Protein Tyrosine Phosphatase 1B Deficiency in Vascular Smooth Muscle Cells Promotes Perivascular Fibrosis following Arterial Injury.
Animals
Cells, Cultured
Fibrosis
Mice
Mice, Knockout
Muscle, Smooth, Vascular
/ pathology
Myocytes, Smooth Muscle
/ pathology
Protein Tyrosine Phosphatase, Non-Receptor Type 1
/ genetics
RNA, Messenger
/ metabolism
RNA, Small Interfering
/ metabolism
Recombinases
/ metabolism
Transforming Growth Factor beta
/ metabolism
Vascular Remodeling
Vascular System Injuries
/ genetics
Journal
Thrombosis and haemostasis
ISSN: 2567-689X
Titre abrégé: Thromb Haemost
Pays: Germany
ID NLM: 7608063
Informations de publication
Date de publication:
Oct 2022
Oct 2022
Historique:
pubmed:
9
9
2022
medline:
28
9
2022
entrez:
8
9
2022
Statut:
ppublish
Résumé
Smooth muscle cell (SMC) phenotype switching plays a central role during vascular remodeling. Growth factor receptors are negatively regulated by protein tyrosine phosphatases (PTPs), including its prototype PTP1B. Here, we examine how reduction of PTP1B in SMCs affects the vascular remodeling response to injury. Mice with inducible PTP1B deletion in SMCs (SMC.PTP1B-KO) were generated by crossing mice expressing Cre.ER Genetic deletion of PTP1B in SMCs resulted in adventitia enlargement, perivascular SMA Chronic reduction of PTP1B in SMCs promotes dedifferentiation, perivascular fibrosis, and adverse remodeling following vascular injury by mechanisms involving an ERK1/2 phosphorylation-driven shift from SMAD2 to KLF4-regulated gene transcription.
Sections du résumé
BACKGROUND
BACKGROUND
Smooth muscle cell (SMC) phenotype switching plays a central role during vascular remodeling. Growth factor receptors are negatively regulated by protein tyrosine phosphatases (PTPs), including its prototype PTP1B. Here, we examine how reduction of PTP1B in SMCs affects the vascular remodeling response to injury.
METHODS
METHODS
Mice with inducible PTP1B deletion in SMCs (SMC.PTP1B-KO) were generated by crossing mice expressing Cre.ER
RESULTS
RESULTS
Genetic deletion of PTP1B in SMCs resulted in adventitia enlargement, perivascular SMA
CONCLUSION
CONCLUSIONS
Chronic reduction of PTP1B in SMCs promotes dedifferentiation, perivascular fibrosis, and adverse remodeling following vascular injury by mechanisms involving an ERK1/2 phosphorylation-driven shift from SMAD2 to KLF4-regulated gene transcription.
Identifiants
pubmed: 36075234
doi: 10.1055/s-0042-1755329
pmc: PMC9512587
doi:
Substances chimiques
RNA, Messenger
0
RNA, Small Interfering
0
Recombinases
0
Transforming Growth Factor beta
0
Protein Tyrosine Phosphatase, Non-Receptor Type 1
EC 3.1.3.48
Ptpn1 protein, mouse
EC 3.1.3.48
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
1814-1826Subventions
Organisme : SCHA 808/15-1
ID : Deutsche Forschungsgemeinschaft
Organisme : DZHK e.V.; Doktoranden-Stipendium
ID : K.S.) and the German Center for Cardiovascular Research
Informations de copyright
The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution-NonDerivative-NonCommercial License, permitting copying and reproduction so long as the original work is given appropriate credit. Contents may not be used for commercial purposes, or adapted, remixed, transformed or built upon. (https://creativecommons.org/licenses/by-nc-nd/4.0/).
Déclaration de conflit d'intérêts
None declared.
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