Localization of proteoheparan sulfate in rat aorta

Clowes, A. W.; Clowes, Monika M.; Gown, Allen M.; Wight, Thomas N.

doi:10.1007/bf00495421

Cited by 26 publications

(12 citation statements)

References 32 publications

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“…With regard to ossification and matrix formation, proteoglycans and bone sialoprotein accumulation might be one of the important factors in initial mineralization (13,18,23). Bone matrix is composed of proteoglycans (PGs), such as chondroitin sulfate PG (CSPG), dermatan sulfate PG (DSPG), heparan sulfate PG (HSPG), and keratan sulfate PG (KSPG) (5), and they are also contained in blood vessel walls, and smooth muscles (4,17,18), cartilage matrix (81, 23 , 24), and so on (7,13). Identification of these PGs has already been described immunohistochemically by the use of specific monoclonal antibodies accompanied with enzymatic digestion (5).…”

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confidence: 99%

Heterotopic bone formation in tumor stromal tissue. Immunohistochemical considerations.

Kumasa

Mori

et al. 1990

Acta Histochem. Cytochem

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Ectopic and heterotopic bone formation rarely occur in stromal tissues of various epithelial tumors. In the present study, ectopic bone forming tumors; calcifying epithelioma Malherbe (6), renal cell carcinoma (1), thyroid adenocarcinoma (1) and ovary carcinoma (1) were examined. The process of ectopic bone formation could be classified into 1) bone formation related to epithelial tissue as found in calcifying epithelioma of Malherbe, 2) bone formation from perivascular smooth muscle, and 3) that due to metaplasia occurring in stromal connective tissue of epithelial tumors. Immunohistochemical detection of proteoglycans (PG) was made in bone-forming matrix areas, and these areas were positive for chondrotin 4 and 6 sulfate, and dermatan and heparan sulfate PGs. Immunohistochemically, fibronectin, collagen III and bone sialoprotein as matrix proteins, and carbonic anhydrase as calcification marker were tested and they appeared in these pre-calcifying tissues.

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confidence: 99%

Heterotopic bone formation in tumor stromal tissue. Immunohistochemical considerations.

Kumasa

Mori

et al. 1990

Acta Histochem. Cytochem

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“…Other molecules that regulate SMC function may be continually present in the untraumatized wall. One such molecule may be heparan sulfate, which appears to be present throughout the arterial wall (Clowes et al, 1982). Heparin has been shown to inhibit SMC proliferation both in vivo (Clowes and Karnovsky, 1977) and in vitro (Hoover et al, 1980;Castellot et al, 1981).…”

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confidence: 99%

Inhibition of vascular smooth muscle cell migration by heparin‐like glycosaminoglycans

Majack

Clowes

1984

Journal Cellular Physiology

196

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Previous studies have suggested that heparin-like glycosaminoglycans may be endogenous inhibitors of smooth muscle proliferation in the vessel wall. The purpose of this study was to determine the effects of exogenous glycosaminoglycans on rat vascular (aortic) smooth muscle cell migration following wounding in vitro. Our data indicate that heparin and related molecules (iota carrageenan, dextran sulfate), but not other glycosaminoglycans (hyaluronate, chondroitin, and dermatan sulfates), inhibit smooth muscle cell motility in a cell-specific, dose-dependent, and reversible fashion. The effect of heparin was maximal (60% inhibition) at 10 micrograms/ml; a half-maximal effect was observed at 1 microgram/ml. Heparin did not significantly affect the migration of bovine aortic endothelium or Swiss 3T3 cells. These observations support the concept that heparin-like glycosaminoglycans may be important regulators of vascular smooth muscle cell function.

