Mechanical Strain Induces Expression of C-Reactive Protein in Human Blood Vessels

Huang, Gailing; Luo, Can; Gu, Xiaolong; Wu, Zhongkai; Wang, Zhiping; Du, Zhiming; Tang, Lilong

doi:10.1124/jpet.109.150961

Cited by 14 publications

(17 citation statements)

References 39 publications

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“…In addition, integrin-dependent MAPKs (ERK1/2) activation mechanism involves Rho GTPase (RhoA, Rac1) [72,76,77]. Ultimately, integrin-dependent MAPKs pathway mechanically leads to activation of transcription factor NF-kB and p53 [72,76,77]. Thereby, integrin MAPK signalling pathway is a critical signal pathway for SMC proliferation and apoptosis under mechanical stimulation.…”

Section: Co-culture Model Under a Haemodynamic Environmentmentioning

confidence: 99%

“…Activated integrins also can lead to integrin-dependent activation of MAPKs via FAK through integrin-dependent Src-Ras-MEK1/2 activation [63]. In addition, integrin-dependent MAPKs (ERK1/2) activation mechanism involves Rho GTPase (RhoA, Rac1) [72,76,77]. Ultimately, integrin-dependent MAPKs pathway mechanically leads to activation of transcription factor NF-kB and p53 [72,76,77].…”

Section: Co-culture Model Under a Haemodynamic Environmentmentioning

confidence: 99%

“…It can induce interleukin (IL)-6 and C-reactive protein expression, and the signal pathway was induced by mechanical stretch in VSMCs via Ras/Rac1-p38 MAPK-NF-kB signalling pathways [76,77]. Mechanical strain induces monocyte adhesion to the vascular wall by increasing the expression of monocyte chemoattractant protein-1, interleukin-6, keratinocyte-derived chemokine and vascular cell adhesion molecule-1 (VCAM-1) [84].…”

Section: Effects Of Vascular Wall Mechanical Forces On Vascular Smootmentioning

confidence: 99%

See 2 more Smart Citations

Biomechanical regulation of vascular smooth muscle cell functions: from in vitro to in vivo understanding

Qiu

Zheng

et al. 2014

J. R. Soc. Interface.

145

115

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Vascular smooth muscle cells (VSMCs) have critical functions in vascular diseases. Haemodynamic factors are important regulators of VSMC functions in vascular pathophysiology. VSMCs are physiologically active in the threedimensional matrix and interact with the shear stress sensor of endothelial cells (ECs). The purpose of this review is to illustrate how haemodynamic factors regulate VSMC functions under two-dimensional conditions in vitro or three-dimensional co-culture conditions in vivo. Recent advances show that high shear stress induces VSMC apoptosis through endothelial-released nitric oxide and low shear stress upregulates VSMC proliferation and migration through platelet-derived growth factor released by ECs. This differential regulation emphasizes the need to construct more actual environments for future research on vascular diseases (such as atherosclerosis and hypertension) and cardiovascular tissue engineering.

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Section: Co-culture Model Under a Haemodynamic Environmentmentioning

confidence: 99%

Section: Co-culture Model Under a Haemodynamic Environmentmentioning

confidence: 99%

Section: Effects Of Vascular Wall Mechanical Forces On Vascular Smootmentioning

confidence: 99%

See 1 more Smart Citation

Biomechanical regulation of vascular smooth muscle cell functions: from in vitro to in vivo understanding

Qiu

Zheng

et al. 2014

J. R. Soc. Interface.

145

115

View full text Add to dashboard Cite

show abstract

“…Stretch increases the expression of C-reactive protein (CRP) mRNA and protein in saphenous vein and internal mammary artery rings exposed to stretch [78]. CRP is a nonspecific marker of inflammation and is considered an independent risk factor for atherosclerosis and atherosclerosis-related diseases [79,80].…”

