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
- Dengue virus (DENV) represents a growing global health challenge with billions of people at risk. Severe Dengue (SD), a complication of DENV infection that involves generalized hemorrhage, is driven, at least in part, by endothelial dysfunction. Endothelial dysfunction refers to increased permeability due to inflammation, mechanical injury and/or modification of the genetic program of endothelial cells. Previous work showed that exposure of endothelial cells to conditioned media from DENV-infected cells (CMDV) increased permeability and cellular stiffness, repressed endothelial markers and induced mesenchymal genes. However, the generality, extent, mechanism and ultimate impact of these events in the onset of SD remain elusive. Here, we integrate analysis from in vitro treatment of endothelial cells with media containing UV-inactivated DENV with computational modeling to investigate the key features of CMDV-induced endothelial alterations and their potential impact on endothelial dysfunction. We found that CMDV increased SNA1 and CDH2 expression, while suppressing endothelial genes OCLN and CDH5. Global transcriptomics analysis revealed that CMDV triggered a transient pro-inflammatory response, followed by induction of selected tissue repair genes and matrix remodeling. A non-directed asynchronous network model (NDAM-CMDV) identified IL6 and FN1 as central nodes of DENV-induced endothelial trans-differentiation, providing new molecular insights that predict the evolution of the disease and identify potential therapeutic targets. - Source: PubMed
Publication date: 2026/07/31
Alfaro-García Jenny PaolaRamírez-Mejía Julieta MaríaRojas-Estevez PaolaÁlvarez-Díaz Diego AlejandroFernández Geysson JavierOrozco-Castaño Carlos AlbertoRodríguez-Rey Boris AngheloGallego-Gómez Juan CarlosVicente-Manzanares Miguel - Endothelial dysfunction is a defining feature of diabetic vascular disease and is characterized by impaired nitric oxide signaling, inflammatory activation, altered mechanotransduction, and disturbed angiogenic responses. The present study investigated whether hyperglycemia modulates endothelial phenotype in a model-dependent manner under distinct structural and mechanical culture conditions. EA.hy926 endothelial cells were cultured for 7 days under normoglycemic (5.5 mM) or high-glucose (25 mM) conditions as static monolayers (G-force = 1 ), adherent clinorotated cells, multicellular spheroids (MCSs) generated during clinorotation, and Matrigel-derived endothelial structures. Gene expression was assessed by qPCR using marker panels related to nitric oxide signaling, signaling, inflammatory adhesion, angiogenesis, and structural adhesion, whereas protein abundance and spatial distribution of eNOS, AKT1, VCAM1, vinculin, and VEGFA together with CDH5/VE-cadherin were analyzed by Western blotting and confocal microscopy. Clinorotation generated both adherent endothelial cells and MCSs. High glucose reduced eNOS-related expression in most models, with the strongest decreases in adherent clinorotated cells and MCSs, whereas Matrigel cultures showed a divergent transcriptional response. PI3K CA expression was markedly suppressed by high glucose in clinostat-derived populations, while was differentially regulated in spheroids and Matrigel cultures. VCAM1 expression was most prominent in MCSs, whereas was highest in Matrigel cultures. VEGF-related signaling differed substantially among models, and Matrigel cultures showed the strongest VEGFA-associated protein signal and the clearest angiogenic organization under normoglycemic conditions, which became less distinct under high glucose. Vinculin protein abundance was highest in MCSs and Matrigel cultures, reflecting pronounced differences in structural organization. Overall, these findings show that endothelial responses to hyperglycemia are strongly shaped by mechanical and structural context and support the use of complementary in vitro models for studying diabetic endothelial dysfunction. - Source: PubMed
Publication date: 2026/07/13
Volkevičiūtė AugustaSahana JayashreePinilla EstéfanoMelnik DanielaGonzález-Torres Luis FernandoWehland MarkusStankevicius EdgarasGrimm DanielaSimonsen Ulf - In vitro vascular models are most informative when they recapitulate endothelial assembly within a 3D microenvironment. Blood vessel organoids (BVOs) enable the study of vascular heterogeneity, function, and organ-instructive cues in development, homeostasis, and disease. Here, we present a robust stepwise method to generate murine blood vessel organoids (mBVOs) from feeder-dependent mouse embryonic stem cells (mESCs) of common genetic backgrounds. Embryoid bodies (EBs) are formed using strain-specific seeding densities (day 0-3), followed by mesoderm induction (day 3-6) and vascular induction (day 6-8). Induced EBs are embedded in collagen I with Geltrex to drive sprouting and network formation (day 8-13). Vascular networks are microdissected and grown in suspension to yield mature mBVOs (day 21-30). The inclusion of a Cre-inducible VE-cadherin-GFP reporter line enables a quantitative quality control, reducing variability by excluding poorly