Induction of SM-α-actin expression by mechanical strain in adult vascular smooth muscle cells is mediated through activation of JNK and p38 MAP kinase

Tock, Jenny; Putten, Vicki Van; Stenmark, Kurt R.; Nemenoff, Raphael A.

doi:10.1016/s0006-291x(03)00087-1

Cited by 61 publications

(75 citation statements)

References 27 publications

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“…7, C and D) suggests that FHL5 levels are likely to be regulated by the mitogen-activated protein (MAP) kinase cascade, which has been demonstrated to be involved in a variety of stress responses (11,24), including mechanical strain-induced muscle cell differentiation and the induction of differentiation marker proteins (12,61,66). Furthermore, activities of MAP kinases have also been shown to be elevated in the gill of the euryhaline killifish Fundulus heteroclitus during hyposmotic stress (23).…”

Section: Discussionmentioning

confidence: 99%

FHL5, a novel actin-binding protein, is highly expressed in eel gill pillar cells and responds to wall tension

Mistry

Kato²,

Tran³

et al. 2004

American Journal of Physiology-Regulatory, Integrative and Comp

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Supporting evidence for the contractile nature of fish branchial pillar cells was provided by demonstrating the presence of actin fibers and a novel four-and-a-half LIM (FHL) protein in which expression is specific for contractile tissues and sensitive to the tension applied to the pillar cell. When eel gill sections were stained with rhodamine-phalloidin, a selective fluorescent probe for fibrous actin, a strong bundle-like staining was observed around collagen columns in pillar cells, suggesting the presence of abundant actin fibers. A cDNA clone encoding a novel member of the actin-binding FHL family, FHL5, was isolated from a subtracted cDNA library of eel gill. Northern analysis revealed that FHL5 mRNA is highly expressed only in gills, heart, and skeletal muscle. In gills, FHL5 was found to be confined to pillar cells by immunohistochemistry. Confocal fluorescence microscopy showed that FHL5 is present in both cytosol and nucleus; within the cytosol, a large portion of FHL5 is colocalized with the phalloidin-positive actin bundles. Furthermore, transfection of myogenic C2C12 cells with FHL5 cDNA demonstrated, in addition to its interaction with actin stress fibers, a nuclear shuttling activity of FHL5. The mRNA and protein levels were found to be elevated on 1) transfer of eels from seawater to freshwater, 2) volume expansion by infusion of isotonic dextran-saline, and 3) constriction of gill vasculature by bolus injection of endothelin-1. These results suggest contractile nature of pillar cells and a role of FHL5 in maintaining the integrity and regulating the dynamics of pillar cells. C2C12 myoblast; endothelin; immunohistochemistry; lamella; zinc finger; four-and-a-half LIM FISH GILLS CONSIST OF a large number of filaments arranged along the gill arches. The surfaces of the filaments are greatly enlarged by a series of plate-like lamellae. Each lamella is composed of two sheets of epithelia separated by a thin space through which the blood circulates to allow the exchange of respiratory gases. The separation between the epithelial sheets is maintained by pillar cells and collagen bundles. Pillar cells are spool-shaped cells connecting two epithelial sheets of the respiratory lamella in fish gills (50,51,64). They are characterized by collagen bundles contained in the infoldings of the plasma membrane and are oriented perpendicularly to the epithelial sheets, which consist of a thin layer of pavement cells and a basal lamina that is continuous with the collagen bundles traversing the pillar cells (49, 64); for the anatomy of gill lamella, see the schematic illustration in Fig. 9D. The membrane-enclosed collagen bundles help prevent ballooning of the lamella. The inner surfaces of the two epithelial sheets are covered with flanges extended from the pillar cells, forming capillary lumen called lacunae. Another feature of the pillar cells is the presence of numerous myofilament-like structures that course through the cytoplasm in an orientation parallel to the collagen bundles. These myofilaments appear to ...

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Section: Discussionmentioning

confidence: 99%

FHL5, a novel actin-binding protein, is highly expressed in eel gill pillar cells and responds to wall tension

Mistry

Kato²,

Tran³

et al. 2004

American Journal of Physiology-Regulatory, Integrative and Comp

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“…To answer these questions and reconcile the paradoxical findings with those reports demonstrating that activation of the ERK and p38 MAPK pathways induces PM [40][41][42][43] and that stretch increases ERK and p38 MAPK activity while maintaining the differentiated phenotype [16,17], we hypothesized that there may exist an early PM of dissociated VSMC that occurs within hours after the removal of the physiological cues acting on the vessel wall, which may have escaped detection. In addition, we posited that early PM has a different molecular mechanism from that of late PM, in which activation of ERK and p38 MAPK pathways is important.…”

Section: Introductionmentioning

confidence: 94%

“…While endothelial cells are primarily subjected to the shear stress resulting from blood flow, VSMC are primarily subjected to the stretch resulting from blood pressure. When VSMC are dissociated, they become deprived of the mechanical stimuli, which have been proved by numerous studies [12][13][14][15][16][17][18][19][20][21] to play a role in PM. Second, if inhibition of ERK and the p38 MAPK pathways is a prerequisite for maintaining the differentiated phenotype [40][41][42][43], how can one explain the findings that stretch not only increased ERK and p38 MAPK activity [44][45][46], but also at the same time was sufficient for maintaining the differentiated phenotype [16,17]?…”

