Stretch-Induced Collagen Synthesis in Cultured Smooth Muscle Cells from Rabbit Aortic Media and a Possible Involvement of Angiotensin II and Transforming Growth Factor-β

Muragaki, Yasuteru; Hatamura, Ikuji; Ueno, Hikaru; Ooshima, Akira

doi:10.1159/000025570

Cited by 158 publications

(113 citation statements)

References 41 publications

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“…Effects of Cyclic Stretch on Ang II Secretion into Culture Medium-A previous study using the Flexercell strain system showed that concentration of immunoreactive Ang II in the conditioned medium was elevated by cyclic stretch of VSMCs (12), and in the present study cyclic stretch of VSMCs caused increases in ACE and AT1 receptor mRNA expression. To determine whether the autocrine/paracrine-secreted Ang II actually contributes to the increase in FN mRNA expression in response to cyclic stretch, incubation medium obtained from VSMCs that were stretched for 12 h was transferred to VSMCs cultured on regular culture dishes.…”

Section: Effects Of Transcriptional Inhibitor and Protein Synthesissupporting

confidence: 66%

“…This process allows cell culture in a uniform mechanically active environment so that all cells stretched over the loading station surface receive the same amount of strain. Previous studies showed that cyclic stretch of VSMCs with the Flexercell Strain Unit induced increases in DNA synthesis and total protein synthesis, thereby suggesting that this system is useful for in vitro analysis of the processes involved in vascular remodeling (11,12).…”

Section: Methodsmentioning

confidence: 99%

“…VSMCs (2). Accumulated evidence suggests that mechanical stretch of cardiovascular cells induces the secretion of Ang II and evokes these hypertrophic responses in an autocrine/paracrine manner (12,27).…”

Section: Functional Importance Of Rfn/ap-1 Element In Stretch-mediatementioning

confidence: 99%

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Molecular Mechanism of Fibronectin Gene Activation by Cyclic Stretch in Vascular Smooth Muscle Cells

Tamura¹,

Chen²,

López-Ilasaca³

et al. 2000

Journal of Biological Chemistry

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Fibronectin plays an important role in vascular remodeling. A functional interaction between mechanical stimuli and locally produced vasoactive agents is suggested to be crucial for vascular remodeling. We examined the effect of mechanical stretch on fibronectin gene expression in vascular smooth muscle cells and the role of vascular angiotensin II in the regulation of the fibronectin gene in response to stretch. Cyclic stretch induced an increase in vascular fibronectin mRNA levels that was inhibited by actinomycin D and CV11974, an angiotensin II type 1 receptor antagonist; cycloheximide and PD123319, an angiotensin II type 2 receptor antagonist, did not affect the induction. In transfection experiments, fibronectin promoter activity was stimulated by stretch and inhibited by CV11974 but not by PD123319. DNA-protein binding experiments revealed that cyclic stretch enhanced nuclear binding to the AP-1 site, which was partially supershifted by antibody to c-Jun. Site-directed mutation of the AP-1 site significantly decreased the cyclic stretch-mediated activation of fibronectin promoter. Furthermore, antisense c-jun oligonucleotides decreased the stretch-induced stimulation of the fibronectin promoter activity and the mRNA expression. These results suggest that cyclic stretch stimulates vascular fibronectin gene expression mainly via the activation of AP-1 through the angiotensin II type 1 receptor.Extracellular matrix of the vascular wall plays an important role in pathophysiological changes including vascular remodeling and atherosclerosis in response to hypertension. Fibronectin (FN) 1 is an important component of the extracellular matrix and is implicated functionally in the regulation of several cellular processes, including cell adhesion, migration, transformation, and motility and wound healing. FN has been found to modulate the phenotype of vascular smooth muscle cells (VSMCs) and regulate VSMC growth (1). We previously found that angiotensin II (Ang II) enhances transcription of the FN gene through the Ang II type 1 receptor (AT1 receptor) in VSMCs, at least in part via activation of the rat FN promoter AP-1 binding motif (rFN/AP-1) (2). Although rFN/AP-1 may not be involved in the regulation of FN gene expression in cells other than VSMCs (3, 4), this result proposes that rFN/AP-1 is functionally important for the regulation of vascular FN expression in response to various stimuli. Accumulated evidence suggests that hemodynamic forces (including stretch and shear stress) as well as endocrine factors (such as Ang II) are among the most important factors implicated in the physiology and pathophysiology of the vascular wall in vivo. Interactions between extracellular matrix proteins and cellular receptors can transduce signals that lead to changes in shape, motility, and growth of VSMCs. Thus, investigation of mechanical stressmediated regulation of the extracellular matrix and the tissue renin-angiotensin system in VSMCs may be important for the elucidation of a molecular mechanism of vascular remodeli...

