Retinoids Repress Human Cardiovascular Cell Calcification With Evidence for Distinct Selective Retinoid Modulator Effects.
Alkaline Phosphatase
Aortic Valve
/ drug effects
Apolipoprotein C-III
/ genetics
Calcium-Binding Proteins
/ genetics
Carotid Arteries
/ drug effects
Carrier Proteins
/ genetics
Cells, Cultured
Cholesterol 7-alpha-Hydroxylase
/ genetics
Coronary Vessels
/ drug effects
Extracellular Matrix Proteins
/ genetics
Heart Valve Diseases
/ genetics
Humans
Isotretinoin
/ pharmacology
Muscle, Smooth, Vascular
/ drug effects
Myocytes, Smooth Muscle
/ drug effects
Osteogenesis
/ drug effects
Receptors, Retinoic Acid
/ agonists
Retinoids
/ pharmacology
Signal Transduction
Tretinoin
/ pharmacology
Vascular Calcification
/ genetics
Matrix Gla Protein
cell differentiation
humans
osteoblasts
retinoids
tretinoin
Journal
Arteriosclerosis, thrombosis, and vascular biology
ISSN: 1524-4636
Titre abrégé: Arterioscler Thromb Vasc Biol
Pays: United States
ID NLM: 9505803
Informations de publication
Date de publication:
03 2020
03 2020
Historique:
pubmed:
20
12
2019
medline:
15
7
2020
entrez:
20
12
2019
Statut:
ppublish
Résumé
Retinoic acid (RA) is a ligand for nuclear receptors that modulate gene transcription and cell differentiation. Whether RA controls ectopic calcification in humans is unknown. We tested the hypothesis that RA regulates osteogenic differentiation of human arterial smooth muscle cells and aortic valvular interstitial cells that participate in atherosclerosis and heart valve disease, respectively. Approach and Results: Human cardiovascular tissue contains immunoreactive RAR (RA receptor)-a retinoid-activated nuclear receptor directing multiple transcriptional programs. RA stimulation suppressed primary human cardiovascular cell calcification while treatment with the RAR inhibitor AGN 193109 or These results establish retinoid regulation of human cardiovascular calcification, provide new insight into mechanisms involved in these responses, and suggest selective retinoid modulators, like acyclic retinoids may allow for treating cardiovascular calcification without the adverse effects associated with cyclic retinoids.
Identifiants
pubmed: 31852220
doi: 10.1161/ATVBAHA.119.313366
pmc: PMC7047603
mid: NIHMS1548899
doi:
Substances chimiques
APOC3 protein, human
0
Apolipoprotein C-III
0
Calcium-Binding Proteins
0
Carrier Proteins
0
Extracellular Matrix Proteins
0
Receptors, Retinoic Acid
0
Retinoids
0
(2E,4E,6E,10E)-3,7,11,15-tetramethyl-2,4,6,10,14-hexadecapentaenoic acid
11ALM7A4RV
Tretinoin
5688UTC01R
CYP7A1 protein, human
EC 1.14.14.23
Cholesterol 7-alpha-Hydroxylase
EC 1.14.14.23
ALPL protein, human
EC 3.1.3.1
Alkaline Phosphatase
EC 3.1.3.1
Isotretinoin
EH28UP18IF
Types de publication
Comparative Study
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
656-669Subventions
Organisme : NHLBI NIH HHS
ID : R01 HL141917
Pays : United States
Organisme : NHLBI NIH HHS
ID : P01 HL048743
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL136431
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL134892
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL114805
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL147095
Pays : United States
Commentaires et corrections
Type : CommentIn
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