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Modulation of endothelial cell migration by ER stress and insulin resistance: a role during maternal obesity?

Overview of attention for article published in Frontiers in Pharmacology, August 2014
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Title
Modulation of endothelial cell migration by ER stress and insulin resistance: a role during maternal obesity?
Published in
Frontiers in Pharmacology, August 2014
DOI 10.3389/fphar.2014.00189
Pubmed ID
Authors

Pablo J. Sáez, Roberto Villalobos-Labra, Francisco Westermeier, Luis Sobrevia, Marcelo Farías-Jofré

Abstract

Adverse microenvironmental stimuli can trigger the endoplasmic reticulum (ER) stress pathway, which initiates the unfolded protein response (UPR), to restore protein-folding homeostasis. Several studies show induction of ER stress during obesity. Chronic UPR has been linked to different mechanisms of disease in obese and diabetic individuals, including insulin resistance (IR) and impaired angiogenesis. Endothelial cell (EC) migration is an initial step for angiogenesis, which is associated with remodeling of existing blood vessels. EC migration occurs according to the leader-follower model, involving coordinated processes of chemotaxis, haptotaxis, and mechanotaxis. Thus, a fine-tuning of EC migration is necessary to provide the right timing to form the required vessels during angiogenesis. ER stress modulates EC migration at different levels, usually impairing migration and angiogenesis, although different effects may be observed depending on the tissue and/or microenvironment. In the context of pregnancy, maternal obesity (MO) induces IR in the offspring. Interestingly, several proteins associated with obesity-induced IR are also involved in EC migration, providing a potential link with the ER stress-dependent alterations observed in obese individuals. Different signaling cascades that converge on cytoskeleton regulation directly impact EC migration, including the Akt and/or RhoA pathways. In addition, ER is the main intracellular reservoir for Ca(2+), which plays a pivotal role during EC migration. Therefore, ER stress-related alterations in Ca(2+) signaling or Ca(2+) levels might also produce distorted EC migration. However, the above findings have been studied in the context of adult obesity, and no information has been reported regarding the effect of MO on fetal EC migration. Here we summarize the state of knowledge about the possible mechanisms by which ER stress and IR might impact EC migration and angiogenesis in fetal endothelium exposed to MO during pregnancy.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 62 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
United Kingdom 1 2%
Chile 1 2%
Unknown 60 97%

Demographic breakdown

Readers by professional status Count As %
Student > Master 18 29%
Student > Ph. D. Student 10 16%
Researcher 7 11%
Student > Bachelor 4 6%
Professor 3 5%
Other 8 13%
Unknown 12 19%
Readers by discipline Count As %
Medicine and Dentistry 13 21%
Agricultural and Biological Sciences 11 18%
Biochemistry, Genetics and Molecular Biology 9 15%
Pharmacology, Toxicology and Pharmaceutical Science 6 10%
Chemistry 3 5%
Other 6 10%
Unknown 14 23%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 19 August 2014.
All research outputs
#20,234,388
of 22,760,687 outputs
Outputs from Frontiers in Pharmacology
#9,985
of 16,010 outputs
Outputs of similar age
#197,546
of 235,512 outputs
Outputs of similar age from Frontiers in Pharmacology
#45
of 62 outputs
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