Estrogen regulates insulin-like growth factor 1, platelet-derived growth factor A and B, and their receptors in the vascular wall

Savolainen-Peltonen, Hanna; Loubtchenkov, Michael; Petrov, Lubomir; Delafontaine, Patrick; Häyry, P

doi:10.1097/01.tp.0000101496.53362.a0

Cited by 8 publications

(6 citation statements)

References 39 publications

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“…How estrogen signals are transduced to modulate IGF-1 expression remains unanswered. It has been speculated the effect of estrogen on IGF-1 was mediated through the recruitment of ERs in neurons, breast tumors, and the heart (37)(38)(39). Nonetheless, there is very little information available on ER expression and distribution in the skeletal muscles.…”

Section: Discussionmentioning

confidence: 99%

Estrogen Effects on Skeletal Muscle Insulin-Like Growth Factor–1 and Myostatin in Ovariectomized Rats

Tsai

McCormick

Brazeau

et al. 2007

Exp Biol Med (Maywood)

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Previous work showed that estrogen replacement attenuates muscle growth in immature rats. The present study examined muscle insulin-like growth factor-1 (IGF-1) and myostatin expression to determine whether these growth regulators might be involved in mediating estrogen's effects on muscle growth. IGF-1 and myostatin message and protein expression in selected skeletal muscles from 7-week-old sham-ovariectomized (SHAM) and ovariectomized rats that received continuous estrogen (OVX/E2) or solvent vehicle (OVX/CO) from an implant for 1 week or 5 weeks was measured. In the 1-week study, ovariectomy increased IGF-1 mRNA expression in fast extensor digitorum longus and gastrocnemius muscles; the increase was reversed by estrogen replacement. A similar trend was observed in the slow soleus muscle, although the change was not statistically significant. In contrast to mRNA, muscle IGF-1 protein expression was not different between SHAM and OVX/ CO animals in the 1-week study. One week of estrogen replacement significantly decreased IGF-1 protein level in all muscles examined. Myostatin mRNA expression was not different among the 1-week treatment groups. One week of estrogen replacement significantly increased myostatin protein in the slow soleus muscle but not the fast extensor digitorum longus and gastrocnemius muscles. There was no treatment effect on IGF-1 and myostatin expression in the 5-week study; this finding suggested a transient estrogen effect or upregulation of a compensatory mechanism to counteract the estrogen effect observed at the earlier time point. This investigation is the first to explore ovariectomy and estrogen effects on skeletal muscle IGF-1 and myostatin expression. Results suggest that reduced levels of muscle IGF-1 protein may mediate estrogen's effect on growth in immature, ovariectomized rats. Increased levels of muscle myostatin protein may also have a role in mediating estrogen's effects on growth in slow but not fast skeletal muscle.

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Section: Discussionmentioning

confidence: 99%

Estrogen Effects on Skeletal Muscle Insulin-Like Growth Factor–1 and Myostatin in Ovariectomized Rats

Tsai

McCormick

Brazeau

et al. 2007

Exp Biol Med (Maywood)

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“…PDGF- B has been detected in cultured neointimal and newborn SMCs27-29, but not in adult SMCs30. In addition, PDGF-B mRNA has been variably detected in vivo in injured rat carotid arteries24,31.…”

