Claudin-5

A claudin subtype that is found localized to TIGHT JUNCTIONS in VASCULAR ENDOTHELIAL CELLS. The protein was initially identified as one of several proteins which are deleted in VELOCARDIOFACIAL SYNDROME and may play an important role in maintaining the integrity of the BLOOD-BRAIN BARRIER.

Also Known As:

Networked: 493 relevant articles (28 outcomes, 54 trials/studies)

Relationship Network

Bio-Agent Context: Research Results

Experts

1.	Zhang, Xiangjian: 9 articles (08/2014 - 03/2010)
2.	Campbell, Matthew: 8 articles (01/2022 - 10/2010)
3.	Liu, Yunhui: 8 articles (10/2018 - 06/2011)
4.	Xue, Yixue: 8 articles (10/2018 - 06/2011)
5.	Wang, Ping: 8 articles (01/2018 - 06/2011)
6.	Wang, Lina: 8 articles (08/2014 - 03/2010)
7.	Cui, Lili: 7 articles (08/2014 - 03/2010)
8.	Greene, Chris: 6 articles (01/2022 - 01/2019)
9.	Kanda, Takashi: 6 articles (12/2020 - 11/2009)
10.	Sano, Yasuteru: 6 articles (12/2020 - 11/2009)

Related Diseases

1.	Infarction (Infarctions) 08/01/2014 - "Compared with Vehicle group, Evo significantly ameliorated neurological deficit, brain water content and infarct size, upregulated the expression of pAkt, pGSK3β and claudin-5, and downregulated the nuclear accumulation of NF-κB (P < 0.05). " 01/01/2013 - "The results indicated that PN dramatically ameliorated neurological deficit, brain water content, and infarct volume, downregulated NF- κ B, phospho-p38MAPK, and caspase-1 expressions, and upregulated claudin-5 expression in ischemic brain tissue. " 06/12/2012 - "Compared with pMCAO group, BBR dramatically lessened neurological deficits scores, brain water contents and infarct sizes, upregulated the expression of pAkt, pGSK3β, pCREB and claudin-5, and decreased the nuclear accumulation of NF-κB (P<0.05) in ischemic brain. " 03/19/2010 - "Compared with pMCAO group, the expressions of these factors significantly decreased in Tan II A-H group, the neurologic deficit, infarct volume and brain water content were alleviated (P<0.05) and claudin-5 was predominantly expressed in brain capillaries. " 10/01/2021 - "Claudin-5 overexpression in mouse heart also significantly decreased cleaved caspase 3 and the infarct size in ischemic heart with improved systolic function. "
2.	Edema (Dropsy) 01/01/2023 - "An inhibitor of claudin-5 interactions, M01, alleviates neuroinflammation and vasogenic edema after blood-spinal cord barrier dysfunction." 01/01/2019 - "We found that the exosomes derived from pericytes could reduce pathological changes, improve the motor function, the blood flow and oxygen deficiency after SCI. In addition, the exosomes could improve the endothelial ability to regulate blood flow, protect the blood-spinal cord barrier, reduce edema, decrease the expression of HIF-1α, Bax, Aquaporin-4, and MMP2, increase the expression of Claudin-5, bcl-2 and inhibit apoptosis. " 07/01/2020 - "Mechanistic study indicated that GJ-4 could alleviate endothelial dysfunction, as GJ-4 markedly reduced endothelial cell edema, as well as improved tight junction structures by up-regulating Zonula occludens-1 (ZO-1), Claudin-5 and Occludin expressions. " 01/01/2021 - "Our results found that FTY720-NSCs-Exos could alleviate pathological alterations and ameliorate the hindlimb function and oxygen insufficiency in model mice after SCI. In addition, exosomes could ameliorate the morphology of neurons, reduce inflammatory infiltration and edema, decrease the expression of Bax and AQP-4, upregulate the expression of claudin-5 and Bcl-2, and inhibit cell apoptosis. " 01/01/2021 - "Yiqifumai injection and Rb1+Sch inhibited mesenteric venule hyperpermeability, suppressed microvillar erosion and submucosal edema, and protected claudin-5 from downregulation and interleukin-1β from upregulation in ileal tissues after LPS. "
