ArticleBioscience reports2012
Primary human endothelial cells secrete agents that reduce responsiveness to lysophosphatidic acid (LPA).
Article in Bioscience reports, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
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Who cites it
5 citing papers in PubMed.
- Development of an Atlantic salmon heart endothelial cell line (ASHe) that responds to lysophosphatidic acid (LPA).In vitro cellular & developmental biology. Animal · 2017Article
- Lysophosphatidic acid does not cause blood/lymphatic vessel plasticity in the rat mesentery culture model.Physiological reports · 2016Article
- Insulin-like growth factor 1 (IGF-1) stabilizes nascent blood vessels.The Journal of biological chemistry · 2015Article
- LSD1 controls metastasis of androgen-independent prostate cancer cells through PXN and LPAR6.Oncogenesis · 2014Article
- Regression activity that is naturally present in vitreous becomes ineffective as patients develop proliferative diabetic retinopathy.Diabetologia · 2013Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
The plasma level of LPA (lysophosphatidic acid) (200-600 nM) is well within the range that promotes proliferation and migration of vascular ECs (endothelial cells), yet vessels are quiescent and stable. In this report, we considered one explanation for this paradox: that ECs secrete agents that attenuate responsiveness to LPA. Indeed, we observed that CM (conditioned medium) from confluent, quiescent cultures of primary HUVECs (human umbilical vein ECs) contained an agent that inhibited LPA-mediated signalling events and cellular responses. The putative inhibitor, which we tentatively call ILMR (inhibitor of LPA-mediated responsiveness) seemed to act on cells (instead of at the level of LPA) by suppressing the ability of LPA receptor 1 to signal. The amount and/or activity of ILMR was regulated by growth factors; exposing HUVECs to VEGF-A (vascular endothelial growth factor A), but not bFGF (basic fibroblast growth factor), reduced the amount and/or activity of ILMR in CM. We conclude that in addition to promoting angiogenesis directly, VEGF-A can also act indirectly by modulating the bioactivity of angiomodulators such as LPA.
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Registered trials
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