IL-10 Accelerates Re-Endothelialization and Inhibits Post-Injury Intimal Hyperplasia following Carotid Artery Denudation

Verma, Suresh; Garikipati, Venkata Naga Srikanth; Krishnamurthy, Prasanna; Khan, Mohsin; Thorne, Tina; Qin, Gangjian; Losordo, Douglas W.; Kishore, Raj

doi:10.1371/journal.pone.0147615

Cited by 25 publications

(16 citation statements)

References 34 publications

(54 reference statements)

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“…Earlier reports have identified increased IL-10 levels following injury of rat sciatic nerve, and a beneficial role of IL-10 has been implicated in tissues such as cardiac muscle, carotid endothelia, and lung epithelia (20)(21)(22). We found that epithelial IL-10Rα mediates the IL-10-driven increase in wound healing.…”

Section: Discussionsupporting

confidence: 56%

Macrophage-derived IL-10 mediates mucosal repair by epithelial WISP-1 signaling

Quirós¹,

Nishio²,

Neumann³

et al. 2017

Journal of Clinical Investigation

155

132

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Section: Discussionsupporting

confidence: 56%

Macrophage-derived IL-10 mediates mucosal repair by epithelial WISP-1 signaling

Quirós¹,

Nishio²,

Neumann³

et al. 2017

Journal of Clinical Investigation

155

132

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“…Several studies have shown an increase on neointima proliferation after angioplasty due to an inhibited endothelial recovery 28 . Since endothelial repair is an important component of the adaptive response of the vessel to injury, we examined this process in our model by immunofluorescent staining for CD31, a specific marker of endothelial cells.…”

Section: Resultsmentioning

confidence: 99%

Hindlimb Ischemia Impairs Endothelial Recovery and Increases Neointimal Proliferation in the Carotid Artery

Sorrentino

Iaconetti

Rosa

et al. 2018

Sci Rep

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Peripheral ischemia is associated with higher degree of endothelial dysfunction and a worse prognosis after percutaneous coronary interventions (PCI). However, the role of peripheral ischemia on vascular remodeling in remote districts remains poorly understood. Here we show that the presence of hindlimb ischemia significantly enhances neointima formation and impairs endothelial recovery in balloon-injured carotid arteries. Endothelial-derived microRNAs are involved in the modulation of these processes. Indeed, endothelial miR-16 is remarkably upregulated after vascular injury in the presences of hindlimb ischemia and exerts a negative effect on endothelial repair through the inhibition of RhoGDIα and nitric oxide (NO) production. We showed that the repression of RhoGDIα by means of miR-16 induces RhoA, with consequent reduction of NO bioavailability. Thus, hindlimb ischemia affects negative carotid remodeling increasing neointima formation after injury, while systemic antagonizzation of miR-16 is able to prevent these negative effects.Peripheral Arterial Disease (PAD) affects approximately 20% of adults over the age of 50, exposing them to the negative impact of peripheral ischemia 1-3 . However, half of these subjects are asymptomatic. Hence, the actual impact of peripheral ischemia is largely under-estimated, leading to under-treatment and seriously undermining prevention strategies 4,5 . Interestingly, in patients with multidistrectual atherosclerosis the presence of peripheral ischemia is associated to a further increase in mortality independently of classical cardiovascular risk factors 6,7 . In line with these observations, it was shown that limb ischemia might remotely influence atherosclerotic vascular remodeling in coronary and cerebral districts 8,9 . Indeed, the presence of limb ischemia is often associated to endothelial dysfunction 10 , and consequently to a more severe atherosclerosis of remote districts 11 . Interestingly, patients with PAD and peripheral ischemia undergoing percutaneous coronary intervention (PCI) have a significantly poorer prognosis suggesting a remote negative impact of peripheral ischemia on coronary artery disease 12,13 . This picture has not improved with the recent significant progresses in medical therapy and introduction of the latest generation of drug eluting stents (DES) 14 . Indeed, it is known that limb ischemia can negatively influence vascular remodeling in other districts, such as coronary and cerebral arteries [12][13][14][15] . MicroRNA (miRNAs), small noncoding RNAs, have emerged in the last decade as epigenetic regulators of essential biological processes [15][16][17] . In particular, they play a key role in the pathophysiology of atherosclerosis, including restenosis after PCI [18][19][20] , and could be used as circulating biomarkers [21][22][23][24] . Recent studies showed that miRNAs could modulate both vascular smooth muscle cells (VSMC) and the endothelium in response to vascular injury 25 . Moreover, miRNAs can mediate intercellular crosstalk, involv...

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“…We previously reported that pMSCs produce many molecules with survival, pro-proliferative, and migratory activities, such as IL-6 [ 28 ], IL-8 [ 29 , 30 ], IL-10 [ 31 ], IL-11 [ 32 ], and PDGF-Rβ [ 33 ]. These molecules potentially mediate the pMSC protective effects on endothelial cells treated with glucose.…”

Section: Discussionmentioning

confidence: 99%

Human chorionic villous mesenchymal stem/stromal cells protect endothelial cells from injury induced by high level of glucose

et al. 2018

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BackgroundMesenchymal stem/stromal cells derived from chorionic villi of human term placentae (pMSCs) protect human endothelial cells from injury induced by hydrogen peroxide (H2O2). In diabetes, elevated levels of glucose (hyperglycaemia) induce H2O2 production, which causes the endothelial dysfunction that underlies the enhanced immune responses and adverse complications associated with diabetes, which leads to thrombosis and atherosclerosis. In this study, we examined the ability of pMSCs to protect endothelial cell functions from the negative impact of high level of glucose.MethodspMSCs isolated from the chorionic villi of human term placentae were cultured with endothelial cells isolated from human umbilical cord veins in the presence of glucose. Endothelial cell functions were then determined. The effect of pMSCs on gene expression in glucose-treated endothelial cells was also determined.ResultspMSCs reversed the effect of glucose on key endothelial cell functions including proliferation, migration, angiogenesis, and permeability. In addition, pMSCs altered the expression of many genes that mediate important endothelial cell functions including survival, apoptosis, adhesion, permeability, and angiogenesis.ConclusionsThis is the first comprehensive study to provide evidence that pMSCs protect endothelial cells from glucose-induced damage. Therefore, pMSCs have potential therapeutic value as a stem cell-based therapy to repair glucose-induced vascular injury and prevent the adverse complications associated with diabetes and cardiovascular disease. However, further studies are necessary to reveal more detailed aspects of the mechanism of action of pMSCs on glucose-induced endothelial damage in vitro and in vivo.

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IL-10 Accelerates Re-Endothelialization and Inhibits Post-Injury Intimal Hyperplasia following Carotid Artery Denudation

Cited by 25 publications

References 34 publications

Macrophage-derived IL-10 mediates mucosal repair by epithelial WISP-1 signaling

Macrophage-derived IL-10 mediates mucosal repair by epithelial WISP-1 signaling

Hindlimb Ischemia Impairs Endothelial Recovery and Increases Neointimal Proliferation in the Carotid Artery

Human chorionic villous mesenchymal stem/stromal cells protect endothelial cells from injury induced by high level of glucose

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