BTLA deficiency promotes HSC activation and protects against hepatic ischemia-reperfusion injury.

ABSTRACT:

Background and aims

Hepatic ischemia-reperfusion injury (IRI) is unavoidable even despite the development of more effective surgical approaches. During hepatic IRI, activated HSC (aHSC) are involved in liver injury and recovery.

Approach and result

A proportion of aHSC increased significantly both in the mouse liver tissues with IRI and in the primary mouse HSCs and LX-2 cells during hypoxia-reoxygenation. "Loss-of-function" experiments revealed that depleting aHSC with gliotoxin exacerbated liver damage in IRI mice. Subsequently, we found that the transcription of mRNA and the expression of B and T lymphocyte attenuator (BTLA) protein were lower in aHSC compared with quiescent HSCs. Interestingly, overexpression or knockdown of BTLA resulted in opposite changes in the activ

SUBMITTER: Shen X 

PROVIDER: S-EPMC11155569 | biostudies-literature | 2024 Jun

REPOSITORIES: biostudies-literature