Section: Introductionmentioning

confidence: 98%

“…Mechanical factors, soluble biochemical factors, and extracellular matrix components have been proved to induce PM. Studies with cultured cells [12][13][14][15][16][17] and with intact cultured vessels [18][19][20][21] have shown that mechanical stimulation is able to maintain VSMC in the differentiated phenotype, typified by a high level of SMC-specific marker genes or a low proliferation rate. Soluble biochemical factors, including platelet-derived growth factor (PDGF) [22][23][24][25], transforming growth factor (TGF)-β [26,27], and retinoic acid [28][29][30][31] have been shown to affect PM.…”

Section: Introductionmentioning

confidence: 99%

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The early- and late stages in phenotypic modulation of vascular smooth muscle cells: Differential roles for lysophosphatidic acid

Guo

Makarova

Cheng

et al. 2008

Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biolog

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Lysophosphatidic acid (LPA) has been implicated as causative in phenotypic modulation (PM) of cultured vascular smooth muscle cells (VSMC) in their transition to the dedifferentiated phenotype. We evaluated the contribution of the three major LPA receptors, LPA 1 and LPA 2 GPCR and PPARγ, on PM of VSMC. Expression of differentiated VSMC-specific marker genes, including smooth muscle α-actin, smooth muscle myosin heavy chain, calponin, SM-22α, and hcaldesmon, was measured by quantitative real-time PCR in VSMC cultures and aortic rings kept in serum-free chemically defined medium or serum-or LPA-containing medium using wild-type C57BL/6, LPA 1 , LPA 2 , and LPA 1&2 receptor knockout mice. Within hours after cells were deprived of physiological cues, the expression of VSMC marker genes, regardless of genotype, rapidly decreased. This early PM was neither prevented by IGF-I, inhibitors of p38, ERK1/2, or PPARγ nor significantly accelerated by LPA or serum. To elucidate the mechanism of PM in vivo, carotid artery ligation with/without replacement of blood with Krebs solution was used to evaluate contributions of blood flow and pressure. Early PM in the common carotid was induced by depressurization regardless of the presence/absence of blood, but eliminating blood flow while maintaining blood pressure or after sham surgery elicited no early PM. The present results indicate that LPA, serum, dissociation of VSMC, IGF-I, p38, ERK1/2, LPA 1 , and LPA 2 are not causative factors of early PM of VSMC. Tensile stress generated by blood pressure may be the fundamental signal maintaining the fully differentiated phenotype of VSMC.

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“…Previous work has shown that mechanical strain has an effect on proliferation and differentiation of vascular SMCs, including up-regulation of various SMC contractile markers (8)(9)(10), and the cells aligned perpendicularly to the axis of strain (11). Similarly, we have shown that when MSCs are subjected to conditions of cyclic uniaxial strain on silicone membranes, the cells show an initial up-regulation of SMC markers that eventually drops back to basal levels after the cells align perpendicularly to the axis of strain as a means of reducing the effective stress on their cytoskeleton (12).…”

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confidence: 99%

Anisotropic mechanosensing by mesenchymal stem cells

Kurpinski

Chu

Hashi

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

361

316

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Mesenchymal stem cells (MSCs) are a potential source for the construction of tissue-engineered vascular grafts. However, how vascular mechanical forces regulate the genetic reprogramming in MSCs is not well understood. Mechanical strain in the vascular wall is anisotropic and mainly in the circumferential direction. We have shown that cyclic uniaxial strain on elastic substrates causes the cells to align perpendicularly to the strain axis, which is different from that in the vascular wall. To simulate the vascular cell alignment and investigate the anisotropic mechanical sensing by MSCs, we used soft lithography to create elastomeric membranes with parallel microgrooves. This topographic pattern kept MSCs aligned parallel to the strain axis, and the cells were subjected to 5% cyclic uniaxial strain (1 Hz) for 2-4 days. DNA microarray analysis revealed global gene expression changes, including an increase in the smooth muscle marker calponin 1, decreases in cartilage matrix markers, and alterations in cell signaling (e.g., down-regulation of the Jagged1 signaling pathway). In addition, uniaxial strain increased MSC proliferation. However, when micropatterning was used to align cells perpendicularly to the axis of mechanical strain, the changes of some genes were diminished, and MSC proliferation was not affected. This study suggests that mechanical strain plays an important role in MSC differentiation and proliferation, and that the effects of mechanotransduction depend on the orientation of cells with respect to the strain axis. The differential cellular responses to the anisotropic mechanical environment have important implications in cardiovascular development, tissue remodeling, and tissue engineering. stem cell engineering ͉ differentiation ͉ genetic reprogramming ͉ uniaxial mechanical strain ͉ micropatterning

show abstract

Induction of SM-α-actin expression by mechanical strain in adult vascular smooth muscle cells is mediated through activation of JNK and p38 MAP kinase

Cited by 61 publications

References 27 publications

FHL5, a novel actin-binding protein, is highly expressed in eel gill pillar cells and responds to wall tension

FHL5, a novel actin-binding protein, is highly expressed in eel gill pillar cells and responds to wall tension

The early- and late stages in phenotypic modulation of vascular smooth muscle cells: Differential roles for lysophosphatidic acid

Anisotropic mechanosensing by mesenchymal stem cells

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