Up-Regulated Expression of Matrix Metalloproteinases in Endothelial Cells Mediates Platelet Microvesicle-Induced Angiogenesis

Sun, Cheng; Feng, Shibin; Cao, Zhengwang; Bei, Jun-Jie; Chen, Qiang; Zhao, Weibo; Xu, Xianjie; Zhou, Zhou; Yu, Zhengping; Hu, Houyuan

doi:10.1159/000475651

Cited by 51 publications

(41 citation statements)

References 46 publications

(57 reference statements)

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“…The cell migration assay was performed according to the manufacturer’s protocol [24]. EPCs (5 × 10 4 ) were incubated in the upper chambers.…”

Section: Methodsmentioning

confidence: 99%

Vitamin D Ameliorates Angiotensin II-Induced Human Endothelial Progenitor Cell Injury via the PPAR-γ/HO-1 Pathway

et al. 2019

J Vasc Res

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Vitamin D has an important protective effect on chronic inflammatory disease. Angiotensin II (AngII) triggers vascular damage and plays a key role in vascular diseases via several mechanisms, including inflammation. Conversely, vitamin D has been shown to have an important protective effect on chronic inflammation. There is evidence showing that vitamin D can reverse the effects of AngII, but the molecular mechanisms by which this occurs are not known. Our results demonstrate that vitamin D improved the viability, migration ability, and tube formation of AngII-pretreated endothelial progenitor cells (EPCs) and inhibited the apoptosis of EPCs induced by AngII. Vitamin D also reversed reactive oxygen species production, vascular inflammatory cytokine generation, and nuclear factor kappa-B activation in EPCs induced by AngII. Furthermore, EPC pretreatment with GW9662 (the antagonist for PPAR-γ) or siHO-1 decreased the protective effect of vitamin D on AngII-induced EPC injury. Overall, our data indicate that vitamin D ameliorated AngII-induced abnormal EPC injury by decreasing oxidative stress and inflammatory cytokine levels. These findings also suggest that vitamin D protected EPCs from AngII-induced vascular injury via the activation of the PPAR-γ/HO-1 signaling pathway.

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“…The cell migration assay was performed according to the manufacturer’s protocol [24]. EPCs (5 × 10 4 ) were incubated in the upper chambers.…”

Section: Methodsmentioning

confidence: 99%

Vitamin D Ameliorates Angiotensin II-Induced Human Endothelial Progenitor Cell Injury via the PPAR-γ/HO-1 Pathway

et al. 2019

J Vasc Res

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“…Moreover, levels of metalloprotease expression and activity; mostly MMP-2 and MMP-9, were upregulated in HUVEC. These pro-angiogenic and pro-migratory effects were abolished with the inhibition of MMPs (Sun et al, 2017). Angiogenesis can also be regulated by lymphocyte-derived EVs.…”

Section: Extracellular Vesicles Promote Endothelial Dysfunction At Thmentioning

confidence: 98%

The Contrasting Role of Extracellular Vesicles in Vascular Inflammation and Tissue Repair

2019

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Extracellular vesicles are a heterogeneous family of vesicles, generated from different subcellular compartments and released into the extracellular space. Composed of a lipid bilayer encompassing both soluble cytosolic material and nuclear components, these organelles have been recently described as novel regulators of intercellular communication between adjacent and remote cells. Due to their diversified composition and biological content, they portray specific signatures of cellular activation and pathological processes, their potential as diagnostic and prognostic biomarkers has raised significant interest in cardiovascular diseases. Circulating vesicles, especially those released from platelets, leukocytes, and endothelial cells are found to play a critical role in activating several fundamental cells within the vasculature, including endothelial cells and vascular smooth muscle cells. Their intrinsic activity and immunomodulatory properties lends them to not only promote vascular inflammation, but also enhance tissue regeneration, vascular repair, and indeed resolution. In this review we aim to recapitulate the recent findings concerning the roles played by EVs that originate from different circulating cells, with particular reference to their action on the endothelium. We focus herein, on the interaction of platelet and leukocyte EVs with the endothelium. In addition, their potential biological function in promoting tissue resolution and vascular repair will also be discussed.

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“…THBS1 prevents the activation of MMPs via type I repeats (Bein & Simons 2000) and suppresses the activation of MMP9 by binding to its inactive form (Rodriguez-Manzaneque et al 2001). In HUVEC cells, inhibition of MMP activation decreased proangiogenic and promigratory effects induced by platelet microvesicles (Sun et al 2017). On the other hand, THBS1 has also been reported to increase MMP2 and -9 activation in several tumor cells (Ren et al 2006) and vascular smooth muscle cells (Lee et al 2003).…”

Section: Role Of Thbs1 In Matrix Remodelingmentioning

confidence: 99%

Thrombospondin-1 at the crossroads of corpus luteum fate decisions

Farberov¹,

Basavaraja²,

Meidan³

2019

Reproduction

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The multimodular matricellular protein thrombospondin-1 (THBS1) was among the first identified endogenous antiangiogenic molecules. Recent studies have shown THBS1-mediated suppression of angiogenesis and other critical activities for corpus luteum (CL) regression. THBS1 is specifically induced by prostaglandin F2alpha in mature CL undergoing regression, whereas luteinizing signals such as luteinizing hormone and insulin reduced its expression. THBS1 interacts both synergistically and antagonistically with other essential luteal factors, such as fibroblast growth factor 2, transforming growth factor beta1 and serpin family E member 1, to promote vascular instability, apoptosis and matrix remodeling during luteal regression. Expression of THBS1 is also downregulated by pregnancy recognition signals to maintain the CL during early pregnancy. This dynamic pattern of luteal expression, the extensive interactivity with other luteal factors and strong antiangiogenic and proapoptotic activities indicate that THBS1 is a major determinant of CL fate.

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Up-Regulated Expression of Matrix Metalloproteinases in Endothelial Cells Mediates Platelet Microvesicle-Induced Angiogenesis

Cited by 51 publications

References 46 publications

Vitamin D Ameliorates Angiotensin II-Induced Human Endothelial Progenitor Cell Injury via the PPAR-γ/HO-1 Pathway

Vitamin D Ameliorates Angiotensin II-Induced Human Endothelial Progenitor Cell Injury via the PPAR-γ/HO-1 Pathway

The Contrasting Role of Extracellular Vesicles in Vascular Inflammation and Tissue Repair

Thrombospondin-1 at the crossroads of corpus luteum fate decisions

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