Retinoic acid upregulates beta(1)-integrin in vascular smooth muscle cells and alters adhesion to fibronectin. Am J Physiol Heart Circ Physiol 2000 Jul;279(1):H382-7
Date
07/19/2000Pubmed ID
10899079DOI
10.1152/ajpheart.2000.279.1.H382Scopus ID
2-s2.0-0033855605 (requires institutional sign-in at Scopus site) 30 CitationsAbstract
Retinoic acid has an established physiological role in differentiation, development, and cellular growth. This study investigated the action of all-trans retinoic acid (ATRA) on vascular integrins, cell-surface receptors that control growth and remodeling of blood vessels. The beta(1)-integrin subunit mRNA and protein was induced after treatment with ATRA in two different rat vascular smooth muscle cell lines. To relate this result to the in vivo state, the aortas from adult rats fed with therapeutic doses of ATRA were examined for beta(1)-integrin protein. A significant upregulation of the integrin subunit was observed in vivo. To assess if this increase contributed to physiological changes in cellular function, cells treated with ATRA were tested for alterations in adhesion to extracellular matrix proteins. The cells exposed to the retinoid were seen to adhere more strongly to fibronectin, via the beta(1)-integrin. These results showed that modulation of vascular integrins by ATRA in adult rats contributes to functional changes that can cause remodeling of blood vessels.
Author List
Medhora MMMESH terms used to index this publication - Major topics in bold
AnimalsAorta
Cell Adhesion
Cell Line
Cells, Cultured
Fibronectins
Gene Expression Regulation
Integrin beta1
Muscle, Smooth, Vascular
Protein Biosynthesis
Pulmonary Artery
RNA, Messenger
Rats
Transcription, Genetic
Tretinoin
