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Cited by 48Cardiovascular, Neuropeptides, and Oxidative Stress ResearchProtein Kinase Regulation and GTPase SignalingTGF-β signaling in diseases

Patterns of Gene Expression Differentially Regulated by Platelet-derived Growth Factor and Hypertrophic Stimuli in Vascular Smooth Muscle Cells

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Kaplan-Albuquerque, Nihal, Bogaert, Yolanda E., Van Putten, Vicki, Weiser-Evans, Mary C., Nemenoff, Raphael A.·2005·Journal of Biological Chemistry
DOI 10.1074/jbc.m500917200
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Abstract

In vascular smooth muscle cells (VSMC), platelet-derived growth factor (PDGF) suppresses expression of multiple smooth muscle contractile proteins, useful markers of differentiation. Conversely, hypertrophic agents induce expression of these genes. The goal of this study was to employ genomic approaches to identify classes of genes differentially regulated by PDGF and hypertrophic stimuli. Changes in gene expression were determined using Affymetrix RAE-230 GeneChips in rat aortic VSMC stimulated with PDGF. For comparison with a model hypertrophic stimulus, a microarray was performed with VSMC stably expressing constitutively active Galpha(16), which strongly induces smooth muscle marker expression. We identified 75 genes whose expression was increased by exposure to PDGF and decreased by expression of Galpha(16) and 97 genes whose expression was decreased by PDGF and increased by Galpha(16). These genes included many smooth muscle-specific proteins; several extracellular matrix, cytoskeletal, and chemotaxis-related proteins; cell signaling molecules; and transcription factors. Changes in gene expression for many of these were confirmed by PCR or immunoblotting. The contribution of signaling pathways activated by PDGF to the gene expression profile was examined in VSMC stably expressing gain-of-function H-Ras or myristoylated Akt. Among the genes that were confirmed to be differentially regulated were CCAAT/enhancer-binding protein delta, versican, and nexilin. All of these genes also had altered expression in injured aortas, consistent with a role for PDGF in the response of injured VSMC. These data indicate that genes that are differentially regulated by PDGF and hypertrophic stimuli may represent families of genes and potentially be biomarkers for vascular injury.

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Authors
Kaplan-Albuquerque, N., Bogaert, Y. E., Van Putten, V., Weiser-Evans, M. C., & Nemenoff, R. A.
Affiliations
University of Colorado Health (US)
Corresponding author
Nemenoff, Raphael A.
ORCID
Nemenoff, Raphael A.
Venue
Journal of Biological Chemistry
Publisher
Elsevier BV
Published
2005-05
Volume
280
Issue
20
Pages
19966-19976
ISSN
0021-9258 (ISSN-L)
DOI
10.1074/jbc.m500917200
OpenAlex
W1996965585
Cited by
48
References
47
Citations by year
2022: 2 · 2021: 3 · 2020: 4 · 2018: 7 · 2017: 2 · 2016: 1 · 2015: 2 · 2014: 4 · 2013: 2 · 2012: 2
FWCI
2.54
Type
journal article
Language
en
Open access
Licence
Locations
  • Journal of Biological Chemistry (publishedVersion, cc-by)
  • PubMed (publishedVersion)
Funders
  • National Cancer Institute (CA103618, R01CA103618)
  • National Institute of Diabetes and Digestive and Kidney Diseases (DK 19928, P01DK019928)
Topics
  • Health Sciences › Medicine › Surgery › Cardiovascular, Neuropeptides, and Oxidative Stress Research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
Keywords
platelet-derived growth factor, vascular smooth muscle cells, smooth muscle hypertrophy, gene expression profiling, Gα16, versican, nexilin, H-Ras, Akt, vascular injury, biomarkers, extracellular matrix, chemotaxis, transcription factors
MeSH terms
Animals, Cells, Cultured, Gene Expression Regulation, Genetic Markers, Muscle, Smooth, Vascular, Phenotype, Platelet-Derived Growth Factor, Transcription Factors, Transfection, Oligonucleotide Array Sequence Analysis, Gene Expression Profiling, Heterotrimeric GTP-Binding Proteins, GTP-Binding Protein alpha Subunits, Gq-G11, Cell Size, Rats

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