Premium
Role of miR‐19a in the development of abdominal aortic aneurysm
Author(s) -
Zhang Yali,
Park HoJin,
Galper Jonas B
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.870.1
Subject(s) - suppressor of cytokine signaling 1 , microrna , socs3 , inflammation , abdominal aortic aneurysm , cancer research , cytokine , medicine , signal transduction , stat3 , suppressor , biology , gene , microbiology and biotechnology , immunology , aneurysm , cancer , surgery , biochemistry
Abdominal aortic aneurysm (AAA) is a significant health problem that affects 6–9% of men over 65 years of age. Surgical repair is the only effective means of AAA treatment. The mechanistic basis for the initiation and progression of the disease which might serve as a therapeutic target for treatment of AAA has not been established. AngII treatment of ApoE−/− mice is a model for AAA formation. MicroRNAs (miRs) are endogenous small RNAs that negatively regulate gene expression in a sequence‐specific manner. MicroRNA arrays demonstrated that miR‐19a is increased in AngII‐induced AAA tissue in ApoE−/− mice. SOCS1 (Suppressor of Cytokine Signaling 1) has been shown to play a protective role in inflammatory diseases via inhibition of p‐STAT3 activity. Based on a computational analysis, we found the binding sequence of miR‐19a in 3′UTR of SOCS1 mRNA suggesting that miR‐19a might inhibit SOCS1 protein expression and decrease the inhibition of inflammation by SOCS1. We demonstrated that SOCS1 is decreased and pSTAT3 is increased in AngII‐induced aneurysmal tissue from ApoE−/− mice. Furthermore, treatment of bone marrow derived macrophages with AngII resulted in increased expression of mir‐19a and decreased SOCS1 and increased pSTAT3. These data suggest the conclusion that miR‐19a might play a role in AngII‐induced AAA formation by inhibiting SOCS1 inhibition of inflammation.