The Hyaluronic Acid Receptors Induced by Stretch Injury of Rat Bladder in Vivo and Influences Smooth Muscle Cell Contraction in Vitro

Bägli, Darius; Joyner, Byron D.; Mahoney, Sean R.; McCulloch, Lori

doi:10.1097/00005392-199909010-00071

Cited by 36 publications

(23 citation statements)

References 37 publications

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“…10,36 Inhibiting RHAMM failed to alter gel contraction in the present study. This is in contrast to a recent report by Bagli et al, 43 who blocked contraction of collagen gels (without exogenous HA) by rat bladder smooth muscle cells using a RHAMM-blocking peptide. The peptide adheres to RHAMM-binding sites on HA to prevent receptor ligation, whereas the antibody used in the present study inhibits RHAMM signaling but not binding to HA.…”

Section: Discussioncontrasting

confidence: 99%

Hyaluronan Enhances Contraction of Collagen by Smooth Muscle Cells and Adventitial Fibroblasts

Travis

Hughes

Wong

et al. 2001

Circulation Research

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Abstract-Remodeling contributes to restenosis when cells shrink the artery wall at sites of injury. This may be analogous to wound healing, where tissue remodeling achieves wound contraction. Hyaluronan (HA) is prominent in wound matrix and inhibits fetal scarring. HA is also produced in the artery wall after angioplasty, where it may inhibit constrictive remodeling. This hypothesis was tested in vitro using a model of matrix contraction. Primate aortic smooth muscle cells and adventitial fibroblasts were seeded into collagen I gels containing increasing amounts of HA (0% to 50%, wt/wt). Both cell types reduced the diameter of collagen alone Ϸ65% at 18 hours. HA significantly increased gel contraction (diameter in mm: 0% HA, 7.7Ϯ0.9; 2%, 7.1Ϯ0.7; 10%, 6.7Ϯ0.5; 50%, 5.6Ϯ0.9; PϽ0.05 for Ն10%), cell spreading and telopodia, and pericellular accumulation of collagen fibrils. These effects were mediated in part by cellular HA binding, because an antibody against CD44 receptors blocked pericellular collagen accumulation and enhanced gel contraction without altering cell shape. The role of CD44 was specific, because inhibiting receptor for hyaluronic acid-mediated motility (RHAMM) had no effect. Blocking ␤ 1 -integrins completely inhibited contraction of collagen, but gels containing HA required CD44 and ␤ 1 -integrin blockade for complete inhibition. Enhanced collagen reorganization and contraction were not attributable to increased collagenase activity, because the metalloproteinase inhibitor batimastat had no effect. In summary, HA enhanced collagen reorganization by the cell types most likely to mediate constrictive remodeling after angioplasty. These effects were CD44-dependent, thus providing a potential target for therapies to prevent constrictive remodeling and restenosis. (Circ Res. 2001;88:77-83.)

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Section: Discussioncontrasting

confidence: 99%

Hyaluronan Enhances Contraction of Collagen by Smooth Muscle Cells and Adventitial Fibroblasts

Travis

Hughes

Wong

et al. 2001

Circulation Research

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“…27 In line with this is the observation that blocking of RHAMM (receptor of HA-mediated motility) is linked to attenuated collagen gel contraction by SMCs isolated from the bladder exposed to stretch injury. 28 Furthermore, in accordance with the minimal strength and stiffness of elastin compared with collagen, 29 the thinning and fragmentation of the elastic membranes in the Tg mice were not found to be reflected in neither reduced mechanical strength, stiffness, and extensibility of the aorta or changes in the toe-part of the load-strain curves corresponding to the normal in vivo range of loading (data not shown). Therefore, the observed changes of the elastic membranes more likely contribute to collagen reorganization resulting in increased strength and stiffness of the aortic wall in Tg mice.…”

Section: Discussionmentioning

confidence: 57%

Overexpression of Hyaluronan in the Tunica Media Promotes the Development of Atherosclerosis

