In:
Journal of Cellular and Molecular Medicine, Wiley, Vol. 20, No. 6 ( 2016-06), p. 1159-1169
Abstract:
Cyclin D2 is involved in the pathology of vascular complications of type 2 diabetes mellitus (T2 DM ). This study investigated the role of cyclin‐D2‐regulated mi RNA s in endothelial cell proliferation of T2 DM . Results showed that higher glucose concentration (4.5 g/l) significantly promoted the proliferation of rat aortic endothelial cells ( RAOEC s), and significantly increased the expression of cyclin D2 and phosphorylation of retinoblastoma 1 (p‐ RB 1) in RAOEC s compared with those under low glucose concentration. The cyclin D2‐3′ untranslated region is targeted by miR‐98, as demonstrated by mi RNA analysis software. Western blot also confirmed that cyclin D2 and p‐ RB 1 expression was regulated by miR‐98. The results indicated that miR‐98 treatment can induce RAOEC apoptosis. The suppression of RAOEC growth by miR‐98 might be related to regulation of Bcl‐2, Bax and Caspase 9 expression. Furthermore, the expression levels of miR‐98 decreased in 4.5 g/l glucose‐treated cells compared with those treated by low glucose concentration. Similarly, the expression of miR‐98 significantly decreased in aortas of established streptozotocin ( STZ )‐induced diabetic rat model compared with that in control rats; but cyclin D2 and p‐ RB 1 levels remarkably increased in aortas of STZ ‐induced diabetic rats compared with those in healthy control rats. In conclusion, this study demonstrated that high glucose concentration induces cyclin D2 up‐regulation and miR‐98 down‐regulation in the RAOEC s. By regulating cyclin D2, miR‐98 can inhibit human endothelial cell growth, thereby providing novel therapeutic targets for vascular complication of T2 DM .
Type of Medium:
Online Resource
ISSN:
1582-1838
,
1582-4934
DOI:
10.1111/jcmm.2016.20.issue-6
Language:
English
Publisher:
Wiley
Publication Date:
2016
detail.hit.zdb_id:
2076114-4
