Procollagen C-Proteinase Enhancer-1 (PCPE-1) deficiency in mice reduces liver fibrosis but not NASH progression

This article is currently being updated. View its version on PubMed.

https://pubmed.ncbi.nlm.nih.gov/35148334

Research summary

This study investigated the role of PCPE-1 in liver fibrosis and nonalcoholic steatohepatitis (NASH) progression. Using Pcolce Knockout (Pcolce^-/-) mice subjected to a choline-deficient, amino acid-defined high-fat diet (CDA HFD) for 8 weeks, researchers observed that PCPE-1 deficiency significantly reduced liver fibrosis, evidenced by decreased collagen deposition and cross-linking. However, PCPE-1 deficiency did not affect hepatic steatosis, inflammation, or liver dysfunction, indicating that while PCPE-1 contributes to fibrosis development, it does not influence the progression of NASH.

Key outcome of the study

PCPE-1 deficiency leads to reduced liver fibrosis without impacting steatosis or inflammation, suggesting its specific role in collagen maturation and fibrosis development in NASH.

Mouse model

Global Pcolce Knockout (Pcolce^-/-) mouse model, generated by constitutive deletion of the Pcolce gene to study its role in liver fibrosis and NASH progression.

TARGET:
Pcolce
Procollagen C-Proteinase Enhancer-1

Keywords

Liver fibrosis, NASH, Collagen maturation, PCPE-1, Extracellular matrix remodeling

Technical specifications

Constitutive Knockout model, Pcolce gene deletion, CDA HFD-induced NASH model

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KO repository

>2000 conditional Knockout mouse models for target discovery and  confirmation, in vivo compound specificity, MOA, and clinical studies

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