The Role of Mesothelin in Activation of Portal Fibroblasts in Cholestatic Liver Injury.
activated Hepatic Stellate Cells
activated Portal Fibroblasts
cholestatic fibrosis
Journal
Biology
ISSN: 2079-7737
Titre abrégé: Biology (Basel)
Pays: Switzerland
ID NLM: 101587988
Informations de publication
Date de publication:
28 Oct 2022
28 Oct 2022
Historique:
received:
21
09
2022
revised:
18
10
2022
accepted:
27
10
2022
entrez:
11
11
2022
pubmed:
12
11
2022
medline:
12
11
2022
Statut:
epublish
Résumé
Fibrosis is a common consequence of abnormal wound healing, which is characterized by infiltration of myofibroblasts and formation of fibrous scar. In liver fibrosis, activated Hepatic Stellate Cells (aHSCs) and activated Portal Fibroblasts (aPFs) are the major contributors to the origin of hepatic myofibroblasts. aPFs are significantly involved in the pathogenesis of cholestatic fibrosis, suggesting that aPFs may be a primary target for anti-fibrotic therapy in cholestatic injury. aPFs are distinguishable from aHSCs by specific markers including mesothelin (Msln), Mucin 16 (Muc16), and Thymus cell antigen 1 (Thy1, CD90) as well as fibulin 2, elastin, Gremlin 1, ecto-ATPase nucleoside triphosphate diphosphohydrolase 2. Msln plays a critical role in activation of PFs, via formation of Msln-Muc16-Thy1 complex that regulates TGFβ1/TGFβRI-mediated fibrogenic signaling. The opposing pro- and anti-fibrogenic effects of Msln and Thy1 are key components of the TGFβ1-induced activation pathway in aPFs. In addition, aPFs and activated lung and kidney fibroblasts share similarities across different organs with expression of common markers and activation cascade including Msln-Thy1 interaction. Here, we summarize the potential function of Msln in activation of PFs and development of cholestatic fibrosis, offering a novel perspective for anti-fibrotic therapy targeting Msln.
Identifiants
pubmed: 36358290
pii: biology11111589
doi: 10.3390/biology11111589
pmc: PMC9687690
pii:
doi:
Types de publication
Journal Article
Review
Langues
eng
Subventions
Organisme : Japan Society for the Promotion of Science
ID : No. 18K16280 (YK) and 21K16444 (TN)
Organisme : NIDDK NIH HHS
ID : P30 DK120515
Pays : United States
Organisme : Takeda Science Foundation
ID : (TN)
Organisme : NIDDK NIH HHS
ID : R01 DK091183
Pays : United States
Organisme : NIH HHS
ID : K099205, AA028550, DK101737, AA011999, DK120515, AA029019, DK091183 (TK), P42ES010337 and R44DK115242 (DB)
Pays : United States
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