ArticleJournal of cellular and molecular medicine2019
Phorbol esters induce PLVAP expression via VEGF and additional secreted molecules in MEK1-dependent and p38, JNK and PI3K/Akt-independent manner.
Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 17 citations in OpenAlex.
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- The senescent secretome drives PLVAP expression in cultured human hepatic endothelial cells to promote monocyte transmigration.iScience · 2023Article
- The role of PLVAP in endothelial cells.Cell and tissue research · 2023Review
- Brain endothelial cells acquire blood-brain barrier properties in the absence of Vegf-dependent CNS angiogenesis.Developmental biology · 2023Article
- Unveiling the gut-brain axis: structural and functional analogies between the gut and the choroid plexus vascular and immune barriers.Seminars in immunopathology · 2022Review
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- Immortalized human choroid plexus endothelial cells enable an advanced endothelial-epithelial two-cell typeiScience · 2022Article
- Bioinformatics analysis reveals biomarkers with cancer stem cell characteristics in kidney renal clear cell carcinoma.Translational andrology and urology · 2021Article
- Single-Cell RNA Sequencing Reveals Multiple Pathways and the Tumor Microenvironment Could Lead to Chemotherapy Resistance in Cervical Cancer.Frontiers in oncology · 2021Article
- The fenestrae-associated protein Plvap regulates the rate of blood-borne protein passage into the hypophysis.Development (Cambridge, England) · 2019Article
- Phorbol esters induce PLVAP expression via VEGF and additional secreted molecules in MEK1-dependent and p38, JNK and PI3K/Akt-independent manner.Journal of cellular and molecular medicine · 2019Article
- The Cytoplasmic Expression Of CLDN12 Predicts An Unfavorable Prognosis And Promotes Proliferation And Migration Of Osteosarcoma.Cancer management and research · 2019Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Endothelial diaphragms are subcellular structures critical for mammalian survival with poorly understood biogenesis. Plasmalemma vesicle associated protein (PLVAP) is the only known diaphragm component and is necessary for diaphragm formation. Very little is known about PLVAP regulation. Phorbol esters (PMA) are known to induce de novo PLVAP expression and diaphragm formation. We show that this induction relies on the de novo production of soluble factors that will act in an autocrine manner to induce PLVAP transcription and protein expression. We identified vascular endothelial growth factor-A (VEGF-A) signalling through VEGFR2 as a necessary but not sufficient downstream event as VEGF-A inhibition with antibodies and siRNA or pharmacological inhibition of VEGFR2 only partially inhibit PLVAP upregulation. In terms of downstream pathways, inhibition of MEK1/Erk1/2 MAP kinase blocked PLVAP upregulation, whereas inhibition of p38 and JNK MAP kinases or PI3K and Akt had no effect on PMA-induced PLVAP expression. In conclusion, we show that VEGF-A along with other secreted proteins act synergistically to up-regulate PLVAP in MEK1/Erk1/2 dependent manner, bringing us one step further into understanding the genesis of the essential structures that are endothelial diaphragms.
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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.