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“…13,19,20,35,[41][42][43] Increased perlecan expression is associated with noncycling SMCs in the developing vasculature, 19,20 and direct inhibition of SMC proliferation in vitro by perlecan has been demonstrated. 16,35 Several inhibitors of SMC proliferation, such as heparin, 14 apolipoprotein E, 35 and transforming growth factor-␤1, 44 increase perlecan expression.…”

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confidence: 99%

“…Perlecan is a large ECM HSPG that is synthesized by vascular cells. 13,19,20,35,[41][42][43] 23,25 However, the pattern of perlecan expression and distribution in the later stages of lesion formation after vascular injury has not been previously described, nor has endogenous HSPG been shown to act as an inhibitor of cell proliferation in the neointimal lesion.Our results indicate that perlecan accumulation is correlated with the attenuation of neointimal SMC proliferation after vascular injury. Specifically, expression and deposition of perlecan are low as SMCs proliferate and migrate in response to growth factors at early times after vascular injury.…”

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Changes in Perlecan Expression During Vascular Injury

Kinsella

Tran

Weiser‐Evans

et al. 2003

ATVB

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Objective-Vascular smooth muscle cells (SMCs), activated by growth factors after arterial injury, migrate and proliferate to expand the intima of the blood vessel. During intimal expansion, proliferation is suppressed and an increasingly large proportion of the neointimal mass is composed of newly synthesized extracellular matrix (ECM). We sough to determine whether the ECM heparan sulfate proteoglycan (HSPG) perlecan, which inhibits SMC proliferation in vitro, also accumulates and limits SMC proliferation during neointimal expansion. Methods and Results-Perlecan expression and accumulation were analyzed by immunohistochemistry and in situ hybridization during neointima formation after balloon catheter injury to the rat carotid artery. Perlecan expression was low in uninjured vessels and up to 7 days after injury, during maximal SMC proliferation. By 14 days after injury, perlecan was dramatically increased, and immunostaining remained heavy throughout the advanced lesion, 35 to 42 days after injury. Finally, explants of intimal tissue from 35-to 42-day neointimal lesions were digested with glycosaminoglycanases to determine whether endogenous HSPGs inhibit intimal SMC proliferation. SMCs within HS-depleted, but not chondroitinase ABC-treated or mock-incubated, explants were found to proliferate in response to plateletderived growth factor BB. Key Words: heparan sulfate Ⅲ perlecan Ⅲ neointimal hyperplasia Ⅲ vascular smooth muscle Ⅲ proliferation A ccumulated evidence indicates that extracellular matrix (ECM) proteins provide both permissive and inhibitory modulation of the cellular responses to growth factors. [1][2][3] Thus, changes in the amounts and types of ECM proteins that are deposited during the development of the atherosclerotic lesion may modify the effects of growth factors during vascular pathogenesis. However, mechanisms by which the ECM may inhibit intimal smooth muscle cell (SMC) proliferation in the ECM-rich advanced lesion remain unresolved. Considerable previous work has suggested that the glycosaminoglycan chains of heparan sulfate proteoglycans (HSPGs), and heparin, are potent inhibitors of SMC proliferation in vitro. 4 -6 Conversely, HS lyases appear to accelerate the conversion of the SMC phenotype from a quiescent, contractile state to a rapidly growing, "synthetic" state. 7 Pioneering studies demonstrated that heparin infusion dramatically suppresses the early wave of medial SMC proliferation that is required for the formation of a neointima after injury to the rat carotid artery. 8 Moreover, heparin was found to inhibit SMC cell growth in vitro, 9,10 suggesting that heparinlike molecules, such as vascular HSPGs, may be endogenous inhibitors of vascular SMC proliferation. Conclusions-HSPGsProteoglycans are among the ECM proteins that are deposited within the late neointimal lesion. [11][12][13][14] Perlecan is an ECM HSPG that is a potent modulator of cellular phenotype and proliferation 3,15,16 and a major vascular wall basement membrane component. 17,18 The induction of perlecan expres...

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Localization of proteoheparan sulfate in rat aorta

Cited by 26 publications

References 32 publications

Heterotopic bone formation in tumor stromal tissue. Immunohistochemical considerations.

Heterotopic bone formation in tumor stromal tissue. Immunohistochemical considerations.

Inhibition of vascular smooth muscle cell migration by heparin‐like glycosaminoglycans

Changes in Perlecan Expression During Vascular Injury

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