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Section: Effects Of Transcriptional Inhibitor and Protein Synthesissupporting

confidence: 66%

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Molecular Mechanism of Fibronectin Gene Activation by Cyclic Stretch in Vascular Smooth Muscle Cells

Tamura¹,

Chen²,

López-Ilasaca³

et al. 2000

Journal of Biological Chemistry

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“…The device consisted of a computer-controlled vacuum unit, a culture well plate with a flexiblepolystyrene culture well bottom coated with type I collagen (Flex I, Flexercell International Corp., McKeesport, PA, USA), and another culture well plate with a non-deformable culture well bottom made of the same materials as Flex I (Flex 11, Flexercell International Corp., McKeesport, PA, USA). Application of a vacuum provides a hemispherically downward deformation to the flexible Flex I bottom, resulting in a non-homogenous strain profile with a maximum at the Table 2 Sequences of RT-PCR primers used in the present study periphery and a geometric decline toward zero at the center or the culture well bottom [2,4,9,19,21]. The cells were placed in Flex I and Flex I1 culture well plates at a density of 1 x 10' cellslwell.…”

Section: Methodsmentioning

confidence: 99%

Mechanical stretching force promotes collagen synthesis by cultured cells from human ligamentum flavum via transforming growth factor‐β1

Nakatani

Marui

Hitora

et al. 2002

Journal Orthopaedic Research

133

125

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Although mechanical stress as a result of spinal instability is known to cause hypertrophy of the ligameiitum flavum resulting in degenerative spinal canal stenosis, the mechanism of the ligament hypertrophy is not well understood. In the present study, we investigated the effect of mechanical stretching force on collagen synthesis and transforming growth factor-/3 1 (TGF-PI) production using ligament cells isolated from human ligamentum flavum in vitro. Ligamenturn flavum cells (LFCs) were isolated from human ligamenturn flavum obtained from patients who underwent lumbar spine surgery. The LFCs were subjected to a mechanical stretching force using a cominercially available stretching device that physically deformed the cells. Collagen synthesis and TGF-PI production levels in the LFCs were then examined. Notable increases were observed in the gene expressions of collagen types I, 111, and V in LFCs subjected to mechanical stretching force. The increase in collagen gene expression of LFCs was inhibited in the presence of anti-TGF-pl antibodies. Production of TGF-PI by the LFCs also increased significantly by the mechanical stretching force. Exogenous application of TGF-PI was confirmed to increase collagen synthesis of the LFCs. This data indicated that mechanical stretching force can promote TGF-Dl production by LFCs, resulting in hypertrophy of the ligament.

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“…Smooth muscle cells, which are contained in the middle layer of an artery, are important constituents of the vascular system and they are responsible for control of short-term changes in lumen diameter and of long-term changes in the extracellular matrix turnover (e.g. Li et al 1998). In this section we provide an overview of the relevant continuum modelling aspects.…”

Section: Active Response Of Artery Wallsmentioning

confidence: 99%

Constitutive modelling of arteries

2010

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This review article is concerned with the mathematical modelling of the mechanical properties of the soft biological tissues that constitute the walls of arteries. Many important aspects of the mechanical behaviour of arterial tissue can be treated on the basis of elasticity theory, and the focus of the article is therefore on the constitutive modelling of the anisotropic and highly nonlinear elastic properties of the artery wall. The discussion focuses primarily on developments over the last decade based on the theory of deformation invariants, in particular invariants that in part capture structural aspects of the tissue, specifically the orientation of collagen fibres, the dispersion in the orientation, and the associated anisotropy of the material properties. The main features of the relevant theory are summarized briefly and particular forms of the elastic strain-energy function are discussed and then applied to an artery considered as a thickwalled circular cylindrical tube in order to illustrate its extension-inflation behaviour. The wide range of applications of the constitutive modelling framework to artery walls in both health and disease and to the other fibrous soft tissues is discussed in detail. Since the main modelling effort in the literature has been on the passive response of arteries, this is also the concern of the major part of this article. A section is nevertheless devoted to reviewing the limited literature within the continuum mechanics framework on the active response of artery walls, i.e. the mechanical behaviour associated with the activation of smooth muscle, a very important but also very challenging topic that requires substantial further development. A final section provides a brief summary of the current state of arterial wall mechanical modelling and points to key areas that need further modelling effort in order to improve understanding of the biomechanics and mechanobiology of arteries and other soft tissues, from the molecular, to the cellular, tissue and organ levels.

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Stretch-Induced Collagen Synthesis in Cultured Smooth Muscle Cells from Rabbit Aortic Media and a Possible Involvement of Angiotensin II and Transforming Growth Factor-β

Cited by 158 publications

References 41 publications

Molecular Mechanism of Fibronectin Gene Activation by Cyclic Stretch in Vascular Smooth Muscle Cells

Molecular Mechanism of Fibronectin Gene Activation by Cyclic Stretch in Vascular Smooth Muscle Cells

Mechanical stretching force promotes collagen synthesis by cultured cells from human ligamentum flavum via transforming growth factor‐β1

Constitutive modelling of arteries

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