Apolipoprotein A-I enhances proliferation of human endothelial progenitor cells and promotes angiogenesis through the cell surface ATP synthase

González-Pecchi, Valentina; Valdés, Sara; Pons, Véronique; Honorato, Paula; Martinez, Laurent O.; Lamperti, Liliana; Aguayo, Claudio; Radojkovic, Claudia

doi:10.1016/j.mvr.2014.11.003

Cited by 41 publications

(34 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Liver-specific overexpression of apoA-I was found to increase apoA-I and HDL-C levels in plasma, thereby reducing atherosclerosis in hyperlipidemic mice [34,35]. In addition, apoA-I enhances the proliferation of human endothelial progenitor cells (EPCs) and promotes angiogenesis through ATP synthase in cell surface [36]. ApoA-I restores neovascularization of the lymphatic system in tumor necrosis factor (TNF)-alpha-mediated inflammatory responses [37].…”

Section: Apolipoprotein A-i (Apoa-i)mentioning

confidence: 99%

High-Density Lipoprotein: From Biological Functions to Clinical Perspectives

Liu¹

2020

Apolipoproteins, Triglycerides and Cholesterol

View full text Add to dashboard Cite

High-density lipoprotein (HDL) is a heterogeneous particle composed of apolipoproteins, enzymes, and lipids. Besides transporting cholesterol to the liver, HDL also exerts many protections on anti-oxidation, anti-inflammation, and anti-apoptosis. Initial understandings of HDL came from its protective roles against atherosclerosis and the observation that high plasma HDL cholesterol (HDL-C) levels seemed to decrease cardiovascular disease (CVD) attack. However, those patients either with cholesterol ester transfer protein (CETP) deficiency or taking CETP inhibitors substantially elevated HDL-C levels but did not necessarily decrease CVD risk. Thus, some researchers suggested that quantitative measurements of HDL particle (HDL-P) might be more valuable than traditional HDL-C measurements. What is more bewildering is that HDL from patients with systemic inflammation decreased its protective effects and even became a pro-inflammatory factor. Recently, synthesized HDL and apolipoprotein mimetic peptides showed biological functions similar to native ones. Expectedly, lots of novel measurement methods and therapeutic agents about HDL would be established soon.

show abstract

Section: Apolipoprotein A-i (Apoa-i)mentioning

confidence: 99%

High-Density Lipoprotein: From Biological Functions to Clinical Perspectives

Liu¹

2020

Apolipoproteins, Triglycerides and Cholesterol

View full text Add to dashboard Cite

show abstract

“…HDL also bind to scavenger receptor class B member 1 (SR-BI) to accelerate re-endothelialization through activation of the Src kinases, PI3K and p44/42 mitogen-activated protein kinases (MAPK) [16]. Finally, apoA-I binds and activates the ecto-F 1 -ATPase receptor on the surface of endothelial cells and endothelial progenitor cells (EPC), to promote cell proliferation [18, 19]. The effects of apoA-I on ecto-F 1 -ATPase activity are strictly limited to this receptor since they were observed following the inhibition of other HDL/apoA-I receptors, such as SR-BI and ABCA1, but were reduced following treatment with inhibitory factor 1 (IF1-H49K), a specific F 1 -ATPase inhibitor.…”

Section: Introductionmentioning

confidence: 99%

PI3Kβ Plays a Key Role in Apolipoprotein A-I-Induced Endothelial Cell Proliferation Through Activation of the Ecto-F1-ATPase/P2Y1 Receptors

