Retinoic acid enhances the proliferation of smooth muscle cells

Peclo, M. M.; Printseva, O. Yu.

doi:10.1007/bf01942850

Cited by 13 publications

(9 citation statements)

References 10 publications

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“…22,23 The action of retinoids on SMC growth has been the subject of contradictory reports indicating that tRA either increases or decreases SMC proliferation. 24,25 It is now considered that tRA activates mitogenesis in quiescent SMCs and decreases growth-stimulated SMC proliferation, suggesting that more than a single mechanism accounts for the growth-regulatory activity of tRA. 26 In this study, we demonstrate that, in serum-stimulated conditions, tRA inhibits both medial and IT SMC proliferation in vitro and that this effect is more rapid on IT SMCs.…”

Section: Discussionmentioning

confidence: 99%

Retinoic Acid Regulates Arterial Smooth Muscle Cell Proliferation and Phenotypic Features In Vivo and In Vitro Through an RARα-Dependent Signaling Pathway

Neuville

Yan

Gidlöf

et al. 1999

ATVB

105

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Abstract-We have recently shown that all-trans retinoic acid (tRA) modulates arterial smooth muscle cell (SMC) morphologic features and biochemical composition in vitro. It has been proposed that different SMC phenotypes coexist in arteries, which may be retrieved in culture: hence, a differential action of tRA on distinct SMC subsets is conceivable.We have examined the effect of tRA on SMC proliferation, migration, plasminogen activator activity, and ␣-smooth muscle actin expression in 2 phenotypically different rat SMC populations, cultured respectively from the normal aortic media and from the intimal thickening (IT) after endothelial injury. tRA inhibited proliferation and increased migration and tissue-type plasminogen activator activity in both SMC populations, but decreased ␣-smooth muscle actin only in SMC cultured from the IT. The action of tRA is mediated by 2 families of nuclear receptors, RAR and RXR, each containing 3 isoforms, ␣, ␤, and ␥. RAR and RAR-␣ agonists, but not RXR agonists, inhibited SMC proliferation in both cell populations and ␣-smooth muscle actin expression only in IT SMC. When administered intraperitoneally to balloon-injured rats, tRA and RAR-␣ agonists reduced the intimal hyperplasia in the carotid artery. Our results show that tRA and synthetic retinoids can affect the proliferation, migration, and differentiation of SMC in vitro. Key Words: smooth muscle cell heterogeneity Ⅲ smooth muscle cell motility Ⅲ smooth muscle cell differentiation Ⅲ intimal thickening S mooth muscle cell (SMC) differentiation, migration, and proliferation are key factors in the development of atherosclerosis and restenosis after angioplasty. 1,2 These phenomena involve an SMC phenotypic modulation characterized by modification of gene expression. 3 It has been suggested that SMC subsets present in the normal media are particularly prone to undergoing phenotypic modulation, and the concept of SMC heterogeneity is gaining wider acceptance (for review see Reference 4). For instance, SMC populations cultured from the rat aortic media and from the intima 15 days after endothelial injury are characterized by a spindle-shaped and an epithelioid morphology, respectively (for discussion of this point see Reference 5). These 2 phenotypes are also obtained when SMC are cloned from the aortic media or the intima, albeit in different proportions. 6 The regulation of SMC phenotype is thought to be exerted by cytokines, growth factors, and agents regulating differentiation. 7 Within the last category, some agents are known to govern SMC differentiation during embryogenesis, and there is a growing body of evidence suggesting that the genetic programs used during embryogenesis may act also during arterial disease processes. 8,9 Vitamin A plays a crucial role in the regulation of cell growth and differentiation, and its active form, retinoic acid, is involved in signal transduction pathways regulating embryonic development. 10 These effects are mediated by 2 families of nuclear receptors that are ligand-dependent trans...

