ArticleThe Biochemical journal1997
Suppression of smooth-muscle alpha-actin expression by platelet-derived growth factor in vascular smooth-muscle cells involves Ras and cytosolic phospholipase A2.
Article in The Biochemical journal, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 53 citations in OpenAlex.
- Spontaneous Helical Alignment of Smooth Muscle Cells to Form a Medial Layer for Engineered Microvasculature.Advanced healthcare materials · 2026Article
- Smooth muscle cell phenotypic modulation during atherosclerosis.Vascular pharmacology · 2026Review
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- Six Shades of Vascular Smooth Muscle Cells Illuminated by KLF4 (Krüppel-Like Factor 4).Arteriosclerosis, thrombosis, and vascular biology · 2021Review
- Transcriptome, Spliceosome and Editome Expression Patterns of the Porcine Endometrium in Response to a Single Subclinical Dose ofInternational journal of molecular sciences · 2020Article
- The Role of Vascular Smooth Muscle Cells in Arterial Remodeling: Focus on Calcification-Related Processes.International journal of molecular sciences · 2019Review
- Fibroblast growth factor (FGF) signaling regulates transforming growth factor beta (TGFβ)-dependent smooth muscle cell phenotype modulation.Scientific reports · 2016Article
- Phenotypic transformation of smooth muscle cells from porcine coronary arteries is associated with connexin 43.Molecular medicine reports · 2016Article
- Smooth muscle phenotype switching in blast traumatic brain injury-induced cerebral vasospasm.Translational stroke research · 2014Review
- Cooperative binding of KLF4, pELK-1, and HDAC2 to a G/C repressor element in the SM22α promoter mediates transcriptional silencing during SMC phenotypic switching in vivo.Circulation research · 2012Article
- The early- and late stages in phenotypic modulation of vascular smooth muscle cells: differential roles for lysophosphatidic acid.Biochimica et biophysica acta · 2008Article
- Role of smooth muscle cells in the initiation and early progression of atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2008Review
- Smooth muscle cell signal transduction: implications of vascular biology for vascular surgeons.Journal of vascular surgery · 2007Review
- Regulation and characteristics of vascular smooth muscle cell phenotypic diversity.Netherlands heart journal : monthly journal of the Netherlands Society of Cardiology and the Netherlands Heart Foundation · 2007Article
- Lung Krüppel-like factor (LKLF) is a transcriptional activator of the cytosolic phospholipase A2 alpha promoter.The Biochemical journal · 2005Article
- Interleukin-1alpha and tumour necrosis factor-alpha modulate airway smooth muscle DNA synthesis by induction of cyclo-oxygenase-2: inhibition by dexamethasone and fluticasone propionate.British journal of pharmacology · 1999Article
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7 authors at 1 institution in 1 country.
Funding
Abstract
Platelet-derived growth factor (PDGF), which is a potent mitogen for vascular smooth-muscle cells (VSMC), also inhibits the expression of specific smooth-muscle proteins, including smooth-muscle alpha-actin (SM-alpha-actin), in these cells. The goal of this study was to identify signalling pathways mediating these distinct effects. In rat aortic VSMC, PDGF caused a rapid activation of Ras and Raf, leading to the activation of mitogen-activated protein kinases (ERKs). Cells stably transfected with constitutively active Ras (H-Ras) expressed low levels of SM-alpha-actin protein. Arginine vasopressin, which stimulated SM-alpha-actin promoter activity in wild-type cells or controls (Neo; transfected with a plasmid lacking an insert), failed to do so in cells transiently expressing H-Ras. The effects of Ras on suppression of SM-alpha-actin expression were not mediated by the Raf/ERK pathway, since cells stably expressing constitutively active Raf (BxB-Raf) had normal levels of SM-alpha-actin protein, and stimulation of SM-alpha-actin promoter activity by vasopressin was unaffected in cells transiently expressing BxB-Raf. Furthermore a specific inhibitor of ERK activation had no effect on SM-alpha-actin expression. Exposure of wild-type VSMC to PDGF, or stable expression of Ras but not Raf, also resulted in constitutive increases in prostaglandin E2 production and cytosolic phospholipase A2 (cPLA2) activity, which was mediated by an increased expression of cPLA2 protein. Transient expression of cPLA2 in wild-type VSMC inhibited the stimulation of SM-alpha-actin promoter activity by vasopressin. These results suggest that PDGF-induced inhibition of SM-alpha-actin expression is mediated through a Ras-dependent/Raf independent pathway involving the induction of cPLA2 and eicosanoid production.
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