Mechanism of paracrine communications between hepatic progenitor cells and endothelial cells.
Angiogenesis
Colony stimulating factor 1
Differentiation
Endothelial cells
Hepatic progenitor cells
Paracrine
Journal
Cellular signalling
ISSN: 1873-3913
Titre abrégé: Cell Signal
Pays: England
ID NLM: 8904683
Informations de publication
Date de publication:
Dec 2022
Dec 2022
Historique:
received:
31
05
2022
revised:
16
08
2022
accepted:
25
08
2022
medline:
23
10
2023
pubmed:
3
9
2022
entrez:
2
9
2022
Statut:
ppublish
Résumé
Hepatic progenitor cells (HPCs) are facultative tissue-specific stem cells lining reactive ductules, which are ubiquitously observed in chronic liver diseases and cancer. Although previous research mainly focused on their contribution to liver regeneration, it turned out that in vivo differentiation of HPCs into hepatocytes only occurs after extreme injury. While recent correlative evidence implies the association of HPCs with disease progression, their exact role in pathogenesis remains largely unknown. Our previous research demonstrated that HPCs expressing angiogenic paracrine factors accumulate in the peritumoral area and are positively correlated with the extent of intratumoral cell proliferation and angiogenesis in the livers of patients with liver cancer. Given the crucial roles of angiogenesis in liver disease progression and carcinogenesis, we aimed to test the hypothesis that HPCs secrete paracrine factors to communicate with endothelial cells, to determine molecular mechanisms mediating HPCs-endothelial interactions, and to understand how the paracrine function of HPCs is regulated. HPCs promoted viability and tubulogenesis of human umbilical vein endothelial cells (HUVECs) and upregulated genes known to be involved in angiogenesis, endothelial cell function, and disease progression in a paracrine manner. The paracrine function of HPCs as well as expression of colony stimulating factor 1 (CSF1) were inhibited upon differentiation of HPCs toward hepatocytes. Inhibition of CSF1 receptor partly suppressed the paracrine effects of HPCs on HUVECs. Taken together, our study indicates that inhibition of the paracrine function of HPCs through modulation of their differentiation status and inhibition of CSF1 signaling is a promising strategy for inhibition of angiogenesis during pathological progression.
Identifiants
pubmed: 36055565
pii: S0898-6568(22)00220-0
doi: 10.1016/j.cellsig.2022.110458
pmc: PMC9971365
mid: NIHMS1836600
pii:
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
110458Subventions
Organisme : NIDDK NIH HHS
ID : P30 DK078392
Pays : United States
Organisme : NCI NIH HHS
ID : R37 CA225807
Pays : United States
Informations de copyright
Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of Competing Interest None.
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