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Find video protocols related to scientific articles indexed in Pubmed.
Oxidized high-density lipoprotein impairs endothelial progenitor cells function by activation of CD36-MAPK-TSP-1 pathways.
Antioxid. Redox Signal.
PUBLISHED: 10-15-2014
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Aims: High density lipoprotein (HDL) levels inversely correlate with cardiovascular events due to the protective effects on vascular wall and stem cells, which is susceptible to oxidative modifications and then leads to potential pro-atherosclerotic effects. We proposed that oxidized high density lipoprotein (ox-HDL) might lead to endothelial progenitor cells (EPCs) dysfunction and investigated underlying mechanisms. Results: ox-HDL was shown to increase apoptosis and intracellular ROS levels, but reduce migration, angiogenesis and cholesterol efflux of EPCs in a dose dependent manner. p38 mitogen-activated protein kinase (MAPK) and NF-?B were activated after ox-HDL stimulation, which also upregulated thrombospondin-1 expression without affecting vascular endothelial growth factor. Effects caused by ox-HDL could be significantly attenuated by pretreatment with shRNA-mediated CD36 knockdown or probucol. Data of in vivo experiments and the inversely correlation of ox-HDL and circulating EPC numbers among patients with coronary artery diseases or CAD and type 2 diabetes also supported it. Meanwhile HDL separated from such patients could significantly increase cultured EPC's caspase 3 activity, furthermore supporting our proposal. Innovation: This is the most complete study to date of how ox-HDL would impair EPCs function, which was involved with activation of CD36-p38 MAPK-TSP-1 pathways and proved by not only the inverse relationship between ox-HDL and circulating EPCs in clinic, but also pro-apoptotic effects of HDL separated from patients' serum. Conclusion: Activation of CD36-p38 MAPK-TSP-1 pathways contributes to the pathological effects of ox-HDL on EPCs' dysfunction, which might be one of potential etiological factors responsible for the disturbed neovascularization in chronic ischemic disease.
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Norepinephrine stimulates mobilization of endothelial progenitor cells after limb ischemia.
PLoS ONE
PUBLISHED: 01-01-2014
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During several pathological processes such as cancer progression, thermal injury, wound healing and hindlimb ischemia, the mobilization of endothelial progenitor cells (EPCs) mobilization was enhanced with an increase of sympathetic nerve activity and norepinephrine (NE) secretion, yet the cellular and molecular mechanisms involved in the effects of NE on EPCs has less been investigated.
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Endothelial progenitor cells may participate in stress-induced tumour angiogenesis.
Med. Hypotheses
PUBLISHED: 03-07-2013
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Epidemiological and animal studies have suggested that chronic stress promotes tumourigenesis by promoting tumour angiogenesis. However, underlying mechanisms have not been fully elucidated. Endothelial progenitor cells (EPCs) are a group of bone marrow-derived cells that have an important function in neovascularisation of various tumour growths. In this study, chronic stress was hypothesised to increase tumour angiogenesis via sympathetic neurotransmitter-induced activation of EPCs through ?1 adrenoreceptor (AR)-extracellular regulated protein kinases and ?2 AR-endothelial nitric oxide synthase signal pathways. This hypothesis should be tested in several clinical and animal studies. Results may have implications on the development of new anti-tumour drugs.
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Rosiglitazone via upregulation of Akt/eNOS pathways attenuates dysfunction of endothelial progenitor cells, induced by advanced glycation end products.
Br. J. Pharmacol.
PUBLISHED: 11-16-2009
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Advanced glycation end products (AGEs) and endothelial progenitor cells (EPCs) play key roles in pathogenesis of diabetes-related vascular complications. AGEs can induce dysfunction in EPCs. The peroxisome proliferator-activated receptor-gamma (PPARgamma) agonists are widely used in the treatment of type 2 diabetes, and it remains unknown if they could attenuate EPC dysfunction induced by AGEs.
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Palmitic acid promotes endothelial progenitor cells apoptosis via p38 and JNK mitogen-activated protein kinase pathways.
Atherosclerosis
PUBLISHED: 03-26-2009
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Recent studies have demonstrated that palmitic acid (PA) could regulate endothelial progenitor cells (EPCs) function (migration, proliferation, survival and angiogenesis) via various signal pathways, but the effect of PA on EPCs apoptosis and associated mechanisms are still elusive.
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What is Visualize?

JoVE Visualize is a tool created to match the last 5 years of PubMed publications to methods in JoVE's video library.

How does it work?

We use abstracts found on PubMed and match them to JoVE videos to create a list of 10 to 30 related methods videos.

Video X seems to be unrelated to Abstract Y...

In developing our video relationships, we compare around 5 million PubMed articles to our library of over 4,500 methods videos. In some cases the language used in the PubMed abstracts makes matching that content to a JoVE video difficult. In other cases, there happens not to be any content in our video library that is relevant to the topic of a given abstract. In these cases, our algorithms are trying their best to display videos with relevant content, which can sometimes result in matched videos with only a slight relation.