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Section: Discussionmentioning

confidence: 99%

Retinoic Acid Regulates Arterial Smooth Muscle Cell Proliferation and Phenotypic Features In Vivo and In Vitro Through an RARα-Dependent Signaling Pathway

Neuville

Yan

Gidlöf

et al. 1999

ATVB

105

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“…Retinoic acid enhances cell growth of several different cell types in vitro (Jetten, 1984;Peclo and Printseva, 1987). Ide and Aono (1988) and Paulsen (1989) reported that retinoic acid has a mitogenic effect on normal distal, but not proximal, limb bud mesoderm in vitro.…”

Section: Discussionmentioning

confidence: 99%

The talpid² chick limb has weak polarizing activity and can respond to retinoic acid and polarizing zone signal

Dvorak

Fallon

1992

Developmental Dynamics

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The tuZpi8 @a2) chick mutant has wide, polydactylous wings and legs. TuZpid2 limb cartilages have abnormal morphology and a very subtle anteroposterior polarity. Specifically, posterior ta2 limb structures are identifiable, while more anterior cartilages are less distinctive. Here, we investigate the development of anteroposterior limb pattern in the tu2 embryo. We show that tu2 posterior limb bud mesoderm is capable of respecifying the anteroposterior axis of a normal wing. However, the average duplication obtained after grafting a tu2 polarizing region was significantly less than the average duplication formed after a graft of normal wing bud polarizing zone. Thus, polarizing activity appears to be weak in tu2. Grafts of normal polarizing zone to the posterior edge of tu2 wing buds had no effect on the tu2 phenotype. This result suggests that a weakly functioning polarizing signal does not account for the altered anteroposterior polarity in tu2 limbs, and that normal polarizing zone activity is not sufficient for formation of normal limb bud cartilages. We demonstrated that transmission of a polarizing signal through the tu2 limb mesoderm was normal. In addition, tu2 anterior border mesoderm had no polarizing activity. We also assessed the ability of tu2 limb bud mesoderm to respond to a polarizing signal. Either normal polarizing zone tissue or a bead containing retinoic acid was placed at the anterior edge of tu2 wing buds at stages 18-23. Both polarizing zone and retinoic acid caused respecification of the tu2 wing anteroposterior axis. The result was that a tu2 ulna replaced the radius, and the most posterior digit was duplicated anteriorly. Limb cartilages with normal morphology never formed. When a bead containing retinoic acid was placed at the posterior edge of tu2 wing buds, there was no effect on anteroposterior pattern. However, beads with retinoic acid always caused a reduction in the number of tu2 wing digits which formed, whether the beads were placed at the anterior or posterior edge of the developing tu2 limb.

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“…It has been reported that RA either increases 81 or decreases 2,5,82 SMC proliferation. This paradoxical effect has recently been clarified by Chen and Gardner 83 : RA stimulates quiescent SMCs by increasing expression of cyclin D1, which is involved in cell entry into the G1 phase, whereas serum-stimulated cells are growth inhibited through a decrease in extracellular signalregulated protein kinase activity.…”

Section: Ra and Smc Biological Featuresmentioning

confidence: 97%

Retinoids and Arterial Smooth Muscle Cells

Neuville

Bochaton‐Piallat

Gabbiani

2000

ATVB

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Retinoic acid enhances the proliferation of smooth muscle cells

Cited by 13 publications

References 10 publications

Retinoic Acid Regulates Arterial Smooth Muscle Cell Proliferation and Phenotypic Features In Vivo and In Vitro Through an RARα-Dependent Signaling Pathway

Retinoic Acid Regulates Arterial Smooth Muscle Cell Proliferation and Phenotypic Features In Vivo and In Vitro Through an RARα-Dependent Signaling Pathway

The talpid² chick limb has weak polarizing activity and can respond to retinoic acid and polarizing zone signal

Retinoids and Arterial Smooth Muscle Cells

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Retinoic acid enhances the proliferation of smooth muscle cells

Cited by 13 publications

References 10 publications

Retinoic Acid Regulates Arterial Smooth Muscle Cell Proliferation and Phenotypic Features In Vivo and In Vitro Through an RARα-Dependent Signaling Pathway

Retinoic Acid Regulates Arterial Smooth Muscle Cell Proliferation and Phenotypic Features In Vivo and In Vitro Through an RARα-Dependent Signaling Pathway

The talpid2 chick limb has weak polarizing activity and can respond to retinoic acid and polarizing zone signal

Retinoids and Arterial Smooth Muscle Cells

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The talpid² chick limb has weak polarizing activity and can respond to retinoic acid and polarizing zone signal