Castaing-Berthou¹,

Malet²,

Radojkovic³

et al. 2017

Cell Physiol Biochem

Self Cite

View full text Add to dashboard Cite

Background/Aims: High-density lipoproteins (HDL) exert multiple cardioprotective functions on the arterial wall, including the promotion of endothelial cell survival and proliferation. Among mechanism contributing to endothelial protection, it has been reported that apolipoprotein A-I (apoA-I), the major protein in HDL, binds and activates the endothelial ecto-F₁-ATPase receptor. This generates extracellular ADP, which in turn promotes endothelial cell survival. In this study we aimed to further investigate the signaling pathway involved downstream of apoA-I-induced ecto-F₁-ATPase activation. Methods: In human umbilical vein endothelial cells (HUVECs), pharmacological and gene silencing approaches were used to study pathways involved downstream ecto-F₁-ATPase activation by apoA-I. Results: ApoA-I and HDL both induced Akt phosphorylation. F₁-ATPase inhibitors such as inhibitory factor 1 and oligomycin completely blocked apoA-I-induced Akt phosphorylaton and significantly blocked HDL-induced phosphorylation, indicating that this signaling pathway is dependent on ecto-F₁-ATPase activation by apoA-I. Further, we were able to specify roles for the P2Y₁-ADPreceptor and the PI3Kβ isoform in this pathway since pharmacological inhibition and silencing of these proteins dramatically inhibited apoA-I-induced Akt phosphorylation and cell proliferation. Conclusion: Altogether, these data highlight a key role of the P2Y₁/PI3Kβ axis in endothelial cell proliferation downstream of ecto-F₁-ATPase activation by apoA-I. Pharmacological targeting of this pathway could represent a promising approach to enhance vascular endothelial protection.

show abstract

“…It has been reported that ApoA-I attenuates the TNF-mediated inhibition of tube formation in lymphatic ECs [26]. Moreover, ApoA-I can enhance the proliferation of human endothelial progenitor cells and promotes angiogenesis through the cell surface ATP synthase [27]. In this study, we found, for the first time, that the protective function of ApoA-I in HCAECs is mediated, at least partially, by the antagonism of TGF-β1-induced EndMT, suggesting a novel cellular mechanism to be involved in the endothelial benefits of ApoA-I.…”

Section: Discussionmentioning

confidence: 99%

Apolipoprotein A1 Inhibits the TGF-β1-Induced Endothelial-to-Mesenchymal Transition of Human Coronary Artery Endothelial Cells

Feng

Zhang²,

Jackson³

et al. 2017

Cardiology

View full text Add to dashboard Cite

Objective: Transforming growth factor β1 (TGF-β1) is the major cytokine for stimulating endothelial cells (ECs) to transdifferentiate to mesenchymal cells (MCs) in the process known as endothelial-to-mesenchymal transition (EndMT). Recently, TGF-β1-induced EndMT has been implicated in the pathogenesis of atherosclerosis (AS). It has been identified that apolipoprotein A1 (ApoA-I) obstructs TGF-β1-induced endothelial dysfunction, providing a protective effect for ECs and also anti-AS activity. However, the exact role of ApoA-I in TGF-β1-induced EndMT is not clear. In this study, we aimed to investigate whether ApoA-I can modulate TGF-β1-induced EndMT in human coronary artery ECs (HCAECs). Methods and Results: The HCAECs were treated with TGF-β1 with or without ApoA-I. Morphological changes in HCAECs and the expression of EndMT-related markers were evaluated. HCAECs treated with TGF-β1 were found to transform to MC morphology, with inconspicuous expression of EC markers such as vascular endothelial cadherin and CD31, and conspicuous expression of fibroblast-specific protein 1 (FSP-1) and α-smooth muscle actin. The treatment of HCAECs with ApoA-I inhibited the TGF-β1-induced EndMT, and elevated expression of EC markers was observed but reduced expression of MC markers. Moreover, ApoA-I impeded the expression level of Slug and Snail, crucial transcriptional factors of EndMT, and it inhibited the TGF-β1-induced phosphorylation of Smad2 and Smad3 which affected the EC morphology. In addition, the knockdown of ABCA1 by RNA interference eliminated the inhibition effect of ApoA-I on TGF-β1-induced EndMT. Conclusions: Our findings revealed a novel mechanism for the ApoA-I protective effect on endothelium function via the inhibition of TGF-β1-induced EndMT. This might provide new insights for developing strategies for modulating AS and vascular remodeling.

show abstract

Apolipoprotein A-I enhances proliferation of human endothelial progenitor cells and promotes angiogenesis through the cell surface ATP synthase

Cited by 41 publications

References 36 publications

High-Density Lipoprotein: From Biological Functions to Clinical Perspectives

High-Density Lipoprotein: From Biological Functions to Clinical Perspectives

PI3Kβ Plays a Key Role in Apolipoprotein A-I-Induced Endothelial Cell Proliferation Through Activation of the Ecto-F1-ATPase/P2Y1 Receptors

Apolipoprotein A1 Inhibits the TGF-β1-Induced Endothelial-to-Mesenchymal Transition of Human Coronary Artery Endothelial Cells

Contact Info

Product

Resources

About