Role of PDGF-A expression in the control of vascular smooth muscle cell growth by transforming growth factor-beta.

Majack, Richard A.; Majesky, Mark W.; Goodman, Linda

doi:10.1083/jcb.111.1.239

Cited by 208 publications

(90 citation statements)

References 44 publications

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“…In AKR-2B cells TGF-fl induces the expression of the PDGF B chain gene (Leof et al, 1986), whereas in fibroblasts the PDGF A chain gene is induced (Paulsson et al, 1987b;Soma and Grotendorst, 1989). The PDGF A chain gene is also induced in vascular smooth muscle cells treated with TGF-f (Battegay et al, 1990;Majack et al, 1990). However, the level of PDGF A chain transcript present in our cells is much lower than the level of CTGF mRNA, and we have not been able to detect Lau and Nathans, 1987).…”

Section: Discussionmentioning

confidence: 99%

Regulation of connective tissue growth factor gene expression in human skin fibroblasts and during wound repair.

Igarashi

Okochi

Bradham

et al. 1993

MBoC

663

581

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Connective tissue growth factor (CTGF) is a cysteine-rich peptide that exhibits platelet-derived growth factor (PDGF)-like biological and immunological activities. CTGF is a member of a family of peptides that include serum-induced immediate early gene products, a v-src-induced peptide, and a putative avian transforming gene, nov. In the present study, we demonstrate that human foreskin fibroblasts produce high levels of CTGF mRNA and protein after activation with transforming growth factor beta (TGF-beta) but not other growth factors including PDGF, epidermal growth factor, and basic fibroblast growth factor. Because of the high level selective induction of CTGF by TGF-beta, it appears that CTGF is a major autocrine growth factor produced by TGF-beta-treated human skin fibroblasts. Cycloheximide did not block the large TGF-beta stimulation of CTGF gene expression, indicating that it is directly regulated by TGF-beta. Similar regulatory mechanisms appear to function in vivo during wound repair where there is a coordinate expression of TGF-beta 1 before CTGF in regenerating tissue, suggesting a cascade process for control of tissue regeneration and repair.

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Section: Discussionmentioning

confidence: 99%

Regulation of connective tissue growth factor gene expression in human skin fibroblasts and during wound repair.

Igarashi

Okochi

Bradham

et al. 1993

MBoC

663

581

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“…For example, PDGF stimulates TGF-/3 production 39 and conversely, TGF-/3 induces PDGF production and modulates expression of PDGF receptors. 40 Like IL-1 and PDGF, TGF-/3 can induce its own gene expression. 41 Cultured endothelial cells and VSMCs secrete constitutively the latent form of TGF-/3, as do many cells in vitro.…”

Section: Resultsmentioning

confidence: 99%

Cytokines and growth factors positively and negatively regulate interstitial collagen gene expression in human vascular smooth muscle cells.

Amento¹,

Ehsani²,

Palmer³

et al. 1991

Arterioscler Thromb

523

276

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Human atheromas accumulate extracellular matrix proteins such as collagen types I and III. We tested whether cytokines or growth factors produced by cells found in human atherosclerotic plaques alter collagen gene expression in vascular smooth muscle cells (VSMCs), which produce the blood vessel matrix. Interleukin-l (IL-1, 1-10 ng/ml) modestly increased the synthesis of collagens I and III (measured by tritiated proline incorporation into specific electrophoretic bands), whereas transforming growth factor-^ (TGF-/3) or platelet-derived growth factor (PDGF) markedly stimulated production of these interstitial collagens. Interferon y (IFN-y)

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“…Both platelet-derived growth factor (PDGF) and transforming growth factor-␤ (TGF-␤) have been shown to induce TSP-1 secretion from vascular smooth muscle cells (VSMCs). 11,12 TSP-1 mRNA levels have been shown to be similarly regulated. Basic fibroblast growth factor upregulates TSP-1 mRNA in 3T3 cells, 13 and PDGF induces upregulation in a manner similar to that of c-myc and c-fos, with TSP-1 being classified as an immediate early response gene.…”

mentioning

confidence: 87%

Phosphatidylinositol 3-Kinase and Focal Adhesion Kinase Are Early Signals in the Growth Factor–Like Responses to Thrombospondin-1 Seen in Human Vascular Smooth Muscle

