Deletion of Annexin A2 protects from liver injury after massive small bowel resection in mice
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Updated: Sep 3, 2026
Ileectomy-induced Bile Overaccumulation in Mouse Intestine
Published on: August 21, 2017
Daniel Alligood1, Alex Park1, Kerry Swanson1
1Department of Surgery, Division of Pediatric Surgery, Washington University in St. Louis, United States.
Background:
Short gut syndrome (SGS) after extensive small bowel resection (SBR) is associated with intestinal failure associated liver disease (IFALD). Previously, we identified Annexin A2 (Anxa2) hepatocytes with fibrotic transcriptional alterations in a murine intestinal failure model. This study investigates Anxa2's role in the pathogenesis of IFALD.
Methods:
Wild type 8 to 12-week-old C57BL/6J (WT control) and B6J.129X1-Anxa2tm1Kah/Mmmh (A2KO) female mice underwent sham or 75% proximal SBR and sacrificed 10-weeks post-operatively. Liver injury was assessed with serum markers, histology and bulk RNA sequencing.
Results:
A2KO SBR liver showed a reduction in liver injury marked by reduction in serum transaminases, liver steatosis, and liver fibrosis. Bulk RNA sequencing found A2KO SBR liver has upregulation of gene sets related to oxidative response and beta-oxidation with reduction in fibrotic and innate immune system responses.
Conclusions:
Anxa2 appears to be a putative factor in fibrogenesis with multifactorial roles. Targeting Anxa2 may serve as a novel therapeutic approach in both IFALD and other liver pathologies.
