Interleukin 6 augments mechanical strain-induced C-reactive protein synthesis via the stretch-activated channel–nuclear factor κ B signal pathway

Zhou, Hongli; Y, Li; Huang, Gailing; Gu, Xiaosong; Zeng, Jianping; Luo, Cheng; B, Ou; ZHANG, YEUJIE; Z, Wu; Tang, Lilong

doi:10.1136/heartjnl-2012-303355

Cited by 10 publications

(10 citation statements)

References 24 publications

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“…Mechanical strain generated by the aortic smooth muscle was measured by using a force transducer (Chengdu, TME Technology Co. Ltd., China) and recorded by using the BL-420S experimental system of biological function (Chengdu, TME Technology Co. Ltd., China) [9,10]. The resting tension was set to 0.2 g. At first, we equilibrated the aortic ring segments for 90 min, during which the K-H solution was changed every 15 min.…”

Section: Methodsmentioning

confidence: 99%

Mechanical Strain Induced Expression of Matrix Metalloproteinase-9 via Stretch-Activated Channels in Rat Abdominal Aortic Dissection

et al. 2017

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BackgroundThe aim of the study was to investigate the expression of matrix metalloproteinase-9 (MMP-9) in rat abdominal aortic dissection (AD) induced by mechanical strain, so as to offer a better understanding of the possible mechanisms of AD.Material/MethodsExperimental AD in rats was achieved by the injection of porcine pancreatic elastase. At days 0, 1, 3, 5, 7, 14, 21, and 30 after the establishment of AD model, serum MMP-9 levels were measured by enzyme-linked immunosorbent assay (ELISA). Four groups of vascular rings were stretched in vitro with a mechanical strength of 0 g, 1 g, 3 g, or 5 g for 30 min. Another four groups were pretreated with GdCl3, streptomycin, SN50, and SN50M, followed by stretching with 3 g for 30 min. The messenger RNA and the protein of MMP-9 were analyzed by real-time RT-PCR and Western blotting, and NF-κB p65 was detected by ELISA.ResultsAfter the establishment of rat abdominal AD model, the serum MMP-9 levels of AD groups increased significantly. The results showed increased expression of MMP-9 in rat AD vessels stretched with mechanical strength of 1 g, 3 g, and 5 g, but this effect was mostly blocked by Gd Cl3 and streptomycin. The NF-κB activity in aortic rings was activated by stretching with a mechanical strength of 3 g and was blocked by SN50, but not by SN50M.ConclusionsThe expression of MMP-9 in serum was increased significantly after rat abdominal AD formation. Mechanical strain induced MMP-9 expression in AD vessels, which was mediated through the activation of the stretch-activated channel-induced NF-κB pathway.

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Section: Methodsmentioning

confidence: 99%

Mechanical Strain Induced Expression of Matrix Metalloproteinase-9 via Stretch-Activated Channels in Rat Abdominal Aortic Dissection

et al. 2017

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“…IL-6 mediates the binding of CCAAT/enhancer-binding protein (C/EBP) β and C/EBPγ to two sites in the CRP promoter at -53 and -219, and it mediates the binding of signal transducer and activator of transcription 3 (STAT3) to a site at -108, which consequently enhances CRP gene transcription [20,21,22]. However, when acute inflammation disappears, inflammation markers in the serum may come from vessels locally with different mechanisms, such as mechanical strain-induced mechanism [16,17,18]. …”

Section: Discussionmentioning

confidence: 99%

“…Different combinations of these factors might produce different cellular activities. We previously reported that IL-6 augments mechanical strain-induced CRP synthesis via the SAC-NF-κB signal pathway in the rabbit vessel rings [18]. SACs are activated under mechanical strain and transduce external mechanical stimuli into physiological signals.…”

Section: Discussionmentioning

confidence: 99%

“…Clearly, CRP does not function solely as an inflammatory factor. We also found that the inflammatory cytokine interleukin (IL)-6 augments mechanical strain-induced CRP synthesis in rabbit vessels via the SAC-nuclear factor-κB (SAC-NF-κB) pathway [18]. In the current study, we investigated the relationship among CRP induction, the inflammatory response, and mechanical strain during the process of vascular injury in human vessels.…”

Section: Introductionmentioning

confidence: 99%

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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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“…So, current evidence suggests that miR-124 function as a key modulator in adhesion-associated processes of podocyte. Previous study suggested that mechanical stress to cells could activate NF-κB transcription factor [31,32] and curcumin treatment could protect against the development of DN through the inhibition of NF-κB activation [21]. …”

Section: Discussionmentioning

confidence: 99%

Curcumin Ameliorates Podocytic Adhesive Capacity Damage Under Mechanical Stress By Inhibiting miR-124 Expression

Liu

Lu²,

Jia³

et al. 2013

Kidney Blood Press Res

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Background/Aims: Curcumin, a kind of plant polyphenolic compound, has been recently discovered to have renoprotective effects on diabetic nephropathy (DN). Podocyte can respond to various injuries including mechanical stress secondary to DN. Our previous study showed that podocyte miR-124 expression was up-regulated accompanied with podocytic adhesive capacity damage in vitro and in vivo. We hypothesized, in the present research that curcumin would ameliorate podocyte adhesion damage under mechanical stress by inhibiting miR-124 expression. Methods: Gene expression of miR-124 was measured by real-time PCR and protein expression of integrin α3 was measured by Western blotting in STZ-induced uninephrectomized diabetic rats and cultured podocytes under mechanical stress treated with curcumin respectively. Western blot and luciferase reporter assays were used to detect the effects of miR-124 overexpression on the Itga3 expression in podocytes. Results: Gene expression of miR-124 was upregulated and α3 was downregulated in renal cortex of diabetic rats and cultured podocytes under mechanical stress which were ameliorated by curcumin treatment significantly. Transient co-transfection of miR-124 mimics with luciferase expression plasmids resulted in a significant repression of luciferase activity in podocytes. Mechanistically, Itga3 may be a regulation target of miR-124. Conclusions: These results provide a novel idea that curcumin prevents against podocytic adhesive capacity damage under mechanical stress by inhibitting miR-124

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Interleukin 6 augments mechanical strain-induced C-reactive protein synthesis via the stretch-activated channel–nuclear factor κ B signal pathway

Abstract: These results indicate that the inflammatory cytokine IL-6 alone does not induce CRP synthesis in vessels in the absence of mechanical strain; however, IL-6 augments mechanical strain-induced CRP synthesis in vessels via the stretch-activated channel-NF-κB pathway.

Cited by 10 publications

References 24 publications

Mechanical Strain Induced Expression of Matrix Metalloproteinase-9 via Stretch-Activated Channels in Rat Abdominal Aortic Dissection

Mechanical Strain Induced Expression of Matrix Metalloproteinase-9 via Stretch-Activated Channels in Rat Abdominal Aortic Dissection

C-Reactive Protein and Inflammatory Cytokines during Percutaneous Coronary Intervention

Curcumin Ameliorates Podocytic Adhesive Capacity Damage Under Mechanical Stress By Inhibiting miR-124 Expression

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