Ask about this productRelated genes to: PLVAP antibody
- Gene:
- PLVAP NIH gene
- Name:
- plasmalemma vesicle associated protein
- Previous symbol:
- -
- Synonyms:
- gp68, PV-1, PV1, FELS
- Chromosome:
- 19p13.11
- Locus Type:
- gene with protein product
- Date approved:
- 2001-04-27
- Date modifiied:
- 2015-07-22
Related products to: PLVAP antibody
Related articles to: PLVAP antibody
- Chronic active antibody-mediated rejection (caABMR) is a major cause of late kidney allograft failure, yet reliable histological indicators of microvascular injury and therapeutic response remain insufficient. Complement C4d deposition reflects complement activation but does not fully capture endothelial remodelling, particularly in ABO-incompatible transplantation. Plasmalemma vesicle-associated protein-1 (PV-1), encoded by PLVAP and normally absent from glomerular endothelium, is upregulated during endothelial remodelling. We investigated whether glomerular PV-1 complements C4d in identifying active endothelial injury in caABMR. - Source: PubMed
Publication date: 2026/04/21
Igarashi YutoShimokawa MayuKawanishi KunioHirai ToshihitoSeino HiroshiShimizu TomokazuIshida HidekiTakagi Toshio - Vasogenic edema, due to inner blood-retinal barrier (BRB) disruption, is a major cause of vision loss across various ocular diseases. Similarly, blood-brain barrier (BBB) breakdown is a hallmark of many neurological disorders. However, the precise molecular and cellular mechanisms underlying barrier dysfunction under pathological conditions remain poorly understood. In this study, we aimed to develop a pathological model to investigate the integrity of the inner BRB and BBB using in vivo live imaging in zebrafish larvae, employing hyperglycemia-induced leakage as a proof of concept. Our results show that external glucose exposure elevates internal glucose levels, inducing hyperglycemia. Hyperglycemia increased midbrain blood vessel diameter and tracer leakage, indicative of barrier dysfunction, without affecting overall larval survival. Using fluorescent reporters, we found that hyperglycemia concurrently reduced claudin-5 and increased PLVAP, suggesting compromised tight junction integrity and impeded BBB maturation. Preliminary studies using transmission electron microscopy further revealed ultrastructural defects of junctions. However, further optimization is needed to reliably assess differences in caveolae between the experimental groups. This proof of concept study establishes an in vivo protocol for visualizing and quantifying barrier permeability, protein expression, and ultrastructure. It provides a valuable foundation for a zebrafish model to dissect the molecular mechanisms of blood-barrier breakdown, with direct implications for investigations of diabetic macular edema and other neurovascular diseases. - Source: PubMed
Publication date: 2026/03/19
Bakker-van Bugnum NoëlleSnijders Emma EHogendorp Eloise F E Evan Noorden Cornelis J FLou LiangVanhollebeke MarieVanhollebeke BenoitGrootemaat Anita Evan der Wel Nicole NSchlingemann Reinier OKlaassen Ingeborg - Diabetic retinopathy (DR), a severe microvascular complication of diabetes mellitus (DM), is recognized worldwide as the leading cause of visual impairment and blindness. FGL2 has been linked to microvascular endothelial cell injury and oxidative stress. This research aims to evaluate the role of FGL2 in influencing retinal microvascular endothelial cell injury and oxidative stress. - Source: PubMed
Publication date: 2026/03/06
Yang HongbinCheng CongcongHui PengbinLiu ShashaTian GegeZhang Xiaoyu - Fenestrated capillaries in the anterior lobe (AL) of the pituitary gland are specialized for efficient hormone exchange and are surrounded by extracellular matrix-rich basement membranes (BMs). Although several collagens have been implicated in the structural regulation of capillaries in the pituitary, the contribution of collagen XV remains unknown. In the present study, we investigated the expression, localization, and regulation of COL15A1, the α1 chain of collagen XV, in the rat pituitary. Real-time quantitative PCR (RT-qPCR) revealed that Col15a1 is highly expressed in the endothelial cell fraction isolated from rat AL. In situ hybridization showed that Col15a1 is expressed in plasmalemma vesicle-associated protein (PLVAP)-positive fenestrated endothelial cells in the AL. Immunohistochemistry demonstrated that COL15A1 is localized to BMs surrounding PLVAP-positive fenestrated capillaries in the AL, the median eminence, and the choroid plexus, but not in those surrounding continuous capillaries in the cerebrum. Because transforming growth factor-β (TGFβ) is a key regulator of collagen expression, we examined its role in Col15a1 regulation. RT-qPCR and in situ hybridization revealed that Tgfbr2 is expressed in fenestrated endothelial cells in the AL. Immunocytochemistry demonstrated that TGFβ1 stimulation induces nuclear translocation of SMAD2 in cultured endothelial cells isolated from the rat AL. RT-qPCR also showed that TGFβ1 significantly increases Col15a1 expression, which is suppressed by the TGFβ receptor I inhibitor SB431542. Together, these results demonstrate that TGFβ signaling regulates Col15a1 expression in fenestrated endothelial cells and suggest that collagen XV contributes to the structural and functional specialization of fenestrated capillaries in the pituitary. - Source: PubMed
Publication date: 2026/02/25
Nakakura TakashiTsukada TakehiroSuzuki Takeshi - The Stromal Vascular Fraction (SVF) derived from human subcutaneous fat has attracted pivotal interest in clinical applications for its regenerative and anti-inflammatory properties. A deeper characterisation of the endothelial cells within the SVF, across both traditional and tissue-engineered culture systems, is essential for advancing our understanding of endothelial cell biology and enhancing regenerative medicine therapies, including skin substitutes. - Source: PubMed
Publication date: 2026/02/11
Schwager TobiasSenn Nathalie ABöni RolandMoehrlen UeliKlar Agnes SBiedermann Thomas