Activation of the phosphatidylinositol 3-kinase/protein kinase Akt pathway mediates CD151-induced endothelial cell proliferation and cell migration

Zheng, Zhenzhong; Liu, Zhengxiang

doi:10.1016/j.biocel.2006.09.001

Cited by 44 publications

(44 citation statements)

References 31 publications

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“…This interesting technique could be used to differentiate between the endogenous gene and the transfected gene, which is also expressed in basal conditions. In the present study, we also observed that CD151 gene delivery promoted endothelial cell proliferation, migration and tube formation, which is consistent with our previous data [8,24] . However, the molecular mechanisms underlying these effects are not known.…”

Section: Discussionsupporting

confidence: 93%

Activation of the ERK signaling pathway is involved in CD151-induced angiogenic effects on the formation of CD151-integrin complexes

et al. 2010

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Aim: To assess the roles of extracellular signal-regulated kinase (ERK), p38, and CD151-integrin complexes on proliferation, migration, and tube formation activities of CD151-induced human umbilical vein endothelial cells (HUVECs). Methods: CD151, anti-CD151 and CD151-AAA mutant were inserted into recombinant adeno-associated virus (rAAV) vectors and used to transfect HUVECs. After transfection, the expression of CD151 was measured. Proliferation was assessed using the 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide (MTT) assay. Cell migration was evaluated in Boyden transwell chambers using FBS as the chemotactic stimulus. The tube formation assay was performed on matrigel. The potential involvement of various signaling pathways was explored using selective inhibitors. Results: CD151 gene delivery increased the expression of CD151 at both the mRNA and protein levels. Overexpression of CD151 promoted cell proliferation, migration and tube formation in vitro, and phosphorylation of ERK was also increased. Further, CD151-induced cell proliferation, migration, and tube formation were attenuated by the ERK inhibitor PD98059 (20 µmol/L) but not by a p38 inhibitor (SB203580, 20 µmol/L). Moreover, there was no significant difference in CD151 protein expression between the CD151 group and the CD151-AAA group, but the CD151-AAA mutant abrogated cellular proliferation, migration, and tube formation and decreased the phosphorylation of ERK. Conclusion: This study suggests that activation of the ERK signaling pathway may be involved in the angiogenic effects of CD151. Activation of ERK was dependent on the formation of CD151-integrin complexes. Therefore modulation of CD151 may be as a novel therapeutic strategy for regulating angiogenesis.

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Section: Discussionsupporting

confidence: 93%

Activation of the ERK signaling pathway is involved in CD151-induced angiogenic effects on the formation of CD151-integrin complexes

et al. 2010

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“…However, in spite of their use as bone substitute, our understanding of the effects of nano-HAP on ECs remains fragmentary. Recently, the production of nitric oxide (NO) through eNOS activation 16,17 has often been reported as a mechanism of the growth of ECs, 18 apoptosis, 19 migration 18,20 and angiogenesis, 21 suggesting a potential role of NO in changes of biological behavior in ECs. Previous studies have shown that NO activation was involved in porous β-CaSiO 3 /Poly-D,L-LactideGlycolide (PDLGA) composite scaffold-induced increased angiogenic activity of ECs.…”

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confidence: 99%

Interaction of hydroxyapatite nanoparticles with endothelial cells: internalization and inhibition of angiogenesis in vitro through the PI3K/Akt pathway

Shi¹,

Zhou²,

Huang³

et al. 2017

IJN

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Nano-hydroxyapatite (nano-HAP) has been proposed as a better candidate for bone tissue engineering; however, the interactions of nano-HAP with endothelial cells are currently unclear. In this study, HAP nanoparticles (HANPs; 20 nm np20 and 80 nm np80) and micro-sized HAP particles (m-HAP; 12 μm) were employed to explore and characterize cellular internalization, subcellular distribution, effects of HANPs on endothelial cell function and underlying mechanisms using human umbilical vein endothelial cells (HUVECs) as an in vitro model. It was found that HANPs were able to accumulate in the cytoplasm, and both adhesion and uptake of the HANPs followed a function of time; compared to np80, more np20 had been uptaken at the end of the observation period. HANPs were mainly uptaken via clathrin- and caveolin-mediated endocytosis, while macropinocytosis was the main pathway for m-HAP uptake. Unexpectedly, exposure to HANPs suppressed the angiogenic ability of HUVECs in terms of cell viability, cell cycle, apoptosis response, migration and capillary-like tube formation. Strikingly, HANPs reduced the synthesis of nitric oxide (NO) in HUVECs, which was associated with the inhibition of phosphatidylinositol 3-kinase (PI3K) and phosphorylation of eNOS. These findings provide additional insights into specific biological responses as HANPs interface with endothelial cells.

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“…A recent study demonstrates that the mouse lung ECs (MLECs) from CD151-null mice display marked reduction in the angiogenesis-related endothelial events including migration, spreading, invasion, Matrigel contraction, tube and cable formation, and spheroid sprouting [28] . Conversely, overexpression of CD151 in human umbilical vein ECs enhances cell proliferation, migration, and capillary tube formation on Matrigel [29] . We have reported that CD151 gene delivery increases the number of microvessels in a rat myocardial ischemia model and an ischemic rat hindlimb model [7,8] .…”

Section: Discussionmentioning

confidence: 96%

Adeno associated viral vector-delivered and hypoxia response element-regulated CD151 expression in ischemic rat heart

et al. 2011

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Aim: The aim of this study was to improve the delivery efficacy and target specificity of the pro-angiogenic gene CD151 to the ischemic heart. Methods: To achieve the inducible expression of adeno-associated viral (AAV)-delivered CD151 gene in only the ischemic myocardium, we generated an AAV construct in which CD151 expression can be controlled by the hypoxia response element (HRE) sequence from the human Enolase gene. The function of this vector was examined in rat H9C2 cardiac myoblasts and in ischemic rat myocardium. The expression of CD151 in the areas of ischemic myocardium was confirmed at the mRNA level by real-time PCR and on the protein level by Western blot, whereas the CD151 expression in the microvessels within the areas of ischemic myocardium was detected by immunohistochemistry. Results: HRE significantly enhances the expression of CD151 under hypoxic conditions or in the ischemic myocardium, and forced CD151 expression increases the number of microvessels in the ischemic myocardium. Conclusion: The AAV-mediated, HRE regulated delivery of the CD151 gene shows higher expression in the ischemic myocardium and more efficiently targets CD151 to the hypoxic regions after myocardial infarction.

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Activation of the phosphatidylinositol 3-kinase/protein kinase Akt pathway mediates CD151-induced endothelial cell proliferation and cell migration

Cited by 44 publications

References 31 publications

Activation of the ERK signaling pathway is involved in CD151-induced angiogenic effects on the formation of CD151-integrin complexes

Activation of the ERK signaling pathway is involved in CD151-induced angiogenic effects on the formation of CD151-integrin complexes

Interaction of hydroxyapatite nanoparticles with endothelial cells: internalization and inhibition of angiogenesis in vitro through the PI3K/Akt pathway

Adeno associated viral vector-delivered and hypoxia response element-regulated CD151 expression in ischemic rat heart

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