ArticleJournal of cellular and molecular medicine2018
Wild-type p53 enhances endothelial barrier function by mediating RAC1 signalling and RhoA inhibition.
Article in Journal of cellular and molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 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
50 citing papers in PubMed, 62 citations in OpenAlex.
- Recent advancements in tissue dissociation techniques for cell manufacturing single-cell analysis and downstream processing.Stem cells translational medicine · 2025Review
- Effects of GHRH and its analogues on the Vascular System.Reviews in endocrine & metabolic disorders · 2025Review
- NEK kinases in cell cycle regulation, DNA damage response, and cancer progression.Tissue & cell · 2025Review
- Growth hormone - releasing hormone in the immune system.Reviews in endocrine & metabolic disorders · 2025Review
- Selective expression and significance of ACKR2 in lung aerocytes.Journal for immunotherapy of cancer · 2025Article
- NEK2 inhibition alleviates lipopolysaccharide-induced endothelial injury.ASPET discovery · 2025Article
- Protective effects of growth hormone - releasing hormone antagonists in the lungs of septic mice.Cellular signalling · 2024Article
- Unfolded protein response suppression potentiates LPS-induced barrier dysfunction and inflammation in bovine pulmonary artery endothelial cells.Tissue barriers · 2024Article
- Involvement of NEK2 and NEK9 in LPS - induced endothelial barrier dysfunction.Microvascular research · 2024Article
- Lysyl oxidase-like 1-antisense 1 (LOXL1-AS1) lncRNA differentially regulates gene and protein expression, signaling and morphology of human ocular cells.Human molecular genetics · 2023Article
- The vascular perspective on acute and chronic lung disease.The Journal of clinical investigation · 2023Review
- Growth hormone-releasing hormone antagonists protect against hydrochloric acid-induced endothelial injury in vitro.Environmental toxicology and pharmacology · 2023Article
- Protective effects of GHRH antagonists against hydrogen peroxide-induced lung endothelial barrier disruption.Endocrine · 2023Article
- Heat shock protein 90 inhibition in the endothelium.Frontiers in medicine · 2023Article
- Syphilis and the host: multi-omic analysis of host cellular responses toFrontiers in microbiology · 2023Article
- Growth Hormone-Releasing Hormone in Endothelial Inflammation.Endocrinology · 2022Review
- Growth Hormone-Releasing Hormone Antagonist JV-1-36 Suppresses Reactive Oxygen Species Generation in A549 Lung Cancer Cells.Endocrines · 2022Article
- P53 in endothelial function and unfolded protein response regulation.Cell biology international · 2022Article
- Activating transcription factor 6 protects against endothelial barrier dysfunction.Cellular signalling · 2022Article
- Unfolded protein response in endothelial injury.Cell cycle (Georgetown, Tex.) · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Inflammation is the major cause of endothelial barrier hyper-permeability, associated with acute lung injury and acute respiratory distress syndrome. This study reports that p53 "orchestrates" the defence of vascular endothelium against LPS, by mediating the opposing actions of Rac1 and RhoA in pulmonary tissues. Human lung microvascular endothelial cells treated with HSP90 inhibitors activated both Rac1- and P21-activated kinase, which is an essential element of vascular barrier function. 17AAG increased the phosphorylation of both LIMK and cofilin, in contrast to LPS which counteracted those effects. Mouse lung microvascular endothelial cells exposed to LPS exhibited decreased expression of phospho-cofilin. 17AAG treatment resulted in reduced levels of active cofilin. Silencing of cofilin pyridoxal phosphate phosphatase (PDXP) blocked the LPS-induced hyper-permeability, and P53 inhibition reversed the 17AAG-induced PDXP down-regulation. P190RHOGAP suppression enhanced the LPS-triggered barrier dysfunction in endothelial monolayers. 17AAG treatment resulted in P190RHOGAP induction and blocked the LPS-induced pMLC2 up-regulation in wild-type mice. Pulmonary endothelial cells from "super p53" mice, which carry additional p53-tg alleles, exhibited a lower response to LPS than the controls. Collectively, our findings help elucidate the mechanisms by which p53 operates to enhance barrier function.
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.