scholarly journals Interleukin-1 and Tumor Necrosis Factor- Stimulate thecat-2Gene of the L-Arginine Transporter in Cultured Vascular Smooth Muscle Cells

1996 ◽  
Vol 271 (19) ◽  
pp. 11280-11283 ◽  
Author(s):  
Denzil J. Gill ◽  
Boon Chuan Low ◽  
Murray R. Grigor
Keyword(s):  
Smooth Muscle ◽  
Tumor Necrosis Factor ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Tumor Necrosis ◽  
Interleukin 1 ◽  
Muscle Cells ◽  
Necrosis Factor

scholarly journals Transcriptional Suppression of CPI-17 Gene Expression in Vascular Smooth Muscle Cells by Tumor Necrosis Factor, Krüppel-Like Factor 4, and Sp1 Is Associated with Lipopolysaccharide-Induced Vascular Hypocontractility, Hypotension, and Mortality

2019 ◽  
Vol 39 (11) ◽  
Author(s):  
Guogang Zhao ◽  
Yu Zhong ◽  
Wen Su ◽  
Shu Liu ◽  
Xiulong Song ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Tumor Necrosis Factor ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Tumor Necrosis ◽  
Muscle Cells ◽  
Mesenteric Arteries ◽  
Vasodilatory Shock ◽  
Necrosis Factor

ABSTRACT Vasodilatory shock in sepsis is caused by the failure of the vasculature to respond to vasopressors, which results in hypotension, multiorgan failure, and ultimately patient death. Recently, it was reported that CPI-17, a key player in the regulation of smooth muscle contraction, was downregulated by lipopolysaccharide (LPS) in mesenteric arteries concordant with vascular hypocontractilty. While Sp1 has been shown to activate CPI-17 transcription, it is unknown whether Sp1 is involved in LPS-induced smooth muscle CPI-17 downregulation. Here we report that tumor necrosis factor (TNF) was critical for LPS-induced smooth muscle CPI-17 downregulation. Mechanistically, we identified two GC boxes as a key TNF response element in the CPI-17 promoter and demonstrated that KLF4 was upregulated by TNF, competed with Sp1 for the binding to the GC boxes in the CPI-17 promoter, and repressed CPI-17 transcription through histone deacetylases (HDACs). Moreover, genetic deletion of TNF or pharmacological inhibition of HDACs protected mice from LPS-induced smooth muscle CPI-17 downregulation, vascular hypocontractility, hypotension, and mortality. In summary, these data provide a novel mechanism of the transcriptional control of CPI-17 in vascular smooth muscle cells under inflammatory conditions and suggest a new potential therapeutic strategy for the treatment of vasodilatory shock in sepsis.

scholarly journals Tumor Necrosis Factor-Related Apoptosis Inducing Ligand Stimulates Migration And Proliferation Of Vascular Smooth Muscle Cells

2018 ◽  
Vol 17 (1) ◽  
Author(s):  
Madia Baizura Baharom ◽  
Nor Saadah Md. Azahri ◽  
Mohd. Ariffin Kaderi ◽  
Suhana Mamat
Keyword(s):  
Smooth Muscle ◽  
Tumor Necrosis Factor ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Tumor Necrosis ◽  
Muscle Cells ◽  
Proliferation Assay ◽  
Necrosis Factor

Introduction: Tumor Necrosis Factor-Related Apoptosis (TRAIL) has the ability to inhibit angiogenesis through programmed cell death, in the same time able to promote pro-angiogenic activity. It seems that TRAIL has an opposite effects make its role in ischemic disease and its function in a normal cell is still unclear. This study determines the effect of TRAIL in Vascular Smooth Muscle Cells (VSMCs). Materials and Methods: In this study, 6 wells in vitro Scratch Assay were conducted for migration and Cellltiter 96® Aqueous One Solution Cell Proliferation Assay (MTS) was performed for proliferation. In both assays, cells were serum arrested for 24, 48 and 72 hours, following stimulation with different concentration (1ng/ml, 20ng/ml, 50ng/ml and 100ng/ml) and different volume (20µL and 100µL) of TRAIL. PDGF-BB was used as positive control. Results of PDGFBB and TRAIL were compared with untreated VSMC. Results: It Is demonstrated that 100µL of 50ng/ml TRAIL-induced VSMC shows significant (p < 0.05) higher migration rate percentage compared to untreated cells, included 100µL of 20ng/ml PDGF-BB after 48 hours. However, in proliferation assay, the lowest concentration of TRAIL (1ng/ml, 20µL) shows significantly higher proliferation rate compared to untreated cells after 24 hours (p < 0.05) meanwhile PDGF-BB (1ng/ml, 20µL) indicates significant higher proliferation after 48 hours. Conclusion: This study demonstrates that TRAIL promotes the VSMC migration and proliferation in vitro. This indicates that migration and proliferation of VSMC upon vascular injury from media to intima not only involves PDGF-BB, but also TRAIL. Therefore, TRAIL contributes to intimal thickening that can lead to the obstruction of the blood vessels and it is a hallmark of atherosclerosis.

scholarly journals Andrographolide Inhibits Nuclear Factor-κB Activation through JNK-Akt-p65 Signaling Cascade in Tumor Necrosis Factor-α-Stimulated Vascular Smooth Muscle Cells

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Yu-Ying Chen ◽  
Ming-Jen Hsu ◽  
Cheng-Ying Hsieh ◽  
Lin-Wen Lee ◽  
Zhih-Cherng Chen ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Tumor Necrosis Factor ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Tumor Necrosis ◽  
Muscle Cells ◽  
Aortic Aneurysms ◽  
Signaling Cascade ◽  
Necrosis Factor

Critical vascular inflammation leads to vascular dysfunction and cardiovascular diseases, including abdominal aortic aneurysms, hypertension, and atherosclerosis. Andrographolide is the most active and critical constituent isolated from the leaves ofAndrographis paniculata, a herbal medicine widely used for treating anti-inflammation in Asia. In this study, we investigated the mechanisms of the inhibitory effects of andrographolide in vascular smooth muscle cells (VSMCs) exposed to a proinflammatory stimulus, tumor necrosis factor-α(TNF-α). Treating TNF-α-stimulated VSMCs with andrographolide suppressed the expression of inducible nitric oxide synthase in a concentration-dependent manner. A reduction in TNF-α-induced c-Jun N-terminal kinase (JNK), Akt, and p65 phosphorylation was observed in andrographolide-treated VSMCs. However, andrographolide affected neither IκBαdegradation nor p38 mitogen-activated protein kinase or extracellular signal-regulated kinase 1/2 phosphorylation under these conditions. Both treatment with LY294002, a phosphatidylinositol 3-kinase/Akt inhibitor, and treatment with SP600125, a JNK inhibitor, markedly reversed the andrographolide-mediated inhibition of p65 phosphorylation. In addition, LY294002 and SP600125 both diminished Akt phosphorylation, whereas LY294002 had no effects on JNK phosphorylation. These results collectively suggest that therapeutic interventions using andrographolide can benefit the treatment of vascular inflammatory diseases, and andrographolide-mediated inhibition of NF-κB activity in TNF-α-stimulated VSMCs occurs through the JNK-Akt-p65 signaling cascade, an IκBα-independent mechanism.

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