Monkey Cadherin 5 ELISA , CDH5
- Known as:
- Monkey Cadherin 5 Enzyme-linked immunosorbent assay test , CDH5
- Catalog number:
- E09C0500
- Product Quantity:
- 96 Tests/kit
- Category:
- -
- Supplier:
- BGene
- Gene target:
- Monkey Cadherin 5 ELISA CDH5
Related genes to: Monkey Cadherin 5 ELISA , CDH5
- 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: Monkey Cadherin 5 ELISA , CDH5
Related articles to: Monkey Cadherin 5 ELISA , CDH5
- Burn injuries, especially in diabetic patients, are difficult to treat because of persistent inflammation, impaired angiogenesis, and defective remodeling of the extracellular matrix (ECM). A hydrogel based on hyaluronic acid, chitosan, and alginate was developed to deliver adipose-derived mesenchymal stem cells (MSC) overexpressing SPARC (secreted protein acidic and rich in cysteine). SPARC is an ECM glycoprotein that promotes angiogenesis, collagen deposition, and matrix remodeling and whose activity is reduced in diabetic wounds - was overexpressed to restore these regenerative functions, and the therapeutic effect of the system was evaluated in diabetic and non-diabetic mice with deep thermal burns. The animals were treated with control (CMV) MSC, SPARC‑MSC, or SPARC‑MSC embedded in the hydrogel (SPARC‑HG). Wound healing was assessed by planimetry, histopathology, immunofluorescence, immunohistochemistry, qRT-PCR, and RNA sequencing. SPARC‑HG accelerated wound healing from day 9 and achieved near-complete re-epithelialization by day 21, even in diabetic mice. Histological analysis showed accelerated granulation-tissue formation, increased collagen deposition, and a more organized skin architecture. Immunofluorescence revealed an increased density of CD31 microvessels, activation of α-SMA myofibroblasts, proliferation of PCNA keratinocytes, and the involvement of CK15 hair-follicle stem cells. Immunohistochemistry confirmed decreased expression of the pro-inflammatory cytokines IL‑6, TNF‑α and IL‑1β. qRT-PCR and RNA-seq demonstrated the upregulation of angiogenic (CD31, Cdh5), matrix (Col1a1), and anti-inflammatory (IL-10) genes, together with the downregulation of Mmp9 and IL-6. Transcriptomic profiling revealed the enrichment of pathways related to ECM organization, collagen fibrillogenesis, endothelial integrity, and PI3K‑Akt signaling. SPARC-MSC and hydrogel in combination generated a synergistic regenerative environment with restoration of angiogenesis and matrix remodeling, promotion of epithelial proliferation and re-establishment of immune balance, resulting in superior healing outcomes. This platform can be a promising approach to treat severe burns, especially in diabetic patients. - Source: PubMed
Publication date: 2026/09/01
Merzlikin NikitaHan MiaoZhu WenlongZhang ZenyuLiu QianqiuTian HongKaiGerunova LiudmilaLi NaHua JinLian - Brain metastasis is the major cause of cancer-related mortality and remains a critical challenge in clinical oncology. Extravasation of circulating cancer cells across blood-brain barrier (BBB) is the first crucial and rate-limiting step for brain metastasis growth. However, the dynamic changes of brain endothelial cell junction and vascular integrity during cancer cell extravasation across BBB remains unclear. Here, we established a knockin zebrafish line, , in which EGFP is fused to the C-terminal of endogenous VE-cadherin, enabling real-time imaging of brain endothelial junction dynamics. Then, we established a brain metastasis model in zebrafish, and tracked the multistep cascade of cancer cell extravasation across BBB. We demonstrated that cancer cells cross brain vascular endothelial cells, accompanied by dynamic remodeling of VE-cadherin and transient disruption of vascular integrity. Our model transforms the BBB into a dynamically observable interface, enabling real-time visualization of junction remodeling during cancer cell extravasation, which will not only facilitate further mechanistic study, but also provide a valuable platform for preclinical drug screening. - Source: PubMed
Publication date: 2026/08/18
Zhang YuDeng ShunzeRen YonggangDu JiulinXu Bing - 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