Collagen Characterization in a Model of Nonalcoholic Steatohepatitis with Fibrosis; A Call for Development of Targeted Therapeutics

Left untreated, nonalcoholic fatty liver disease can progress to nonalcoholic steatohepatitis (NASH), fibrosis, and end-stage liver disease. To date, few if any therapies have proven effective against NASH with fibrosis. Quantification and qualification of hepatic scar might enable development of mo...

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Published inMolecules (Basel, Switzerland) Vol. 26; no. 11; p. 3316
Main Authors Pellicano, Anthony J., Spahn, Kiera, Zhou, Ping, Goldberg, Itzhak D., Narayan, Prakash
Format Journal Article
LanguageEnglish
Published Basel MDPI AG 01.06.2021
MDPI
Subjects
Animal models
Biomarkers
Biopsy
Collagen
Collagen (type I)
collagen type III
Deposition
Drug development
Extracellular matrix
Fatty liver
Fibrosis
Gene expression
Hydroxyproline
Hypotheses
Inflammation
Liver
Liver diseases
Microscopic analysis
Microscopy
NASH
Parenchyma
Patients
precision therapeutics
Scars
Stains & staining
Tissue analysis
transcriptomic
Transplants & implants
United States > US
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Summary:Left untreated, nonalcoholic fatty liver disease can progress to nonalcoholic steatohepatitis (NASH), fibrosis, and end-stage liver disease. To date, few if any therapies have proven effective against NASH with fibrosis. Quantification and qualification of hepatic scar might enable development of more effective targeted therapies. In a murine model of NASH induced by diet, we characterized fibrillar collagen deposition within the hepatic parenchyma. At harvest, livers from the modified diet cohort exhibited NASH with fibrosis. Transcriptomic analysis of hepatic tissue revealed increased col1a1, col1a2, and col3a1, each of which correlated directly with hepatic hydroxyproline content. Circular polarized microscopic analysis of Picrosirius red-stained liver sections revealed deposition of collagen type I within the parenchyma. Development of therapeutics designed to mitigate collagen type I accumulation might prove effective in NASH with fibrosis.
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These authors contributed equally to this work.
ISSN:1420-3049
1420-3049
DOI:10.3390/molecules26113316