Open AccessLong non‐coding RNA MALAT 1 regulates hyperglycaemia induced inflammatory process in the endothelial cells
Author(s) -
Puthanveetil Prasanth,
Chen Shali,
Feng Biao,
Gautam Anirudh,
Chakrabarti Subrata
Publication year - 2015
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.12576
Subject(s) - tumor necrosis factor alpha , rna , umbilical vein , endocrinology , biology , medicine , downregulation and upregulation , inflammation , antisense rna , messenger rna , cancer research , chemistry , immunology , biochemistry , gene , in vitro
To examine whether the long non‐coding RNA (lnc RNA ) metastasis associated lung adenocarcinoma transcript 1 ( MALAT 1) is altered in the endothelial cells in response to glucose and the significance of such alteration. We incubated human umbilical vein endothelial cells with media containing various glucose levels. We found an increase in MALAT 1 expression peaking after 12 hrs of incubation in high glucose. This increase was associated with parallel increase in serum amyloid antigen 3 ( SAA3 ), an inflammatory ligand and target of MALAT 1 and was further accompanied by increase in mRNA s and proteins of inflammatory mediators, tumour necrosis factor alpha ( TNF ‐α) and interleukin 6 ( IL ‐6). Renal tissue from the diabetic animals showed similar changes. Such cellular alterations were prevented following MALAT 1 specific si RNA transfection. Results of this study indicate that Lnc RNA MALAT 1 regulates glucose‐induced up‐regulation of inflammatory mediators IL ‐6 and TNF ‐α through activation of SAA 3. Identification of such novel mechanism may lead to the development of RNA ‐based therapeutics targeting MALAT 1 for diabetes‐induced micro and macro vascular complications.