Differential recruitment of monocyte-derived macrophages in control and stellate cell-depleted mice during recurrent carbon tetrachloride-induced acute liver injury.

ABSTRACT: Liver depleted of hepatic stellate cells (HSCs) is resistant to ischemia/reperfusion-, concanavalin A-, and acetaminophen-induced acute injury. Whether HSCs regulate carbon tetrachloride (CCl₄ )-induced acute liver injury is not known. CCl₄ treatment damages pericentral hepatocytes that express CCl₄ -metabolizing Cyp2E1 and activates HSCs. We investigated whether HSC-depletion in mice transgenic for thymidine kinase under the glial fibrillary acidic protein promoter (GFAP-TK-Tg) confers resistance to injury and inflammation due to CCl₄ rechallenge. GFAP-TK-Tg or wild type (WT) mice were administered 0.16 ml/kg CCl₄ (3× at 3 days intervals), then 40 μg/g/day ganciclovir for 10 days. The treatment depletes ~70%-75% HSCs from GFAP-TK-Tg b

SUBMITTER: Sharma A 

PROVIDER: S-EPMC11296225 | biostudies-literature | 2022 Nov

REPOSITORIES: biostudies-literature