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Last update 23 Jan 2025

PLVAP

Last update 23 Jan 2025

Basic Info

Synonyms

FELS, Fenestrated endothelial-linked structure protein, gp68

+ [6]

Introduction

Endothelial cell-specific membrane protein involved in the formation of the diaphragms that bridge endothelial fenestrae. It is also required for the formation of stomata of caveolae and transendothelial channels. Functions in microvascular permeability, endothelial fenestrae contributing to the passage of water and solutes and regulating transcellular versus paracellular flow in different organs. Plays a specific role in embryonic development.

Drugs associated with PLVAP

CSR02-Fab-TF

Target

PLVAP

Mechanism

PLVAP inhibitors

Active Org.

Koo Foundation Sun Yat-Sen Cancer Center

Originator Org.

Koo Foundation Sun Yat-Sen Cancer Center

Active Indication

Hepatocellular Carcinoma

Inactive Indication-

Drug Highest PhaseEarly Phase 1

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

CN118359711

Patent Mining

Target

PLVAP

Mechanism-

Active Org.

Chong Qing Hua Zhi Sheng Wu Zhi Yao You Xian Gong Si

Originator Org.

Chong Qing Hua Zhi Sheng Wu Zhi Yao You Xian Gong Si [+1]

Active Indication

Virus Diseases

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with PLVAP

NCT04601428

/ RecruitingEarly Phase 1IIT

CSR02-Fab-TF as Hepatic Intra-arterial Therapy in Intermediate Stage B or Limited Advanced Stage C Hepatocellular Carcinoma (HCC): Dose-Escalation Study to Assess Safety and Tolerability

Intra-arterial (IA) therapy is generally used to treat HCC tumors that are too extensive to excise or treat with potentially curative local therapy. IA therapy takes advantage of the fact that the blood supply of HCC comes predominantly from the hepatic artery compared with the surrounding normal liver which is predominantly supplied by portal venous blood. The intent is to deprive the HCC of its blood supply, leading to the death of the tumor. Traditionally, various methods have been used to block the HCC blood supply, but improvements are needed. This study will investigate a new agent designed in the laboratory to block only tumor blood vessels, not blood vessels in the normal liver.

Start Date26 Jan 2021

Sponsor / Collaborator

Koo Foundation Sun Yat-Sen Cancer Center

100 Clinical Results associated with PLVAP

100 Translational Medicine associated with PLVAP

0 Patents (Medical) associated with PLVAP

340

Literatures (Medical) associated with PLVAP

01 Feb 2025·American Journal of Physiology-Renal Physiology

Induction of plasmalemmal vesicle-associated protein exacerbates glomerular endothelial injury in thrombotic microangiopathy

Article

Author: Mallipattu, Sandeep K. ; Estrada, Chelsea C. ; Gujarati, Nehaben ; Daehn, Ilse S. ; Guo, Yiqing ; Revelo, Monica P. ; Wilson, Craig ; Bronstein, Robert ; Ahmed, Sumaya

This study investigated the mechanism(s) underlying glomerular endothelial cell (GEnC) injury in thrombotic microangiopathy (TMA). We identified plasmalemmal vesicle-associated protein (PLVAP) as specifically upregulated in injured GEnCs in TMA, which was accompanied by pathways involved in angiogenesis and loss of differentiation. Induction of Plvap increased proliferation and migration of GEnCs. Human kidney biopsies with TMA demonstrated an increase in glomerular PLVAP, which correlated with histological markers of GEnC injury, confirming its pathologic role in TMA.

