C-reactive protein and vein graft disease: evidence for a direct effect on smooth muscle cell phenotype via modulation of PDGF receptor-β

Ho, Karen J.; Owens, Christopher D.; Longo, Thomas A.; Sui, Xin; Ifantides, Cristos; Conte, Michael S.

doi:10.1152/ajpheart.00079.2008

Cited by 16 publications

(18 citation statements)

References 64 publications

(69 reference statements)

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“…Recently, our laboratory demonstrated that CRP may also play an active role in the vessel wall by stimulating both the expression and activity of the PDGR receptor, as well as the enhancement of VSMC migration, which could have implications for vein graft disease. 13 Accordingly, elevated hsCRP levels correlate with preoperative PAD severity, as well as adverse postoperative events in a cohort of patients undergoing lower extremity vein bypass surgery. 12,22 The results of the present study demonstrate that both ATL and RvE1 attenuate PDGF-stimulated VSMC migration and receptor phosphorylation without altering PDGF-R expression levels.…”

Section: Discussionmentioning

confidence: 95%

“…12 Exogenous application of human CRP to vascular smooth muscle cells (VSMCs) derived from human saphenous vein increases platelet-derived growth factor (PDGF)-stimulated chemotaxis in a PDGFR␤-dependent fashion. 13 These data and others suggest that VSMCs may integrate local pro-and anti-inflammatory signals in ways that have relevance to lesion development.…”

mentioning

confidence: 80%

“…Cell viability was performed using trypan blue exclusion. Chemotaxis was assayed using modified Boyden chambers as previously described, 13 except that PDGF-BB was used at a concentration of 10 ng/ml. Imatinib (Novartis), a tyrosine kinase inhibitor, was used at a concentration of 4 mol/L, which we previously determined to be the IC 50 (data not shown).…”

Section: Cell Viability and Chemotaxismentioning

confidence: 99%

“…Protein lysates were prepared for immunoprecipitation of total PDGFR-␤ and Western blotting of phosphotyrosine as previously described. 13 Bound antibody was detected with enhanced chemiluminescent substrate (West Pico, Pierce) according to the manufacturer's instructions.…”

Section: Immunoprecipitation and Western Blottingmentioning

confidence: 99%

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Aspirin-Triggered Lipoxin and Resolvin E1 Modulate Vascular Smooth Muscle Phenotype and Correlate with Peripheral Atherosclerosis

Spite

Owens

et al. 2010

The American Journal of Pathology

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182

189

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Atherosclerosis is a chronic inflammatory disease of the vessel wall. Recent evidence suggests that chronic vascular inflammation ensues as an imbalance between pro-and anti-inflammatory mediators. Recently identified lipid mediators (eg, lipoxins and resolvins) play active roles in promoting the resolution of inflammation. Alterations in vascular smooth muscle cell (VSMC) phenotype, which manifest as a loss of contractile protein expression and increased proliferation and migration, are prominent mechanistic features of both atherosclerosis and restenosis following various interventions (eg, angioplasty and bypass grafting). We sought to determine whether human atherosclerosis is associated with a "resolution deficit" and whether lipoxins and resolvins influence VSMC phenotype. Here we report that plasma levels of aspirin-triggered lipoxin are significantly lower in patients with symptomatic peripheral artery disease than in healthy volunteers. Both aspirintriggered lipoxin and resolvin E1 block platelet-derived growth factor-stimulated migration of human saphenous vein SMCs and decrease phosphorylation of the platelet-derived growth factor receptor-␤. Importantly, receptors for aspirin-triggered lipoxin and resolvin E1 (ALX and ChemR23, respectively) were identified in human VSMCs. Overall, these results demonstrate that stimulatory lipid mediators confer a protective phenotypic switch in VSMCs and elucidate new functions for these mediators in the regulation of SMC biology. These results also suggest that peripheral artery disease is associated with an inflammation-resolution deficit and highlight a potential therapeutic opportunity for the regulation of vascular injury responses. (Am J Pathol

