Antifibrogenic Activities of CYP11A1-derived Vitamin D3-hydroxyderivatives Are Dependent on RORγ.


Journal

Endocrinology
ISSN: 1945-7170
Titre abrégé: Endocrinology
Pays: United States
ID NLM: 0375040

Informations de publication

Date de publication:
01 01 2021
Historique:
received: 27 07 2020
pubmed: 28 10 2020
medline: 15 5 2021
entrez: 27 10 2020
Statut: ppublish

Résumé

Previous studies showed that noncalcemic 20(OH)D3, a product of CYP11A1 action on vitamin D3, has antifibrotic activity in human dermal fibroblasts and in a bleomycin mouse model of scleroderma. In this study, we tested the role of retinoic acid-related orphan receptor γ (RORγ), which is expressed in skin, in the action of CYP11A1-derived secosteroids using murine fibroblasts isolated from the skin of wild-type (RORγ +/+), knockout (RORγ -/-), and heterozygote (RORγ +/-) mice. CYP11A1-derived 20(OH)D3, 20,23(OH)2D3, 1,20(OH)2D3, and 1,20,23(OH)3D3 inhibited proliferation of RORγ +/+ fibroblasts in a dose-dependent manner with a similar potency to 1,25(OH)2D3. Surprisingly, this effect was reversed in RORγ +/- and RORγ -/- fibroblasts, with the most pronounced stimulatory effect seen in RORγ -/- fibroblasts. All analogs tested inhibited TGF-β1-induced collagen synthesis in RORγ +/+ fibroblasts and the expression of other fibrosis-related genes. This effect was curtailed or reversed in RORγ -/- fibroblasts. These results show that the antiproliferative and antifibrotic activities of the vitamin D hydroxy derivatives are dependent on a functional RORγ. The dramatic changes in the transcriptomes of fibroblasts of RORγ -/- versus wild-type mice following treatment with 20(OH)D3 or 1,20(OH)2D3 provide a molecular basis to explain, at least in part, the observed phenotypic differences.

Identifiants

pubmed: 33107570
pii: 5940802
doi: 10.1210/endocr/bqaa198
pmc: PMC7717072
pii:
doi:

Substances chimiques

Nuclear Receptor Subfamily 1, Group F, Member 3 0
Bleomycin 11056-06-7
Cholecalciferol 1C6V77QF41
Cholesterol Side-Chain Cleavage Enzyme EC 1.14.15.6

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, N.I.H., Intramural

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : NIAMS NIH HHS
ID : R01 AR071189
Pays : United States
Organisme : NIAMS NIH HHS
ID : R01 AR073004
Pays : United States
Organisme : NIAMS NIH HHS
ID : R01 AR052190
Pays : United States
Organisme : BLRD VA
ID : I01 BX004293
Pays : United States
Organisme : NIAID NIH HHS
ID : R21 AI149267
Pays : United States

Informations de copyright

© The Author(s) 2020. Published by Oxford University Press on behalf of the Endocrine Society. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

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Auteurs

Zorica Janjetovic (Z)

Department of Dermatology, University of Alabama at Birmingham, Birmingham, Alabama.

Arnold Postlethwaite (A)

Department of Medicine, University of Tennessee Health Science Center, Veteran Administration Medical Center, Memphis, Tennessee.

Hong Soon Kang (HS)

Cell Biology Section, Immunity, Inflammation and Disease Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina.

Tae-Kang Kim (TK)

Department of Dermatology, University of Alabama at Birmingham, Birmingham, Alabama.

Robert C Tuckey (RC)

School of Molecular Sciences, the University of Western Australia, Crawley, Western Australia, Australia.

David K Crossman (DK)

Department of Genetics, UAB.

Shariq Qayyum (S)

Department of Dermatology, University of Alabama at Birmingham, Birmingham, Alabama.

Anton M Jetten (AM)

Cell Biology Section, Immunity, Inflammation and Disease Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina.

Andrzej T Slominski (AT)

Department of Dermatology, University of Alabama at Birmingham, Birmingham, Alabama.
VA Medical Center, Birmingham, Alabama.

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Classifications MeSH