differentiated organoids. The protocol reliably produces ~100 mBVOs per differentiation and is compatible with engineered mouse strains for gain- and loss-of-function studies, functional assays of vascular plasticity, and syngeneic grafting to assess perfusion. Thus, mBVOs provide a scalable and traceable 3D platform that bridges endothelial assays, mouse models, and human organoid systems. Key features • A detailed timeline to differentiate feeder-dependent mESCs into mBVOs, with key success readouts and troubleshooting. • Efficient across three genetic backgrounds with strain-specific EB seeding densities and typical yields of ~100 mBVOs per differentiation. • The inducible VE-cadherin-GFP lineage tracing/reporter system provides an endothelial quality control to quantify efficiency and exclude poorly differentiated organoids. • Compatible with engineered mouse strains for gain/loss-of-function, with in vitro assays of vascular plasticity/remodeling, and with syngeneic in vivo validation. - Source: PubMed
Publication date: 2026/07/05
Guelfi SophieBopp SarahBergers Gabriele - Triple-negative breast cancer (TNBC) is an aggressive subtype associated with high metastatic potential and poor outcomes, with lung metastasis representing one of the most frequent and life-threatening events. However, the mechanism how cellular plasticity and reprogramming that enable TNBC cells to colonize in the lung remain incompletely understood. Here, we integrated single-cell RNA sequencing and spatial transcriptomics on paired MMTV-PyMT primary mammary tumors and lung metastatic tumors, complemented by functional assays in 4T1 mouse models, to delineate the cellular heterogeneity and molecular mechanisms driving TNBC lung metastasis. We identified three metastasis-associated subtypes-C12-Cd, Cdh5-like, and Wfdc12-each enriched in metastatic lesions and exhibiting distinct biological programs. The C12-Cd subcluster was characterized by the upregulation of Exoc4, a vesicle-trafficking regulator associated with a poor prognosis in patients with TNBC. The Cdh5-like cluster displayed a hypoxia-driven vascular phenotype, in which Hif-2α-mediated Cd36 expression promoted vasculogenic mimicry and metastatic colonization. The Wfdc12 cluster secreted Cxcr2 ligands (Cxcl1/2) and Cxcr2 blockade significantly reduced lung metastasis in vivo, underscoring therapeutic potential. Notably, cross-subtypes of lung metastatic TNBC analysis revealed Sftpc upregulation, reflecting organ-adaptive transcriptional reprogramming that may facilitate tumor cell survival in the pulmonary niche. Collectively, our findings provide a comprehensive cellular and molecular atlas of TNBC lung metastasis. We establish Exoc4, the Hif-2α-Cd36 vasculogenic mimicry axis, Cxcrl1/2-Cxcr2 signaling, and Sftpc as critical mediators of metastatic adaptation. These results not only bridge key knowledge gaps in metastatic heterogeneity and organ-specific adaptation but also highlight novel prognostic markers and therapeutic vulnerabilities with translational potential for treating TNBC lung metastasis. - Source: PubMed
Publication date: 2026/07/07
Lee Hsiao-ChenKuo Chia-YuChen Fang-MingHou Ming-FengTsai Hung-PeiWu Yu-YuanChuang Kai-ChienWu Ling-YuPan Sheng-FengTsai Ying-MingHsu Ya-Ling - Lagopsis supina is a traditional Chinese medicinal herb used for activating blood circulation and nourishing the blood. This study aims to investigate the pro-angiogenic constituents of L. supina and their mechanisms of their action. 30 compounds derived from the active fraction LS-D (L. supina 60% ethanol-water extract) were screened, of which 15 showed angiogenesis-promoting activity, were screened in a PTK787-induced vascular injury zebrafish model. The active constituents were primarily phenolic acids and phenylpropanoids, among which compounds LS21 (vanillic acid) and LS22 (syringic acid) exhibited the most potent pro-angiogenic effects. These constituents (LS21 and LS22) were selected for further investigation of mechanisms of promoting angiogenesis. Transcriptomic analysis followed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment revealed differentially expressed genes and predicted involved pathways. Molecular docking simulated interactions between compounds and key pathway proteins, and RT-qPCR validated gene expression patterns. Mechanistic studies integrating transcriptomics, molecular docking, and RT-qPCR revealed that both LS21 and LS22 downregulated immune-related cell adhesion molecules, while upregulating cdh5 and pecam1a. Additionally, LS21 specifically downregulated the signaling molecules smad2 and smad3a, and upregulated the transcriptional corepressors skila and ncor1. In contrast, LS22 downregulated extracellular matrix-related adhesion molecules and itga2b, while upregulating thbs1a and integrin itgb3b. In conclusion, the L. supina constituents LS21 and LS22 that are primarily phenolic acids and phenylpropanoids, exert their angiogenesis-promoting effects mainly via modulating cell adhesion and suppressing TGF-β signaling pathway. - Source: PubMed
Publication date: 2026/07/06
Yu JiahaoWang XiaoyiJia LiyanFu LuluHe JunweiZhang ShanshanHe QiuxiaLiu KechunLi XiaobinLi Na