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Gene. 2018 Jun 5;658:129-135. doi: 10.1016/j.gene.2018.02.050. Epub 2018 Mar 22.

MicroRNA-216b actively modulates diabetic angiopathy through inverse regulation on FZD5.

Author information

1
Department of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
2
Department of Cardiology, Xinhua Hospital of Zhejiang Province, The Second Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou 310003, China.
3
Department of Geratology, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
4
Department of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai 200032, China. Electronic address: jbge@zs-hospital.sh.cn.

Abstract

BACKGROUND:

In this work, we examined the angiogenic function of microRNA-216b in an in vitro rat diabetic model of myocardial microvascular endothelial cells (MMECs).

METHODS:

MMECs were extracted from Wistar rats (MMEC(WI)) or diabetic Goto-Kakizaki (GK) rats (MMEC(GK)) and cultured in vitro. QRT-PCR was applied to compare miR-216b between MMEC(WI) and MMEC(GK). MiR-216b was downregulated in MMEC(GK). Its effects on angiogenic development, including invasion and proliferation, were evaluated. In MMEC(GK), putative miR-216b downstream target gene, frizzled class receptor 5 (FZD5), was evaluated by dual-luciferase reporter, qRT-PCR and western blot assays, respectively. FZD5 was further downregulated in MMEC(GK) with stable miR-216b downregulation to evaluate its functional role in regulating diabetic angiogenesis.

RESULTS:

MiR-216b was markedly overexpressed in MMEC(GK). MiR-216b downregulation significantly enhanced angiogenesis in MMEC(GK) by promoting invasion and proliferation. FZD5 was inversely upregulated in miR-216b-downregulated MMEC(GK). Subsequently, FZD5 downregulation suppressed angiogenic development, by inhibiting invasion and proliferation in miR-216b-downregulated MMEC(GK).

CONCLUSION:

MicroRNA-216b was overexposed in diabetic MMECs and its downregulation may actively enhance angiogenesis in diabetic angiopathy through inverse regulation on FZD5.

KEYWORDS:

Angiopathy; FZD5; Microvascular, endothelial; Type-II diabetes; miR-216b

PMID:
29477872
DOI:
10.1016/j.gene.2018.02.050
[Indexed for MEDLINE]

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