Chai

Chai²,

Danielsen³

et al. 2005

Circulation Research

130

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Abstract-The arterial content of hyaluronan (HA) undergoes diffuse changes as part of the diabetic macroangiopathy.Because HA influences the phenotype of vascular cells in vitro such as proliferation, migration, and secretion, it is tempting to speculate that diabetes-induced hastened cardiovascular disease may be linked to the increased amount of HA. To explore the pathophysiological role of altered HA content in the arterial wall in vivo, we created transgenic (Tg) mice with HA overexpression in smooth muscle cells (SMCs) in large and small vessels, targeted by the ␣ smooth-muscle-cell-actin (␣SMA) promoter fused to the human hyaluronan synthase 2 (hHAS2) cDNA. RT-PCR demonstrated hHAS2 mRNA expression in the tunica media of large and small vessels. In situ hybridization confirmed that hHAS2 mRNA was targeted to the SMCs. The aortic HA content was elevated in the Tg mice, and by immunohistochemistry, it was seen that HA accumulated in the tunica media. The secretory profile of high-and low-molecular HA was similar in wild-type and Tg animals. Overproduction of HA in the aorta resulted in thinning of the elastic lamellae in Tg mice. Our data suggest that this may lead to increased mechanical stiffness and strength, as determined by controlled stretching until failure. Finally, overproduction of HA on the genetic background of the ApoE-deficient mouse strain promoted atherosclerosis development in the aorta. Key Words: hyaluronan Ⅲ biomechanics Ⅲ atherosclerosis Ⅲ diabetes Ⅲ transgenic H yaluronan (HA) is a large, nonsulfated glycosaminoglycan (GAG) produced in the vasculature by smooth muscle cells (SMCs) and endothelial cells (ECs). It is synthesized at the inner face of the cell membrane by hyaluronan synthases 1 to 3 (HAS 1 to 3), followed by translocation to the outer surface and the intercellular space. 1 Recent in vitro investigations have shown that high (HMW) as well as low molecular (LMW) forms of HA influence important cellular functions, such as proliferation, migration, and secretory capabilities. [1][2][3][4] There seems to exist a delicately regulated balance between production, sizing, and removal of HA that is central to its biological functions during normal conditions. If this balance is disturbed, it has been hypothesized that disease may develop. 5 The notion that HA is likely to take part in the development of vascular pathologies has been nourished by a number of observations, which show altered HA amounts in several arterial disease entities such as diabetic angiopathy, atherosclerosis, and restenosis. 6 -8 During the build-up of the atherosclerotic plaques in humans, some areas with local accumulation of HA appear. 9 -11 This is in contrast to the situation in patients with diabetes in whom the HA accumulation is disseminated in tunica media and is regarded as one important element in a series of diffuse matrix changes in the vessels. 6,12 The diabetic angiopathy deserves some specific comments. First, a very high and equal frequency of cardiovascular disease (CVD) exists among men and...

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“…FAK, focal adhesion kinase. (53), and after stretch injury (54). Activation of Src through cell surface RHAMM is transient (5) but is nevertheless required for turnover of lamellae focal adhesions and consequently for RHAMM-regulated cell motility (5).…”

Section: Fig 2 a Current Model For Hyaluronan (Ha)-dependent Rhammmentioning

confidence: 99%

Signaling Properties of Hyaluronan Receptors

Turley¹,

Noble²,

Bourguignon³

2002

Journal of Biological Chemistry

959

843

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The Hyaluronic Acid Receptors Induced by Stretch Injury of Rat Bladder in Vivo and Influences Smooth Muscle Cell Contraction in Vitro

Cited by 36 publications

References 37 publications

Hyaluronan Enhances Contraction of Collagen by Smooth Muscle Cells and Adventitial Fibroblasts

Hyaluronan Enhances Contraction of Collagen by Smooth Muscle Cells and Adventitial Fibroblasts

Overexpression of Hyaluronan in the Tunica Media Promotes the Development of Atherosclerosis

Signaling Properties of Hyaluronan Receptors

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