Role of miR-148a in Mitigating Hepatic Ischemia-Reperfusion Injury by Repressing the TLR4 Signaling Pathway via Targeting CaMKIIα in Vivo and in Vitro | Zendy

Daofeng Zheng | Zendy; Zhongtang Li | Zendy; Xufu Wei | Zendy; Rui Liu | Zendy; Ai Shen | Zendy; Diao He | Zendy; Chengyong Tang | Zendy; Zhongjun Wu | Zendy

Open Access

Role of miR-148a in Mitigating Hepatic Ischemia-Reperfusion Injury by Repressing the TLR4 Signaling Pathway via Targeting CaMKIIα in Vivo and in Vitro

Author(s) -

Daofeng Zheng,

Zhongtang Li,

Xufu Wei,

Rui Liu,

Ai Shen,

Diao He,

Chengyong Tang,

Zhongjun Wu

Publication year - 2018

Publication title -

cellular physiology and biochemistry

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.486

H-Index - 87

eISSN - 1421-9778

pISSN - 1015-8987

DOI - 10.1159/000493716

Subject(s) - inflammation , reperfusion injury , liver injury , in vivo , signal transduction , apoptosis , western blot , biology , tlr4 , downregulation and upregulation , chemistry , microbiology and biotechnology , ischemia , immunology , endocrinology , medicine , biochemistry , gene

Hepatic ischemia-reperfusion (I/R) injury, which is mainly induced by inflammation and unstable intracellular ions, is a major negative consequence of surgery that compromises hepatic function. However, the exact mechanisms of liver I/R injury have not been determined. Positive crosstalk with the Ca2+/CaMKII pathway is required for complete activation of the TLR4 pathway and inflammation. We previously found that miR-148a, which decreased in abundance with increasing reperfusion time, targeted and repressed the expression of CaMKIIα. In the present study, we examined the role of the miR-148a machinery in I/R-induced Ca2+/CaMKII and TLR4 signaling changes, inflammation, and liver dysfunction in vivo and in vitro.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.

Having issues? You can contact us here

Accelerating Research