CDH5 (Human) ELISA Kit
- Known as:
- CDH5 (Human) Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- KA0152
- Product Quantity:
- 1 Kit
- Category:
- Peptides
- Supplier:
- Abno
- Gene target:
- CDH5 (Human) ELISA Kit
Related genes to: CDH5 (Human) ELISA Kit
- Gene:
- CDH5 NIH gene
- Name:
- cadherin 5
- Previous symbol:
- -
- Synonyms:
- 7B4, CD144
- Chromosome:
- 16q21
- Locus Type:
- gene with protein product
- Date approved:
- 1992-11-20
- Date modifiied:
- 2016-10-05
Related products to: CDH5 (Human) ELISA Kit
Related articles to: CDH5 (Human) ELISA Kit
- Chronic kidney disease is associated with neurovascular complications including cognitive impairment, potentially involving blood-brain barrier (BBB) impairment. The protein-bound uremic toxin indoxyl sulfate (IS) promotes endothelial injury, but its effects on human brain microvascular endothelial cells remain incompletely understood. Human cerebral microvascular endothelial cells (hCMEC/D3) were exposed to IS 200 and 900 μM. BBB integrity was assessed by the FITC-dextran (4 kDa) transwell permeability assay and claudin-5 immunofluorescence. Transcriptional responses were quantified by qPCR for aryl hydrocarbon (AhR) target genes, oxidative stress-associated and inflammatory markers, senescence, and junction-associated genes. Senescence-associated phenotypic changes were evaluated by SA-β-galactosidase staining and cytokine array profiling. IS increased endothelial permeability at 24 and 48 h (~1.5-fold relative to control) without evidence of cytotoxicity and reduced claudin-5 staining intensity. IS strongly upregulated AhR target genes, including CYP1A1, CYP1B1, and CYP1A2. NFE2L2 and IDO1 increased, while NFKB1 remained unchanged. SA-β-gal positivity increased, accompanied by elevated GM-CSF and G-CSF secretion, while CDKN1A decreased at IS 900 µM and CDKN2A remained unchanged. CDH5 was downregulated, TJP1 increased at 900 µM, and CLDN5 remained unchanged. These findings indicate that IS exposure is associated with impaired BBB integrity, AhR-related transcriptional responses, oxidative stress-associated transcriptional changes, junctional remodeling, and senescence-like endothelial features. However, causal attribution to individual pathways requires inhibition or knockdown studies. - Source: PubMed
Publication date: 2026/08/01
Hernandez LeahStrizzi Camillo TancrediRosina MiriamSchwarz AngelinaKronqvist NinaArefin SamsulStenvinkel PeterKublickiene Karolina - Although Dirofilaria repens induces perivascular proliferation in subcutaneous nodules, the molecular factors driving this angiogenic response remain unknown. The objective of this study is to investigate the activation of the angiogenic mechanism in an in vitro model of human vascular endothelial cells (HUVECs) stimulated with D. repens somatic antigen (DrSA) and Dr20/22 protein, identifying the key pathways underlying the vascular pathology caused by the parasite. - Source: PubMed
Publication date: 2026/08/20
Collado-Cuadrado ManuelMontero-Calle AnaVázquez-Ávila SaraBarderas RodrigoPękacz MateuszZawistowska-Deniziak AnnaSotillo JavierPericacho MiguelMorchón Rodrigo - Germline deletion of the core circadian transcription factor Bmal1 has been shown to reduce blood-spinal cord barrier (BSCB) disruption and tissue loss following moderate T9 contusive spinal cord injury (SCI) in mice. Therefore, effects of conditional Bmal1 deletions were tested using the same model. A strong reduction of Bmal1 expression in the brain or spinal cord followed tamoxifen treatment of Bmal1 young adult mice who carried the broadly expressed Cag-CreERT2 recombinase transgene. Supporting functional consequences of such a deficit, canonical BMAL1 target genes Nr1d1 and Dbp were also downregulated. However, only few tissue damage markers were moderately reduced at 3 days post SCI. Furthermore, neither locomotor recovery nor long-term white matter sparing was improved. Similar SCI phenotype was observed in endothelia-selective Bmal1 mice (Cdh5-Cre:Bmal1) including modest attenuation of few acute injury markers, but no significant effects on functional recovery or long-term tissue sparing. These data suggest that germline deletion of Bmal1 is protective against SCI due to compensatory changes in gene expression that originate during development and involve cells beyond endothelia. Therefore, a direct role for BMAL1 in secondary injury cascades that are activated after SCI is unlikely. - Source: PubMed
Publication date: 2026/08/11
Slomnicki Lukasz PArmstrong Christine DMorehouse Johnny RAndres KarienaMusiek Erik SOhri Sujata SaraswatHetman Michal - Severe COVID-19 is frequently associated with vascular complications, raising ongoing debate about whether SARS-CoV-2 can directly infect endothelial cells and thereby contribute to disease pathogenesis. Although endothelial cells express angiotensin-converting enzyme 2 (ACE2), the relevance of endothelial-restricted viral tropism remains unclear. To directly assess the consequences of endothelial-restricted SARS-CoV-2 tropism , we generated a transgenic mouse model expressing human ACE2 under control of the endothelial-specific promoter (-hACE2). Despite confirmed pulmonary endothelial expression and protein presence of hACE2, SARS-CoV-2 infection of -hACE2 mice did not induce clinical illness, detectable viral replication, immune cell influx in the lung, or histopathological abnormalities in the lung or brain. These findings indicate that endothelial-restricted SARS-CoV-2 tropism alone is insufficient to drive productive infection and clinical disease , suggesting that endothelial involvement in COVID-19 likely arises in the context of broader cellular infection or systemic host responses rather than from primary endothelial infection. - Source: PubMed
Publication date: 2026/08/11
Lameire SahineDebeuf NincyDeckers JulieDe Wolf CarolineVanheerswynghels ManonToussaint WendyDe Vlieger LizeVan Hoecke LienBruggeman ArnoutDe Cae SieglindeSchepens BertVanhee StijnLambrecht Bart N - Internal N7-methylguanosine (mG) is a recently identified chemical modification of mammalian mRNA. Although the epitranscriptome plays a key role in regulating RNA metabolism and cellular function, the specific contribution of internal mG to cardiovascular disease remains unknown. Atherosclerosis preferentially develops at sites of disturbed blood flow, which promotes endothelial activation; however, whether internal mG regulates endothelial mechanotransduction and atherogenesis remains unclear. - Source: PubMed
Publication date: 2026/08/11
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