 and ‐2. In the present study, we investigated the regulation of Col6A3 expression by ATF3 in pre‐ and matured adipocytes using 3T3 cell model. Undifferentiated predipocyte treated with TNF‐α, Thapsigargin or DTT induced an increased expression of ATF3 with a concomitant suppression of Col6A3. Moreover, an inverse relationship between ATF3 expression and the expression ofadipocyte maturation markers, such as CEBPα and PPARγ was observed in undifferentiated cells treated with TNF‐α. Similar inverse relation between ATF3 and col6A3 expression was observed in the cells differentiated by insulin alone suggesting a physiological role of ATF3 in adipocyte differentiation and Col6a3 transcriptional regulation. These findings suggest a novel ATF3 mediated pathway regulating expression of Col6A3 expression which, in turn is known to affect adipose tissue inflammation.