Section: Discussionmentioning

confidence: 99%

Syndecan-1

Fukai

Kenagy

Chen

et al. 2009

ATVB

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Objective-Arterial injury induces smooth muscle cell (SMC) proliferation, migration, and intimal accumulation of cells and extracellular matrix. These processes are regulated by the administration of the glycosaminoglycans heparin and heparan sulfate, but little is known about the role of endogenous heparan sulfate proteoglycans in the vessel wall. We investigated the response to carotid injury of syndecan-1-null mice to assess the function of one of a conserved family of transmembrane heparan and chondroitin sulfate proteoglycans. Methods and Results-Syndecan-1-null mice developed a large neointimal lesion after injury, whereas wild-type mice made little or none. This was accompanied by a significant increase in both medial and intimal SMC replication. Cultured syndecan-1-null SMCs showed a significant increase in proliferation in response to PDGF-BB, thrombin, FGF2, EGF, and serum. In response to thrombin, PDGF-BB, and serum syndecan-1-null SMCs expressed more PDGF-B chain message than did wild-type SMCs. Downregulation of PDGF-BB or PDGFR␤ inhibited thrombin-, PDGF-BB-, and serum-induced DNA synthesis in syndecan-1-null SMCs. Key Words: syndecan Ⅲ platelet-derived growth factor Ⅲ smooth muscle Ⅲ arterial injury A rterial injury induces smooth muscle cells (SMCs) to proliferate, migrate, and accumulate in the intima. These processes may be modulated by components of the extracellular matrix (ECM), particularly heparin and the related glycosaminoglycan heparan sulfate. These glycosaminoglycans inhibit arterial SMC migration and proliferation and alter SMC ECM composition. 1-3 Although perlecan, an ECM-associated heparan sulfate proteoglycan (HSPG), has been shown to inhibit SMC proliferation and intimal thickening, 4,5 the role of other HSPGs in the injured vessel wall has not been defined. Conclusions-TheseSyndecan-1 is a member of a conserved family of 4 heparanand chondroitin-sulfate-containing transmembrane HSPGs (syndecans 1 to 4) that are expressed in a developmental-, cell-type-, and tissue-specific manner. 6 Syndecans bind various components of the ECM and are important regulators of cellcell and cell-ECM interactions. All syndecans are normally expressed in the artery. After injury, the levels of mRNA for syndecan-1 slowly rise and peak at about 2 weeks, whereas syndecan-4 peaks at 4 hours, falls toward baseline, and then rises again along with syndecan-1. 7,8 Although all syndecans can bind heparin-binding growth factors and syndecan-4 is known to be required for thrombin-induced migration and proliferation in human aortic SMCs, 9 little is known about the role of syndecan-1 in SMC function. In addition, although it is known that syndecan-4 null mice exhibit a delayed skinwound healing response and syndecan-1-null mice develop a hypocellular scar, 10,11 no studies have been performed to define role for syndecans in the response to vascular injury. Therefore, we have investigated the effects of carotid artery injury in wild-type and syndecan-1-null mice and the growth and migratory properties of vascul...

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“…For example, Natoli et al found that neither MMP-2 expression nor protein are affected by estrogen exposure in human VSMCs from a young female [27]. SavolainenPeltonen et al found that estrogen inhibits migration and proliferation of young rat VSMC [28] and Kolodgie et al found this effect to be receptor mediated [29]. The contrasting reports from us and others suggest alterations of the regulatory mechanisms at play in VSMCs of younger origin and lead one to postulate that inhibition of MT1-MMP in premenopausal VSMCs would have different cellular effects from those presented in the current study.…”

Section: Figmentioning

confidence: 96%

Role of MT1-MMP in Estrogen-Mediated Cellular Processes of Intimal Hyperplasia

Mountain

Kirkpatrick

Freeman

et al. 2012

Journal of Surgical Research

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Estrogen regulates insulin-like growth factor 1, platelet-derived growth factor A and B, and their receptors in the vascular wall

Abstract: Our findings demonstrate that estrogen regulates IGF-1, PDGF-A, PDGF-B, and PDGF-Ralpha, which may be related to the vasculoprotective effect of estrogen, but has no effect on IGF-1R or PDGF-Rbeta.

Cited by 8 publications

References 39 publications

Estrogen Effects on Skeletal Muscle Insulin-Like Growth Factor–1 and Myostatin in Ovariectomized Rats

Estrogen Effects on Skeletal Muscle Insulin-Like Growth Factor–1 and Myostatin in Ovariectomized Rats

Syndecan-1

Role of MT1-MMP in Estrogen-Mediated Cellular Processes of Intimal Hyperplasia

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