Lymn

Rao

Clunn

et al. 1999

ATVB

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Abstract-Thrombospondin-1 (TSP-1) is a matricellular protein that is expressed in negligible amounts in normal blood vessels but is markedly upregulated in vascular injury. Although TSP-1 can act as a pleiotropic regulator for human vascular smooth muscle cells (HVSMCs), the intracellular signaling pathways stimulated by this protein remain obscure. In cultured HVSMCs derived from saphenous vein, TSP-1 induces tyrosine phosphorylation of a number of cellular proteins, with a complex temporal pattern of activation. Immunoprecipitation techniques have identified the early tyrosine-phosphorylated signals as being the p85 regulatory subunit of phosphatidylinositol 3-kinase (PI 3-K) and focal adhesion kinase (FAK). Tyrosine phosphorylation of the p85 subunit of PI 3-K showed a biphasic response to TSP-1 stimulation, which corresponded to a biphasic activation of the lipid kinase. Treatment with both wortmannin and LY294002 inhibited PI 3-K activity of HVSMCs but did not affect tyrosine phosphorylation of the p85 regulatory subunit. TSP-1-stimulated FAK phosphorylation, however, was substantially reduced by these inhibitors, as was the TSP-1-induced chemotaxis of these cells. These results suggest that activation of PI 3-K is an early signal induced by TSP-1 and is critical for chemotaxis. Activation of this kinase precedes and may occur upstream from FAK phosphorylation, although the nature of the interaction between these 2 enzymes remains obscure. Key Words: thrombospondin-1 Ⅲ focal adhesion kinase Ⅲ phosphatidylinositol 3-kinase Ⅲ human vascular smooth muscle T hrombospondin-1 (TSP-1), a large, homotrimeric glycoprotein, is a member of the TSP family of matricellular proteins. This family currently consists of 5 isoforms: TSP-1 through TSP-4 and TSP-5/cartilage oligomeric matrix protein, 1 which, although implicated in a wide variety of biological processes, 2 show differential tissue expression both temporally and spatially. 3,4 TSP-1 was originally described as a product of platelet ␣-granules 5 but has since been shown to be synthesized by a number of different cell types, including vascular endothelial and smooth muscle cells. 6,7 TSP-1 is present in negligible amounts in normal human blood vessels, but the expression of this protein is markedly upregulated in injured and diseased vasculature, 8 -10 suggesting a possible role for TSP-1 in the abnormal cellular response to vascular injury.Literature evidence would suggest that TSP-1 levels are regulated by growth factors. Both platelet-derived growth factor (PDGF) and transforming growth factor-␤ (TGF-␤) have been shown to induce TSP-1 secretion from vascular smooth muscle cells (VSMCs). 11,12 TSP-1 mRNA levels have been shown to be similarly regulated. Basic fibroblast growth factor upregulates TSP-1 mRNA in 3T3 cells, 13 and PDGF induces upregulation in a manner similar to that of c-myc and c-fos, with TSP-1 being classified as an immediate early response gene. 14 These data, in conjunction with the role of TSP-1 in potentiating the chemotactic response of VS...

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Role of PDGF-A expression in the control of vascular smooth muscle cell growth by transforming growth factor-beta.

Cited by 208 publications

References 44 publications

Regulation of connective tissue growth factor gene expression in human skin fibroblasts and during wound repair.

Regulation of connective tissue growth factor gene expression in human skin fibroblasts and during wound repair.

Cytokines and growth factors positively and negatively regulate interstitial collagen gene expression in human vascular smooth muscle cells.

Phosphatidylinositol 3-Kinase and Focal Adhesion Kinase Are Early Signals in the Growth Factor–Like Responses to Thrombospondin-1 Seen in Human Vascular Smooth Muscle

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