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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2000;20:1882.)
© 2000 American Heart Association, Inc.

Brief Reviews

Retinoids and Arterial Smooth Muscle Cells

Pascal Neuville; Marie-Luce Bochaton-Piallat; Giulio Gabbiani

From the Department of Pathology, University of Geneva-CMU, Geneva, Switzerland.

Correspondence to Prof Giulio Gabbiani, Department of Pathology, University of Geneva-CMU, 1 Rue Michel Servet, 1211 Geneva 4/Switzerland. E-mail Giulio.Gabbiani@medecine.unige.ch (Arterioscler Thromb Vasc Biol. 2000;20:1882-1888.)

Key Words: -smooth muscle actin • myofibroblast • atheroma • wound healing • TGF-ß

	Introduction

 
Retinoic acid (RA), the active metabolite of vitamin A, is a crucial signaling molecule during vertebrate development and plays key roles in establishing cell lineages as well as in cell differentiation and proliferation.¹ RA has been shown to influence the expression of many genes (see the Table) through interactions between RA receptors (RARs) and the RA response element (RARE) located in promoter regions.^{42 43} RARs, transducers of the RA signal at the gene expression level, are members of the nuclear receptor superfamily. Essentially 2 subfamilies of nuclear receptor are known to function as RA-dependent transcription factors: the RARs and the retinoid X receptors (RXRs).⁴⁴ These receptors, in the form of homodimers or heterodimers, recognize response elements located in the promoter regions of target genes. For each subfamily, 3 different genes (RAR-, -ß, and -; RXR-, -ß, and -) generate multiple isoforms with specific patterns of expression in both the embryo and adult, suggesting that they perform specific functions in the control of RA target genes.⁴⁵ The uptake, transport, and metabolism of all-trans retinol is regulated by the cellular retinol-binding proteins (CRBP I and CRBP II), whereas the cellular RA-binding proteins (CRABP I and CRABP II) exert the same function for RA.¹ Unlike RARs, retinoid-binding proteins modulate the effect of RA by regulating its intracellular level. Several lines of evidence indicate that CRBPs and CRABPs have distinct physiological roles. CRBPs provide the substrate for RA biosynthesis,⁴⁶ whereas CRABPs are substrates for RA catabolism.⁴⁷ Retinoids have . . . [Full Text of this Article]

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