Section: Stretch-regulated Genes Affecting the Inflammatory Response mentioning

confidence: 99%

The Effect of Pressure-Induced Mechanical Stretch on Vascular Wall Differential Gene Expression

et al. 2012

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High blood pressure is responsible for the modulation of blood vessel morphology and function. Arterial hypertension is considered to play a significant role in atherosclerotic ischaemic heart disease, stroke and hypertensive nephropathy, whereas high venous pressure causes varicose vein formation and chronic venous insufficiency and contributes to vein bypass graft failure. Hypertension exerts differing injurious forces on the vessel wall, namely shear stress and circumferential stretch. Morphological and molecular changes in blood vessels ascribed to elevated pressure consist of endothelial damage, neointima formation, activation of inflammatory cascades, hypertrophy, migration and phenotypic changes in vascular smooth muscle cells, as well as extracellular matrix imbalances. Differential expression of genes encoding relevant factors including vascular endothelial growth factor, endothelin-1, interleukin-6, vascular cell adhesion molecule, intercellular adhesion molecule, matrix metalloproteinase-2 and -9 and plasminogen activator inhibitor-1 has been explored using ex vivo cellular or organ stretch models and in vivo experimental animal models. Identification of pertinent genes may unravel new therapeutic strategies to counter the effects of pressure-induced stretch on the vessel wall and hence minimise its notable complications.

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“…Previous studies have demonstrated that CRP expression is induced under mechanical strain, which in turns activates stretch-activated channels (SACs) in the absence of an inflammatory reaction in case of rabbit and human vessel rings and models [16,17]. Clearly, CRP does not function solely as an inflammatory factor.…”

Section: Introductionmentioning

confidence: 99%

C-Reactive Protein and Inflammatory Cytokines during Percutaneous Coronary Intervention

Gu²,

Li³

et al. 2016

J Vasc Res

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Background: C-reactive protein (CRP) is significantly associated with cardiovascular diseases; however, whether CRP plays a causal role in coronary artery disease has yet to be determined. In addition, the relationship between CRP, atherosclerosis, and inflammation remains controversial. Methods and Results: Serum interleukin (IL)-6, IL-1β, and CRP levels were determined in 160 patients at time points around percutaneous coronary intervention (PCI) with drug-eluting stent implantation. The levels were found to be at peak at 24 h post-PCI and gradually declined to the level before PCI at day 30 post-PCI. These inflammation markers around PCI have no statistical difference in the different postdilation pressures (≤14, 14-18, and ≥18 atm) and stent number (1 and ≥2 stents) groups. Treatment of cultured human vascular smooth muscle cells (VSMCs) with a combination of IL-6 and IL-1β at concentrations associated with PCI did not result in any significant change in the CRP mRNA levels. The IL-6-augmented CRP expression in human internal mammary arteries (IMAs) stretched with a mechanical strength of 3 g was blocked by the nuclear factor-κB (NF-κB) peptide inhibitor SN50 and not by the inactive SN50 analog SN50M. IL-6 treatment increased NF-κB activity in human IMAs stretched with 3 g, and this effect was further blocked by stretch-activated channel (SAC) inhibitors (streptomycin or GdCl₃) and SN50. Conclusions: The current study provides evidence that increased serum IL-6, IL-1β, and CRP levels around PCI are not different between different postdilation pressure and stent number groups. The combination of IL-6 and IL-1β at concentrations associated with PCI cannot induce CRP expression in human VSMCs, but they can augment mechanical strain-induced CRP synthesis via the SAC-NF-κB pathway in human IMAs.

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Mechanical Strain Induces Expression of C-Reactive Protein in Human Blood Vessels

Cited by 14 publications

References 39 publications

Biomechanical regulation of vascular smooth muscle cell functions: from in vitro to in vivo understanding

Biomechanical regulation of vascular smooth muscle cell functions: from in vitro to in vivo understanding

The Effect of Pressure-Induced Mechanical Stretch on Vascular Wall Differential Gene Expression

C-Reactive Protein and Inflammatory Cytokines during Percutaneous Coronary Intervention

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