Effect of stretch on growth and collagen synthesis in cultured rat and lamb pulmonary arterial smooth muscle cells

Kulik, Thomas J.; Alvarado, Stephen P.

doi:10.1002/jcp.1041570322

Cited by 57 publications

(23 citation statements)

References 43 publications

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“…Mechanical stretching of SMCs cultured on distensible substrata or entrapped in collagen gels has been shown to have profound effects on SMC phenotypic state, [99][100][101][102][103][104][105][106]101,[106][107][108][109]9,96,[110][111][112][113][114][115][116][117][118][119] growth factor release, 120 -122 proliferation, 100,123,124 and vascular tone, 125,126 leading several groups to investigate these mechanisms as a means of enhancing the development and maturation of tissue-engineered arteries. In particular, Kanda et al showed that adult bovine SMCbased collagen MEs that were cyclically loaded at 1 Hz with a strain amplitude of 10% for up to 4 weeks exhibited increases in contractile components such as myofilaments, dense bodies, and basement membranes, 106 indicating that cyclic stretching induces SMC reversion to a more contractile phenotype.…”

Section: Cyclic Stretching/distension Of Constructsmentioning

confidence: 99%

Small-Diameter Artificial Arteries Engineered In Vitro

Isenberg

Williams

Tranquillo

2006

Circulation Research

439

320

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Abstract-Although the need for a functional arterial replacement is clear, the lower blood flow velocities of small-diameter arteries like the coronary artery have led to the failure of synthetic materials that are successful for large-diameter grafts. Although autologous vessels remain the standard for small diameter grafts, many patients do not have a vessel suitable for use because of vascular disease, amputation, or previous harvest. As a result, tissue engineering has emerged as a promising approach to address the shortcomings of current therapies. Investigators have explored the use of arterial tissue cells or differentiated stem cells combined with various types of natural and synthetic scaffolds to make tubular constructs and subject them to chemical and/or mechanical stimulation in an attempt to develop a functional small-diameter arterial replacement graft with varying degrees of success. Here, we review the progress in all these major facets of the field. Key Words: tissue engineering Ⅲ artery Ⅲ collagen Ⅲ elastin Ⅲ vascular graft I n 2002, more than 500 000 surgical procedures were performed involving replacement of small-caliber blood vessels. 1 Despite a clear clinical need for a functional arterial graft, success has been limited to arterial replacements of large-caliber vessels such as the thoracic and abdominal aorta, arch vessels, iliac, and common femoral arteries; however, small-caliber (Ͻ6 mm) arterial substitutes, which account for a majority of the demand, have generally proved inadequate largely because of acute thrombogenicity of the graft, anastomotic intimal hyperplasia, aneurysm formation, infection, and progression of atherosclerotic disease. 2 The lower blood flow velocities of smaller vessels pose a different set of design criteria and introduce a host of new problems not encountered in large-caliber arterial substitutes where Dacron and expanded polytetrafluorethylene grafts have succeeded.Although autologous vessels, such as the saphenous vein, remain the standard for small diameter grafts, many patients do not have a vessel suitable for use because of vascular disease, amputation, or previous harvest. Moreover, this method requires a second surgical procedure to obtain the vessel. Tissue engineering has emerged as a promising approach to address the shortcomings of current options. Investigators have explored the use of arterial tissue cells combined with various types of natural and synthetic scaffolds to make tubular constructs and subject them to chemical and/or mechanical stimulation in an attempt to develop a functional small-diameter arterial replacement graft with varying degrees of success. There have been several reviews of vascular tissue engineering studies in recent years. [3][4][5][6] Here, we review the progress in Many design criteria have been proposed for the development of a functional small-diameter arterial replacement graft. 2,5,6,9 -13 It must be biocompatible, ie, nonthrombogenic, nonimmunogenic, and resistant to infection, all of which are associated wi...

