Interleukin-10 Inhibits Postinjury Tumor Necrosis Factor-Mediated Human Vascular Smooth Muscle Proliferation

Selzman, Craig H.; Meldrum, Daniel R.; Cain, Brian S.; Meng, Xianzhong; Shames, Brian D.; Ao, Lihua; Harken, Alden H.

doi:10.1006/jsre.1998.5486

Cited by 35 publications

(25 citation statements)

References 30 publications

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“…NO molecule and two anti-inflammatory cytokines, IL-10 and TGF-β, have potent anti-inflammatory effects on vascular cells [13,14,15,16]. Although in this study both IL-10 and TGF-β mRNA expressions were significantly higher in the injured LCA of group 1 and 2 animals compared to those in group 3, their expressions did not fluctuate significantly over time in both groups 1 and 2 following surgery (fig.…”

Section: Discussioncontrasting

confidence: 44%

“…Moreover, experimental studies have previously shown that CD40 ligand [10] and interleukin (IL)-18 [11], two key proinflammatory mediators, and connexin 43 (Cx43) [12] directly participate in neointimal and smooth muscle cell (SMC) proliferation, which in turn cause vessel wall thickening and narrowing. Conversely, two antiproinflammatory cytokines, IL-10 [13] and transforming growth factor (TGF)-β [14], as well as nitric oxide (NO) molecule [15], are known to inhibit cytokine expression in vascular cells [13,14,15,16]. These results [10,11,12,13,14,15,16] further underscore the possible causal relationship between the inflammatory response cascade and atherosclerotic plaque formation, suggesting that broad-spectral inhibition of various inflammatory pathways may be required in preventing postinjury vascular proliferation rather than blocking merely one specific inflammatory mediator.…”

Section: Introductionmentioning

confidence: 99%

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Shock Wave Therapy Effectively Attenuates Inflammation in Rat Carotid Artery following Endothelial Denudation by Balloon Catheter

Shao

Chiu

Yuen³

et al. 2009

Cardiology

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Background: This study investigates the effectiveness of extracorporeal shock wave (ECSW) in ameliorating inflammatory mediator expression and neointimal formation in a rat model of vascular injury. Methods and Results: Male Sprague-Dawley rats with left carotid artery (LCA) injury induced by balloon dilatation (BD; group 1) were compared with group 2 [LCA injury plus ECSW-181 (defined as 181 total shocks given in LCA at 0.011 mJ/mm²) on day 2 post-LCA injury], and group 3 (normal controls). The rats in each group were further divided into 3 subgroups (n = 6, each) that were sacrificed on postoperative day 3, 7 and 14, respectively. The results demonstrated that, compared to groups 2 and 3, group 1 had significantly increased cellular expression of CD40, interleukin-18, and connexin 43 at each analyzed time point (all p < 0.001). Additionally, LCCA macrophage (CD68) recruitment was substantially increased in group 1 compared to groups 2 and 3 (all p < 0.001). Furthermore, LCA neointimal proliferation and media thickness were markedly higher in group 1 than in groups 2 and 3 on days 7 and 14 post-BD (all p < 0.001). Conclusions: ECSW markedly attenuates inflammatory responses, proliferation of neointima and smooth muscle cells in a rat vascular injury model.

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Section: Discussioncontrasting

confidence: 44%

Section: Introductionmentioning

confidence: 99%

Shock Wave Therapy Effectively Attenuates Inflammation in Rat Carotid Artery following Endothelial Denudation by Balloon Catheter

Shao

Chiu

Yuen³

et al. 2009

Cardiology

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“…Moreover, the effects of IL-10 on vascular cells may vary according to the origin of the cells and the signaling pathways induced by the proinflammatory stimuli. Accordingly, in other studies it was found that IL-10 downregulates the expression of ICAM-1 and VCAM-1 on IL-1-activated HUVECs, 25 decreases both IL-8 and IL-6 production by irradiated HUVECs, 26 inhibits TNF-induced or fibroblast growth factor-2 (FGF-2)-induced human aortic SMC proliferation, 27 and partially antagonizes IFN-␥-induced expression of the secretory nonpancreatic phospholipase A 2 in human SMCs. 28 Moreover, pretreatment of human aortic ECs with recombinant IL-10 as well as transfection with an adenovirus expressing viral IL-10 causes a significant decrease in minimally modified LDL-induced monocyte binding.…”

