Abstract:
:Advanced glycation end products (AGEs), formed at an accelerated rate under diabetes, play a role in inflammation and fibrosis in mesangial areas in diabetic nephropathy (DN). However, the transcriptional modulator that mediates the cellular response to AGEs remains largely obscure. Our goal was to determine whether myocardin-related transcription factor (MRTF)-A, a key protein involved in the transcriptional regulation of smooth muscle cell phenotype, was responsible for the glomerular mesangial cells (GMCs) injury by AGEs, and, if so, how MRTF-A promoted mesangial dysfunction initiated by AGEs. In this study, MRTF-A was activated by AGEs in terms of protein expression and nuclear translocation in rat GMCs. MRTF-A overexpression synergistically enhanced the induction of FN and ICAM-1 by AGEs. In contract, depletion of MRTF-A abrogated the pathogenic program triggered by AGEs. Then, by interfering with MRTF-A, STAT1, STAT3 and STAT5 nuclear translocation were observed and we screened out STAT5, which was decreased obviously when MRTF-A depleted. Further investigation showed that MRTF-A interacted with STAT5 and promoted its nuclear accumulation and transcriptional activity. Therefore, our present findings suggested a role of MRTF-A in AGEs-induced GMCs injury, and further revealed that the underlying molecular mechanism was related to activating the nuclear factor STAT5.
journal_name
Mol Cell Endocrinoljournal_title
Molecular and cellular endocrinologyauthors
Chen Q,Huang J,Gong W,Chen Z,Huang J,Liu P,Huang Hdoi
10.1016/j.mce.2017.07.014subject
Has Abstractpub_date
2018-01-15 00:00:00pages
123-133eissn
0303-7207issn
1872-8057pii
S0303-7207(17)30368-4journal_volume
460pub_type
杂志文章abstract::Prostaglandin A1 (PGA1) increases heat shock element (HSE)-mediated transcription, thereby enhancing expression of HSE-bearing genes, including heat shock proteins. Because we recently found functional HSEs in the human and rodent c-fos promoters, we hypothesized that PGA1 might increase c-fos expression through the H...
journal_title:Molecular and cellular endocrinology
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journal_title:Molecular and cellular endocrinology
pub_type: 杂志文章
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pub_type: 杂志文章
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journal_title:Molecular and cellular endocrinology
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journal_title:Molecular and cellular endocrinology
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