ArticleMicrocirculation (New York, N.Y. : 1994)2012
Homocysteine impairs endothelial wound healing by activating metabotropic glutamate receptor 5.
Article in Microcirculation (New York, N.Y. : 1994), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 7 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Homocysteine metabolism as the target for predictive medical approach, disease prevention, prognosis, and treatments tailored to the person.The EPMA journal · 2021Review
- Regulatory Roles of Metabotropic Glutamate Receptors on Synaptic Communication Mediated by Gap Junctions.Neuroscience · 2021Review
- Astaxanthin inhibits homocysteine‑induced endothelial cell dysfunction via the regulation of the reactive oxygen species‑dependent VEGF‑VEGFR2‑FAK signaling pathway.Molecular medicine reports · 2019Article
- The connexin 43/ZO-1 complex regulates cerebral endothelial F-actin architecture and migration.American journal of physiology. Cell physiology · 2015Article
- Homocysteine disrupts outgrowth of microvascular endothelium by an iNOS-dependent mechanism.Microcirculation (New York, N.Y. : 1994) · 2014Article
- Genetic variants of glutamate receptor gene family in Taiwanese Kawasaki disease children with coronary artery aneurysms.Cell & bioscience · 2014Article
- Phyllanthus emblica L. Enhances Human Umbilical Vein Endothelial Wound Healing and Sprouting.Evidence-based complementary and alternative medicine : eCAM · 2013Article
Corrections and comments
- Erratum issued
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
objectiveHcy is an independent risk factor for cerebrovascular disease and cognitive impairment. The purpose of this study was to elucidate the role of mGluR5 in Hcy-mediated impairment of cerebral endothelial wound repair.
methodsMouse CMVECs (bEnd.3) were used in conjunction with directed pharmacology and shRNA. AutoDock was used to simulate the docking of ligand-receptor interactions.
resultsHcy (20 μM) significantly increased Cx43-pS368 by mGluR5- and PKC-dependent mechanisms. Hcy attenuated wound repair by an mGluR5-dependent mechanism over the six-day study period but did not alter cell proliferation in a proliferation assay, suggesting that the attenuation of wound repair may be due to dysfunctional migration in HHcy. Hcy increased the expression of Cx43 and Cx43-pS368 at the wound edge by activating mGluR5. Direct activation of mGluR5, using the specific agonist CHPG, was sufficient to reproduce the results whereas KO of mGluR5 with shRNA, or inhibition with MPEP, blocked the response to Hcy.
conclusionsInhibition of mGluR5 activation could be a novel strategy for promoting endothelial wound repair in patients with HHcy. Activation of mGluR5 may be a viable strategy for disrupting angiogenesis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.