01 Jan 2025·Phytomedicine

Dachengqi decoction ameliorated liver injury in liver fibrosis mice by maintaining gut vascular barrier integrity

Article

Author: Yuju, Cai ; Fangyuan, Zhou ; Qifeng, Lin ; Mengqi, Zhang ; Junli, Zhang ; Luorui, Shang ; Yao, Wang ; Shuhan, Wang ; Jinxiao, Li ; Liuying, Chen ; Shenglan, Yang

BACKGROUNDSevere liver fibrosis may be accompanied by intestinal barrier damage, such as bacterial peritonitis, suggesting that the role of the gut-liver axis is nonnegligible. Dachengqi decoction (DCQD) was reported to improve bowel movements, but whether DCQD was effective for intestinal damage caused by liver fibrosis remained unclear.PURPOSETo investigate the role of DCQD in liver fibrosis-related gut vascular barrier (GVB) damage in mice.STUDY DESIGNDCQD was verified to reduce the imbalance of the intestinal vascular barrier and restore intestinal homeostasis to prove that DCQD acts through the gut-liver axis.METHODSThree graded doses of DCQD were gavaged into the CCL₄-induced mice for 12 weeks to evaluate the resistance to liver and intestinal damage. Immunoblotting and primary flow cytometry were used to assess organ damage; PV-1 to indicate gut vascular barrier damage; serum endotoxin, fecal SCFAs, and liver microbiota translocation to examine the gut-liver axis's crosstalk. Network pharmacology and RNA sequencing were used to analyze and verify the signaling pathway of DCQD.RESULTSDCQD significantly ameliorated fibrosis and inflammatory response in the CCL₄-induced mice, alleviated gut leakage, downregulated PV-1, relieved liver enterobacterial translocation, restored intestinal homeostasis, and reduced infiltration of myeloid cells in the lamina propria. Network pharmacology and RNA sequencing results indicated that DCQD exerted anti-fibrotic and anti-inflammatory effects in the liver through inhibition of the ESR1/NF-κB/TNFα pathway and maintained GVB homeostasis through the FUT2/Wnt/β-Catenin pathway.CONCLUSIONSDCQD broke the closed-loop damage of the gut-liver axis to improve GVB injury in mice with liver fibrosis.

31 Dec 2024·Pharmaceutical Biology

Berberine decreases S100B generation to regulate gut vascular barrier permeability in mice with burn injury

Article

Author: Feng, Aiwen ; Li, Cheng ; Kang, Yutian ; Zhou, Jun ; Qiu, Jiasheng ; Su, Shaosheng

Context: Berberine (BBR) can regulate enteric glial cells (EGCs) and the gut vascular barrier (GVB).Objective: To explore whether BBR regulates GVB permeability via the S100B pathway.Materials and methods: GVB hyperpermeability in C57BL/6J mice was induced by burns or S100B enema. BBR (25 or 50 mg/kg/d, 3 d) was gavaged preburn. S100B monoclonal antibody (S100BmAb) was i.v. injected postburn. Mouse intestinal microvascular endothelial cells (MIMECs) were treated with S100B, S100B plus BBR, or Z-IETD-FMK. GVB permeability was assayed by FITC-dextran, S100B by ELISA, caspase-8, β-catenin, occludin and PV-1 by immunoblot.Results: Burns elevated S100B in serum and in colonic mucosa to a peak (147.00 ± 4.95 ng/mL and 160.30 ± 8.50 ng/mg, respectively) at 36 h postburn, but BBR decreased burns-induced S100B in serum (126.20 ± 6.30 or 90.60 ± 3.78 ng/mL) and in mucosa (125.80 ± 12.40 or 91.20 ± 8.54 ng/mg). Burns raised GVB permeability (serum FITC-dextran 111.40 ± 8.56 pg/mL) at 48 h postburn, but BBR reduced GVB permeability (serum FITC-dextran 89.20 ± 6.98 or 68.60 ± 5.50 ng/mL). S100B enema (1 μM) aggravated burns-raised GVB permeability (142.80 ± 8.07 pg/mL) and PV-1, but the effect of S100B was antagonized by BBR. Z-IETD-FMK (5 μM) increased S100B-induced permeability to FITC-dextran (205.80 ± 9.70 to 263.80 ± 11.04 AUs) while reducing β-catenin in MIMECs. BBR (5 μM) reduced S100B-induced permeability (104.20 ± 9.65 AUs) and increased caspase-8, β-catenin and occludin.Discussion and conclusion: BBR decreases burns-induced GVB hyperpermeability via modulating S100B/caspase-8/β-catenin pathway and may involve EGCs.

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