2. Academic Validation
  3. FAM49B, restrained by miR-22, relieved hepatic ischemia/reperfusion injury by inhibiting TRAF6/IKK signaling pathway in a Rac1-dependent manner

FAM49B, restrained by miR-22, relieved hepatic ischemia/reperfusion injury by inhibiting TRAF6/IKK signaling pathway in a Rac1-dependent manner

  • Mol Immunol. 2022 Mar;143:135-146. doi: 10.1016/j.molimm.2022.01.015.
Zuotian Huang 1,  Junliang Pu 2,  Yunhai Luo 2,  Jing Fan 2,  Kaili Li 2,  Dadi Peng 2,  Kezhen Zong 2,  Baoyong Zhou 2,  Xiangdong Guan 3,  Fachun Zhou 4
Affiliations

Affiliations

  • 1 The First Affiliated Hospital of Chongqing Medical University, Chongqing, China; Department of Critical Care Medicine, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China.
  • 2 The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
  • 3 Department of Critical Care Medicine, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China. Electronic address: guanxiangdong1962@163.com.
  • 4 The First Affiliated Hospital of Chongqing Medical University, Chongqing, China. Electronic address: cyzfc1966@126.com.
PMID: 35131594 DOI: 10.1016/j.molimm.2022.01.015
Abstract

Hepatic ischemia/reperfusion (I/R) injury plays a pivotal pathogenic role in trauma, hepatectomy, and liver transplantation. However, the whole mechanism remains undescribed. The objective of this study is to investigate the internal mechanism by which microRNA-22 (miR-22) targets family with sequence similarity 49 member B (FAM49B), thus aggravating hepatic I/R injury. Here, we found that miR-22 was upregulated while FAM49B was reduced in hepatic I/R injury. Inhibition of miR-22 in vitro was able to intensify expression of FAM49B, thus reducing phosphorylation of inhibitors of nuclear factor kappa-B kinase (IKK) and downstream pro-inflammatory proteins. A dual luciferase reporter assay indicated that miR-22 directly targeted FAM49B. Remission of hepatic pathologic alterations, Apoptosis, and release of cytokines derived from constraints of miR-22 were abolished in vivo by repressing FAM49B. Further interference of Ras-related C3 botulinum toxin substrate 1 (Rac1) reversed the function of FAM49B inhibition, thus achieving anti-inflammatory consequences.

Keywords

FAM49B; IKK; Inflammation; Ischemia/reperfusion injury; MiR-22.

Figures
Products
嗨！很高兴为您提供帮助！

尊敬的 MCE 客户您好，
请您选择所在区域，我们将转接对应客服为您服务！

热门区域

A

B

C

F

G

H

J

L

N

Q

S

T

X

Y

Z

热 A B C F G H J L N Q S T X Y Z