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Section: Discussionmentioning

confidence: 95%

mentioning

confidence: 80%

Section: Cell Viability and Chemotaxismentioning

confidence: 99%

Section: Immunoprecipitation and Western Blottingmentioning

confidence: 99%

See 2 more Smart Citations

Aspirin-Triggered Lipoxin and Resolvin E1 Modulate Vascular Smooth Muscle Phenotype and Correlate with Peripheral Atherosclerosis

Spite

Owens

et al. 2010

The American Journal of Pathology

Self Cite

182

189

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show abstract

“…Thus, although frequently viewed as a non-specific biomarker of inflammation, CRP may act directly as a modulator of acute vascular injury. [81-86]…”

Section: Molecular Remodelingmentioning

confidence: 99%

Vein graft failure

Owens

Gasper

Rahman

et al. 2015

Journal of Vascular Surgery

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115

104

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Following the creation of an autogenous lower extremity bypass graft, the vein must undergo a series of dynamic structural changes to stabilize the arterial hemodynamic forces. These changes, commonly referred to as remodeling, include an inflammatory response, the development of a neointima, matrix turnover, and cellular proliferation and apoptosis. The sum total of these processes results in dramatic alterations in the physical and biomechanical attributes of the arterialized vein. The most clinically obvious and easily measured of these is lumen remodeling of the graft. However, though somewhat less precise, wall thickness, matrix composition, and endothelial changes can be measured in vivo within the healing vein graft. Recent translational work has demonstrated the clinical relevance of remodeling as it relates to vein graft patency and the systemic factors influencing it. By correlating histologic and molecular changes in the vein, insights into potential therapeutic strategies to prevent bypass failure and areas for future investigation are explored.

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Correlation between platelet‐derived growth factor‐B gene polymorphism and coronary heart disease

Liu

Dong

et al. 2022

Clinical Laboratory Analysis

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Object:The aim of the present work was to investigate the correlation of plasma platelet-derived growth factor (PDGF)-BB level and single nucleotide polymorphism (SNP, rs1800817 and rs2285094) of PDGF-B gene with the onset and stability condition of coronary heart disease (CHD).Methods: Totally, 335 subjects were included in and divided into CHD (n = 247) and control group (n = 88) according to coronary angiography. Besides, the patients in the CHD group were divided into acute coronary syndrome (ACS) group (n = 165) and stable angina pectoria (SAP) group (n = 82), based on CHD stability condition. The plasma PDGF-BB level was measured by ELISA, and the genotype of PDGF-B was examined through qPCR assay. Results:The PDGF-BB level was positively correlated with hsCRP level (r = 0.149, p < 0.05). The genotype frequencies of SNP rs1800817 and rs2285094 match Hardy-Weinberg equilibrium. There was weak linkage disequilibrium between SNP rs1800817 and rs2285094: D′ = 0.419, r 2 = 0.04, which has no correlation with CHD. There was no statistical difference in plasma PDGF-BB level among different genotypes in rs1800817 and rs2285094. There were no differences in the plasma PDGF-BB level among patients with any genotype of SNP rs1800817 and rs2285094, no matter how it was grouped. Logistic regression results indicated that the plasma PDGF-BB level was the independent risk factor of CHD onset (OR = 1.003, 95% CI 1.001-1.006, p = 0.014).Conclusions: High plasma PDGF-BB level is the risk factor of CHD and has correlation with instability of CHD. The plasma PDGF-BB level change may be related to inflammatory response. PDGF-B gene rs1800817 and rs2285094 polymorphisms are not correlated with CHD.

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C-reactive protein and vein graft disease: evidence for a direct effect on smooth muscle cell phenotype via modulation of PDGF receptor-β

Abstract: Ho KJ, Owens CD, Longo T, Sui XX, Ifantides C, Conte MS. C-reactive protein and vein graft disease: evidence for a direct effect on smooth muscle cell phenotype via modulation of PDGF receptor-␤.

Cited by 16 publications

References 64 publications

Aspirin-Triggered Lipoxin and Resolvin E1 Modulate Vascular Smooth Muscle Phenotype and Correlate with Peripheral Atherosclerosis

Aspirin-Triggered Lipoxin and Resolvin E1 Modulate Vascular Smooth Muscle Phenotype and Correlate with Peripheral Atherosclerosis

Vein graft failure

Correlation between platelet‐derived growth factor‐B gene polymorphism and coronary heart disease

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