Inhibition of miR-450b-5p ameliorates hepatic ischemia/reperfusion injury via targeting CRYAB.


Journal

Cell death & disease
ISSN: 2041-4889
Titre abrégé: Cell Death Dis
Pays: England
ID NLM: 101524092

Informations de publication

Date de publication:
12 06 2020
Historique:
received: 03 02 2020
accepted: 25 05 2020
revised: 21 05 2020
entrez: 14 6 2020
pubmed: 14 6 2020
medline: 13 4 2021
Statut: epublish

Résumé

Hepatic ischemia/reperfusion injury (IRI) is an unavoidable course in liver transplantation, during which the immune response of inflammation plays a leading part. MicroRNA-450b-5p (miR-450b-5p), which has been reported to participate in several inflammatory diseases, was investigated in this study. The purpose of this study is to identify the potential function of miR-450b-5p toward remission of hepatic IRI and elucidate the specific mechanism. Herein we found that expression of miR-450b-5p, interleukin (IL)-1β, tumor necrosis factor-α (TNF-α), and IL-6 was stimulated in hepatic IRI. Inhibition of miR-450b-5p could remarkably alleviate mouse hepatic IRI and improve liver function measured by hematoxylin-eosin (HE) staining, terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL), and enzyme-linked immunosorbent assay (ELISA). We further assessed protein expression undergoing Western blot and immunofluorescence, and discovered that miR-450b-5p suppressed alpha B-crystallin (CRYAB), thus restraining the inhibitory κB kinase (IKK) β-mediated canonical nuclear factor-κB (NF-κB) signaling, instead of the noncanonical path guided by IKKα in hepatic IRI. In addition, we demonstrated CRYAB as an activator of M2 polarization through protein kinase B (Akt) 1/mammalian target of rapamycin (mTOR), thus resulting in relief of liver IRI. Combination treatment containing both paths revealed a better antidamage efficacy than adjusting either path alone, suggesting that the joint therapy might be a promising solution in hepatic IRI.

Identifiants

pubmed: 32532961
doi: 10.1038/s41419-020-2648-0
pii: 10.1038/s41419-020-2648-0
pmc: PMC7293338
doi:

Substances chimiques

CRYAB protein, human 0
MIRN450 microRNA, human 0
MicroRNAs 0
alpha-Crystallin B Chain 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

455

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Auteurs

Zuotian Huang (Z)

Department of Hepatobiliary Surgery, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China.

Tong Mou (T)

Department of Hepatobiliary Surgery, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China.

Yunhai Luo (Y)

Department of Hepatobiliary Surgery, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China.

Xingyu Pu (X)

West China School of Medicine, Sichuan University, Chongqing, China.

Junliang Pu (J)

Department of Hepatobiliary Surgery, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China.

Lei Wan (L)

Phase I Clinical Trial Ward, First Affiliated Hospital of Chongqing Medical University, Chongqing, China.

Junhua Gong (J)

Department of Hepatobiliary Surgery, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China.

Hang Yang (H)

Department of Hepatobiliary Surgery, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China.

Yanyao Liu (Y)

Department of Hepatobiliary Surgery, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China.

Zhongtang Li (Z)

Department of Hepatobiliary Surgery, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China.

Ai Shen (A)

Hepatobiliary Pancreatic Tumor Center, Chongqing University Cancer Hospital, Chongqing, China.

Zhongjun Wu (Z)

Department of Hepatobiliary Surgery, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China. wzjtcy@126.com.

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