Impaired cross-activation of β3 integrin and VEGFR-2 on endothelial progenitor cells with aging decreases angiogenesis in response to hypoxia

Di, Qun; Cheng, Zeen; Kim, Weon; Liu, Zexuan; Song, Hui; Li, Xiang; Nan, Yongshan; Wang, Chengya; Cheng, Xianwu

doi:10.1016/j.ijcard.2013.01.240

Cited by 31 publications

(33 citation statements)

References 29 publications

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“…It should be noted that Lee et al 34 show that in the absence of any pathological insult, autocrine VEGF is required for the vascular homoeostasis. Here, Di et al 23 reported that VEGFR2 silencing impaired old HUVEC tubulogenesis under hypoxia. Further study will be needed to investigate the role of the autocrine signalling in the angiogenic cascade under pathological ischaemic stress.…”

Section: Article Nature Communications | Doi: 101038/ncomms4838mentioning

confidence: 77%

“…10). We previously reported that silencing of Akt, VEGF or Notch1 by each related siRNA blunted the tubulogenic actions of cultured HUVECs and aorta rings 17,18,23 . Thus, CatK-mediated Notch1 processing appears to represent a mechanism in EC angiogenic actions in response to hypoxic stress.…”

Section: Expression Of Catk In Ecsmentioning

confidence: 99%

“…In 2007, lee and colleagues demonstrated that genetic deletion of VEGF specifically in the endothelial lineage leads progressive endothelial degeneration and sudden death in 55% of mutant mice by 25 weeks mice of age 34 . Recently, we have reported that silencing of VEGF or VEGFR2 enhanced EC apoptosis and proliferation 23 . These results suggest a cellautonomous VEGF signalling pathway that holds significance for vascular homoeostasis but is dispensable for the angiogenic action.…”

Section: Article Nature Communications | Doi: 101038/ncomms4838mentioning

confidence: 99%

“…Endothelial cell proliferation was assessed with the Cell Titer 96AQ Assay kit (Promega, Madison, WI, USA) 23 . Cells were plated on collagen-coated 96-well plates at 5,000 cells in 100 ml of 0.3% bovine serum albumin/DMEM per well and incubated with EBM-2 in the presence of VEGF (50 ng ml À 1 ) for 24 h. Then, 20 ml of a mixture of tetrazolium compound and phenazine methosulfate was added, and the absorbance was determined at 492 nm.…”

Section: Article Nature Communications | Doi: 101038/ncomms4838mentioning

confidence: 99%

“…Then, the cells were fixed for 10 min with 8% paraformaldehyde and washed with 1% glycerol. Following blocking with 0.1% bovine serum albumin/phosphate-buffered saline, the cells were studied by immunofluorescence as described previously 23 . Coverslips were treated with Prolong mounting medium (Molecular Probes) and visualized by confocal microscopy.…”

Section: Article Nature Communications | Doi: 101038/ncomms4838mentioning

confidence: 99%

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Cathepsin K-mediated notch1 activation contributes to neovascularization in response to hypoxia

et al. 2014

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Section: Article Nature Communications | Doi: 101038/ncomms4838mentioning

confidence: 77%

Section: Expression Of Catk In Ecsmentioning

confidence: 99%

Section: Article Nature Communications | Doi: 101038/ncomms4838mentioning

confidence: 99%

Section: Article Nature Communications | Doi: 101038/ncomms4838mentioning

confidence: 99%

Section: Article Nature Communications | Doi: 101038/ncomms4838mentioning

confidence: 99%

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Cathepsin K-mediated notch1 activation contributes to neovascularization in response to hypoxia

et al. 2014

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Exercise restores muscle stem cell mobilization, regenerative capacity and muscle metabolic alterations via adiponectin/AdipoR1 activation in SAMP10 mice

Inoue

Cheng

Huang

et al. 2016

J cachexia sarcopenia muscle

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BackgroundExercise train (ET) stimulates muscle response in pathological conditions, including aging. The molecular mechanisms by which exercise improves impaired adiponectin/adiponectin receptor 1 (AdipoR1)‐related muscle actions associated with aging are poorly understood. Here we observed that in a senescence‐accelerated mouse prone 10 (SAMP10) model, long‐term ET modulated muscle‐regenerative actions.Methods25‐week‐old male SAMP10 mice were randomly assigned to the control and the ET (45 min/time, 3/week) groups for 4 months. Mice that were maintained in a sedentary condition served controls.ResultsET ameliorated aging‐related muscle changes in microstructure, mitochondria, and performance. The amounts of proteins or mRNAs for p‐AMPKα, p‐Akt, p‐ERK1/2, p‐mTOR, Bcl‐XL, p‐FoxO3, peroxisome proliferators‐activated receptor‐γ coactivator, adiponectin receptor1 (adpoR1), and cytochrome c oxidase‐IV, and the numbers of CD34+/integrin‐α7 + muscle stem cells (MuSCs) and proliferating cells in the muscles and bone‐marrow were enhanced by ET, whereas the levels of p‐GSK‐3α and gp91phox proteins and apoptotic cells were reduced by ET. The ET also resulted in increased levels of plasma adiponectin and the numbers of bone‐marrow (BM)‐derived circulating CD34+/integrin‐α7 + MuSCs and their functions. Integrin‐α7 + MuSCs of exercised mice had improved changes of those beneficial molecules. These ET‐mediated aged muscle benefits were diminished by adiponectin and AdipoR1 blocking as well as AMPK inhibition. Finally, recombinant mouse adiponectin enhanced AMPK and mTOR phosphorylations in BM‐derived integrin‐α7 + cells.ConclusionsThese findings suggest that ET can improve aging‐related impairments of BM‐derived MuSC regenerative capacity and muscle metabolic alterations via an AMPK‐dependent mechanism that is mediated by an adiponectin/AdipoR1 axis in SAMP10 mice.

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Impact of VEGFA −583C > T polymorphism on serum VEGF levels and the susceptibility to acute chest syndrome in pediatric patients with sickle cell disease

Redha

Mahdi

Al-Habboubi

et al. 2014

Pediatric Blood & Cancer

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We investigated the association of VEGFA -583C > T on VEGF serum levels and acute chest syndrome (ACS) in 351 pediatric patients with sickle cell disease (SCD), of whom 90 had ACS, and 261 were ACS-free controls. Significant differences in -583C > T minor allele and genotype frequencies were seen between ACS cases and controls, evidenced by enrichment of -583T/T genotypes in patients with ACS, which were linked with reduction in VEGF serum levels. VEGFA -583C > T and reduced VEGF serum levels may influence ACS risk in patients with SCD, which will aid in identifying patients with SCD who are at high risk of ACS.

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Impaired cross-activation of β3 integrin and VEGFR-2 on endothelial progenitor cells with aging decreases angiogenesis in response to hypoxia

Cited by 31 publications

References 29 publications

Cathepsin K-mediated notch1 activation contributes to neovascularization in response to hypoxia

Cathepsin K-mediated notch1 activation contributes to neovascularization in response to hypoxia

Exercise restores muscle stem cell mobilization, regenerative capacity and muscle metabolic alterations via adiponectin/AdipoR1 activation in SAMP10 mice

Impact of VEGFA −583C > T polymorphism on serum VEGF levels and the susceptibility to acute chest syndrome in pediatric patients with sickle cell disease

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