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Section: Cyclic Stretching/distension Of Constructsmentioning

confidence: 99%

Small-Diameter Artificial Arteries Engineered In Vitro

Isenberg

Williams

Tranquillo

2006

Circulation Research

439

320

View full text Add to dashboard Cite

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“…43 In brief, medium was mixed with buffer containing 0.65 mol/L NaCl, 100 mmol/L Tris-Cl, pH 7.4, 4.7 mmol/L CaCl 2 , 1.25 mg/mL n-ethyl maleimide, and 50 g/mL BSA. Samples were split into 2 equal portions and highly specific collagenase (Sigma type VII, 10 U/mL) was added to 1 portion.…”

Section: Collagen Synthesis Assaymentioning

confidence: 99%

Angiotensin II Stimulates Collagen Synthesis in Human Vascular Smooth Muscle Cells

Ford

Pickering

1999

ATVB

100

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Abstract-Angiotensin II is an established regulator of vascular tone and smooth muscle cell (SMC) growth. However, there are little data about its effect on collagen synthesis by SMCs and none regarding the mechanism of such an effect. We studied the effect of angiotensin II on collagen production by human arterial SMCs, using uptake of [ 3 H]proline into collagenase-digestible proteins, and by ribonuclease protection assay for mRNA encoding the pro␣1 chain of type I collagen, the major collagen in arteries. This revealed a dose-dependent increase in relative collagen synthesis rate and a dose-dependent increase in pro␣1(I) collagen mRNA abundance, with the half-maximal effect at 1.7 nmol/L. Angiotensin II-stimulated collagen expression was associated with a 6-fold increase in transforming growth factor-␤ (TGF-␤) production and was inhibited by a neutralizing antibody to TGF-␤. Both collagen production and TGF-␤ release were inhibited by the AT 1 -specific antagonist, losartan, but not by the AT 2 receptor antagonist, PD123319. To determined if tyrosine phosphorylation was functionally linked to collagen synthesis, we studied the effect of 2 mechanistically distinct inhibitors of tyrosine kinase, genistein, and tyrphostin A25. These inhibitors abrogated angiotensin II-mediated procollagen mRNA expression and angiotensin II-mediated TGF-␤ production, whereas the inactive homolog tyrphostin A1 had no effect. We conclude that angiotensin II stimulates collagen production in human arterial SMCs via the AT 1 receptor and an autocrine loop of TGF-␤, induction of which requires tyrosine phosphorylation.

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“…Endothelial cells are known to respond to shear stress and cardiac myocytes to strain with teleologically understandable alterations (Li et al, 1999a;Wung et al, 1999). As well, the response of cells of the kidney (Hirakata et al, 1997;Ingram et al, 1999) and lung (Kulik and Alvarado, 1993), to name but a few other organs, demonstrably respond to their mechanical environments. Indeed, as onecelled organisms are known to respond to pressure generated by the height of fluid in which they exist (Sukharev et al, 1997), it would seem logical that an ability to respond to the mechanical environment would be an adaptive evolutionary stress that might have affected the joining of cells into complex organisms during evolution.…”

Section: Introductionmentioning

confidence: 99%

Molecular pathways mediating mechanical signaling in bone

Rubin

Jacobs

2006

Gene

400

303

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Bone tissue has the capacity to adapt to its functional environment such that its morphology is "optimized" for the mechanical demand. The adaptive nature of the skeleton poses an interesting set of biological questions (e.g., how does bone sense mechanical signals, what cells are the sensing system, what are the mechanical signals that drive the system, what receptors are responsible for transducing the mechanical signal, what are the molecular responses to the mechanical stimuli). Studies of the characteristics of the mechanical environment at the cellular level, the forces that bone cells recognize, and the integrated cellular responses are providing new information at an accelerating speed. This review first considers the mechanical factors that are generated by loading in the skeleton, including strain, stress and pressure. Mechanosensitive cells placed to recognize these forces in the skeleton, osteoblasts, osteoclasts, osteocytes and cells of the vasculature are reviewed. The identity of the mechanoreceptor(s) is approached, with consideration of ion channels, integrins, connexins, the lipid membrane including caveolar and noncaveolar lipid rafts and the possibility that altering cell shape at the membrane or cytoskeleton alters integral signaling protein associations. The distal intracellular signaling systems on-line after the mechanoreceptor is activated are reviewed, including those emanating from G-proteins (e.g., intracellular calcium shifts), MAPKs, and nitric oxide. The ability to harness mechanical signals to improve bone health through devices and exercise is broached. Increased appreciation of the importance of the mechanical environment in regulating and determining the structural efficacy of the skeleton makes this an exciting time for further exploration of this area.

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Effect of stretch on growth and collagen synthesis in cultured rat and lamb pulmonary arterial smooth muscle cells

Cited by 57 publications

References 43 publications

Small-Diameter Artificial Arteries Engineered In Vitro

Small-Diameter Artificial Arteries Engineered In Vitro

Angiotensin II Stimulates Collagen Synthesis in Human Vascular Smooth Muscle Cells

Molecular pathways mediating mechanical signaling in bone

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