ArticleFrontiers in physiology2014
Lysophosphatidic acid induces integrin activation in vascular smooth muscle and alters arteriolar myogenic vasoconstriction.
Article in Frontiers in physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 20 citations in OpenAlex.
- LPA-Induced Thromboxane A2-Mediated Vasoconstriction Is Limited to Poly-Unsaturated Molecular Species in Mouse Aortas.International journal of molecular sciences · 2024Article
- Engineering Smooth Muscle to Understand Extracellular Matrix Remodeling and Vascular Disease.Bioengineering (Basel, Switzerland) · 2022Review
- Modification of Fibronectin by Non-Enzymatic Glycation Impairs KFrontiers in physiology · 2022Article
- PKCε stimulation of TRPV1 orchestrates carotid body responses to asthmakines.The Journal of physiology · 2021Article
- Calcium in Vascular Smooth Muscle Cell Elasticity and Adhesion: Novel Insights Into the Mechanism of Action.Frontiers in physiology · 2019Review
- Lysophosphatidic acid acts on LPABritish journal of pharmacology · 2018Article
- Mechanisms underlying modulation of podocyte TRPC6 channels by suPAR: Role of NADPH oxidases and Src family tyrosine kinases.Biochimica et biophysica acta. Molecular basis of disease · 2018Article
- Nonenzymatic glycation interferes with fibronectin-integrin interactions in vascular smooth muscle cells.Microcirculation (New York, N.Y. : 1994) · 2017Article
- The phospholipase A2 activity of peroxiredoxin 6 modulates NADPH oxidase 2 activation via lysophosphatidic acid receptor signaling in the pulmonary endothelium and alveolar macrophages.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
- The role of reactive oxygen species in microvascular remodeling.International journal of molecular sciences · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
In vascular smooth muscle cells (VSMC) increased integrin adhesion to extracellular matrix (ECM) proteins, as well as the production of reactive oxygen species (ROS) are strongly stimulated by lysophosphatidic acid (LPA). We hypothesized that LPA-induced generation of ROS increases integrin adhesion to the ECM. Using atomic force microscopy (AFM) we determined the effects of LPA on integrin adhesion to fibronectin (FN) in VSMC isolated from rat (Sprague-Dawley) skeletal muscle arterioles. In VSMC, exposure to LPA (2 μM) doubled integrin-FN adhesion compared to control cells (P < 0.05). LPA-induced integrin-FN adhesion was reduced by pre-incubation with antibodies against β1 and β3 integrins (50 μg/ml) by 66% (P < 0.05). Inhibition of LPA signaling via blockade of the LPA G-protein coupled receptors LPAR1 and LPAR3 with 10 μM Ki16425 reduced the LPA-enhanced adhesion of VSCM to FN by 40% (P < 0.05). Suppression of ROS with tempol (250 μM) or apocynin (300 μM) also reduced the LPA-induced FN adhesion by 47% (P < 0.05) and 59% (P < 0.05), respectively. Using confocal microscopy, we observed that blockade of LPA signaling, with Ki16425, reduced ROS by 45% (P < 0.05), to levels similar to control VSMC unexposed to LPA. In intact isolated arterioles, LPA (2 μM) exposure augmented the myogenic constriction response to step increases in intraluminal pressure (between 40 and 100 mm Hg) by 71% (P < 0.05). The blockade of LPA signaling, with Ki16425, decreased the LPA-enhanced myogenic constriction by 58% (P < 0.05). Similarly, blockade of LPA-induced ROS release with tempol or gp91 ds-tat decreased the LPA-enhanced myogenic constriction by 56% (P < 0.05) and 55% (P < 0.05), respectively. These results indicate that, in VSMC, LPA-induced integrin activation involves the G-protein coupled receptors LPAR1 and LPAR3, and the production of ROS, and that LPA may play an important role in the control of myogenic behavior in resistance vessels through ROS modulation of integrin activity.
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.