Section: Il-10mentioning

confidence: 94%

Anti-Inflammatory Mechanisms in the Vascular Wall

Tedgui

Mallat

2001

Circulation Research

381

258

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Abstract-The role of vascular cells during inflammation is critical and is of particular importance in inflammatorydiseases, including atherosclerosis, ischemia/reperfusion, and septic shock. Research in vascular biology has progressed remarkably in the last decade, resulting in a better understanding of the vascular cell responses to inflammatory stimuli. Most of the vascular inflammatory responses are mediated through the IB/nuclear factor-B system. Much recent work shows that vascular inflammation can be limited by anti-inflammatory counteregulatory mechanisms that maintain the integrity and homeostasis of the vascular wall. The anti-inflammatory mechanisms in the vascular wall involve anti-inflammatory external signals and intracellular mediators. The anti-inflammatory external signals include the anti-inflammatory cytokines, transforming growth factor-␤, interleukin-10 and interleukin-1 receptor antagonist, HDL, as well as some angiogenic and growth factors. Physiological laminar shear stress is of particular importance in protecting endothelial cells against inflammatory activation. Its effects are partly mediated through NO production. Finally, endogenous cytoprotective genes or nuclear receptors, such as the peroxisome proliferator-activated receptors, can be expressed by vascular cells in response to proinflammatory stimuli to limit the inflammatory process and the injury. nflammation is a basic pathological mechanism that underlies a variety of diseases. The inflammatory reaction involves the complex interactions between inflammatory cells (neutrophils, lymphocytes, and monocytes/macrophages) and vascular cells (endothelial cells [ECs] and smooth muscle cells [SMCs]). The role of vascular cells during the inflammatory process is critical. Multiple cytokines and growth factors are present at sites of inflammation, and each of these can potentially influence the nature of the inflammatory response. ECs and SMCs must integrate the signals generated by these multiple factors to effectively regulate the immunoinflammatory response through the expression of adhesion molecules, cytokines, chemokines, matrix metalloproteinases, and growth factors. Research in vascular biology has progressed remarkably in the last decade, resulting in a better understanding of the vascular cell responses to inflammatory stimuli and resulting in the identification of major intracellular inflammatory signaling pathways, particularly the IB/nuclear factor-B (NF-B) system. Much recent work shows that vascular inflammation can be limited by anti-inflammatory counteregulatory mechanisms that maintain the integrity and homeostasis of the vascular wall. This might be of particular importance in inflammatory diseases, such as atherosclerosis, septic shock, or ischemia/reperfusion. The purpose of the present review is to describe recent advances in the understanding of the anti-inflammatory mechanisms in vascular cells, focusing on anti-inflammatory external signals and intracellular mediators Original

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“…Moreover, TNF-α stimulates VSMC migration, one of the key processes of vascular stenotic lesion formation [29]. It was also shown that TNF-α may stimulate proliferation of VSMC [30] and enhance VSMC proliferation induced by monocytes [31], which is important for neointima growth and vessel remodeling. Finally, TNF-α was shown to be a key transcriptional inducer of several MMPs [32, 33], active participants of arterial response to intravascular injury promoting VSMC migration and replication [34, 35].…”

Section: Discussionmentioning

confidence: 99%

Oligonucleotide Microarrays Reveal Regulated Genes Related to Inward Arterial Remodeling Induced by Urokinase Plasminogen Activator

Плеханова

Berk²,

Bashtrykov³

et al. 2008

J Vasc Res

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Accumulating evidence suggests that urokinase plasminogen activator (uPA) is involved in vascular remodeling and lumen stenosis after angioplasty and stenting. We have shown previously that increased uPA expression greatly promotes neointima formation and inward arterial remodeling after balloon injury. To evaluate the role of inflammation in early mechanisms responsible for inward arterial remodeling induced by uPA and elucidate the mechanisms of remodeling, we characterized changes in the expression profiles of 8,799 genes in injured rat carotid arteries 1 and 4 days after recombinant uPA treatment compared to vehicle. We used a standard model of the balloon catheter injury of the rat carotid followed by periadventitial application to the injured vessel of either uPA dissolved in Pluronic gel, or plain gel. Vessels were harvested and analyzed by immunohistochemistry, morphometry, microarray gene expression profiling and quantitative RT-PCR. Periadventitial application of uPA significantly reduced lumen size and vessel area encompassed by the external elastic lamina at both 1 and 4 days after treatment. Inflammatory cells accumulated in the arterial adventitia at both 1 and 4 days after uPA treatment. On the 4th day, increases in the areas and arterial cell numbers of all arterial layers were found. Among 79 differentially expressed known genes 1 day after uPA application, 12 proinflammatory genes, including TNF-α and TACE, and 15 genes related to mitochondrial metabolism and oxidative stress regulation were identified. Four days after injury in uPA-treated arteries, 3 proinflammatory and 2 oxidation-related genes were differentially expressed. We conclude that uPA likely promotes inward arterial remodeling by regulating oxidative stress and inflammation after arterial injury.

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Interleukin-10 Inhibits Postinjury Tumor Necrosis Factor-Mediated Human Vascular Smooth Muscle Proliferation

Cited by 35 publications

References 30 publications

Shock Wave Therapy Effectively Attenuates Inflammation in Rat Carotid Artery following Endothelial Denudation by Balloon Catheter

Shock Wave Therapy Effectively Attenuates Inflammation in Rat Carotid Artery following Endothelial Denudation by Balloon Catheter

Anti-Inflammatory Mechanisms in the Vascular Wall

Oligonucleotide Microarrays Reveal Regulated Genes Related to Inward Arterial Remodeling Induced by Urokinase Plasminogen Activator

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