3.	Brain Edema (Cerebral Edema) 12/01/2009 - "The results of our study indicate that the interaction between tPA and microglial LRP1 increases MMP-9 expression and activity resulting in the degradation of claudin-5 and development of cerebral edema." 09/01/2018 - "The administration of soluble ligand EphrinA1 enhanced CD68+ cell accumulation, brain edema and dysfunction of the BBB, with lower expression levels of zonula occludens-1 (ZO-1) and Claudin-5. " 12/06/2010 - "Combination therapy with tPA plus cilostazol prevented development of hemorrhagic transformation, reduced brain edema, prevented endothelial injury via reduction MMP-9 activity, and prevented the blood-brain barrier opening by inhibiting decreased claudin-5 expression. " 01/01/2016 - "NBP, as a novel treatment approach, may effectively inhibit the down-regulation of ZO-1 and claudin-5 proteins (but not AQP-4), thereby preserving the barrier function and reducing cerebral edema after CO poisoning." 07/30/2014 - "Following pMCAO, Rhy treatment not only ameliorated neurological deficits, infarct volume and brain edema, but also increased claudin-5 and BDNF expressions (p < 0.05). "
4.	Heart Failure 12/01/2022 - "Claudin-5 has recently attracted increasing attention by its potential as a novel treatment target in the early stage of heart failure. " 07/01/2012 - "This experiment demonstrates that claudin-5 may represent a novel treatment target for prevention of heart failure." 07/01/2012 - "The goal of this study was to determine whether sustaining claudin-5 levels is sufficient to prevent the onset of histological and functional indicators of heart failure. " 10/01/2021 - "Downregulation of claudin-5 in the heart is associated with the end-stage heart failure. " 05/01/2015 - "These data support that loss of claudin-5 in cardiomyocytes and endothelial cells is prevalent in human heart failure. "
5.	Hypoxia (Hypoxemia) 06/05/2019 - "In the hypoxia cell model, NBP pre-treatment improved TJ ultrastructure, decreased intracellular ROS level, and increased the expression of claudin-5 (P < 0.01) and ZO-1 (P < 0.01) in comparison with the corresponding values in the hypoxia group. " 12/01/2022 - "In this study, we identified reduced levels of Claudin-5 in the hearts of mice subjected to acute myocardial IR injury and murine HL-1 cardiomyocytes subjected to hypoxia and reoxygenation (HR). " 10/17/2022 - "Hypoxia upregulated CAV-1 transcription via the activation of NRF1 in endothelial cells, thus inducing the internalization and autophagic degradation of claudin-5. " 01/04/2022 - "Endothelial cell morphology, claudin-5 and ZO-1 localization and barrier integrity were unaffected by hypoxia, indicating that the tight junctions in the BBB model were not compromised. " 10/01/2021 - "Autophagy alleviates hypoxia-induced blood-brain barrier injury via regulation of CLDN5 (claudin 5)."

Related Drugs and Biologics

1.	Proteins (Proteins, Gene)
2.	Tight Junction Proteins
3.	Occludin
4.	Claudin-1
5.	Vascular Endothelial Growth Factor A (Vascular Endothelial Growth Factor)
6.	cadherin 5
7.	Messenger RNA (mRNA)
8.	Matrix Metalloproteinases (MMPs)
9.	Matrix Metalloproteinase 9 (Gelatinase B)
10.	Connexin 43 (Connexin43)

Related Therapies and Procedures

1.	Therapeutics
2.	Oral Administration
3.	Ischemic Postconditioning
4.	Ligation
5.	Warm Ischemia