CDH5 antibody - N-terminal region (OAAB01399)
- Known as:
- CDH5 (anti-) - N-terminal region (OAAB01399)
- Catalog number:
- oaab01399
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- CDH5 antibody - N-terminal region (OAAB01399)
Related genes to: CDH5 antibody - N-terminal region (OAAB01399)
- 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 antibody - N-terminal region (OAAB01399)
Related articles to: CDH5 antibody - N-terminal region (OAAB01399)
- A high triglyceride/high-density lipoprotein cholesterol (TG/HDL-C) ratio is strongly associated with insulin resistance and atherosclerotic cardiovascular risk, but the cellular mechanisms linking this lipid imbalance to vascular injury remain incompletely defined. This study established a combined hyperglycemic/high TG/low HDL-C ratio-mimetic in vitro model using human coronary artery endothelial cells and THP-1-derived macrophages to investigate endothelial inflammation, glycocalyx disruption, monocyte recruitment, foam-cell formation, oxidative stress, and cholesterol efflux. High TG/low HDL-C ratio-mimetic stress significantly reduced endothelial viability, increased cytotoxicity, impaired transendothelial resistance, increased fluorescein isothiocyanate (FITC)-dextran permeability, and promoted syndecan-1 shedding. The lipid-stress condition induced endothelial inflammatory activation, with increased vascular cell adhesion molecule 1 (VCAM1), intercellular adhesion molecule 1 (ICAM1), E-selectin (SELE), C-C motif chemokine ligand 2 (CCL2), interleukin 6 (IL6), and C-X-C motif chemokine ligand 8 (CXCL8) expression, accompanied by enhanced THP-1 adhesion and transmigration. Glycocalyx and junctional injury were supported by increased heparanase (HPSE) expression and reduced syndecan-1 (SDC1), tight junction protein 1 (TJP1), cadherin 5 (CDH5), wheat germ agglutinin (WGA) staining, zonula occludens-1 (ZO-1) continuity, and vascular endothelial cadherin (VE-cadherin) integrity. Endothelial-conditioned lipid stress promoted macrophage foam-cell formation, increased CD36 scavenger receptor (CD36), oxidized low-density lipoprotein receptor 1 (OLR1), and peroxisome proliferator-activated receptor gamma (PPARG) expression, enhanced cholesterol accumulation, and suppressed ATP-binding cassette transporter A1 (ABCA1)-, ATP-binding cassette transporter G1 (ABCG1)-, scavenger receptor class B member 1 (SCARB1)-, and apolipoprotein E (APOE)-associated cholesterol efflux pathways. HDL rescue broadly attenuated endothelial inflammation, oxidative stress, barrier disruption, and macrophage foam-cell formation, whereas ApoA-I exerted protective effects across the selected endothelial and macrophage endpoints in which it was evaluated. CD36 inhibition reduced macrophage lipid accumulation, whereas heparanase inhibition preserved glycocalyx integrity. These findings identify the endothelial glycocalyx-nuclear factor kappa B (NF-κB)-CD36/ABCA1 axis as a mechanistic link between the high TG/low HDL-C ratio and diabetic atherosclerotic vascular dysfunction. - Source: PubMed
Publication date: 2026/09/10
Bi LechangZhao WenLu MingjingJiang NanWang GaofengHuang FeilaiLuo PengchaoWang Guofu - Atopic dermatitis (AD) is increasingly recognized as a systemic inflammatory disease associated with increased cardiovascular risk, yet the mechanisms linking AD to atherosclerosis and clinically relevant biomarkers of early vascular involvement remain poorly defined. We characterized the circulating proteomic profile of moderate-to-severe AD and identified biomarkers associated with subclinical atherosclerosis. In this cross-sectional study, serum samples from patients with AD (n=34), psoriasis (n=34), and healthy controls (n=20) were analyzed using proteomic panels targeting inflammatory and cardiovascular pathways. Participants underwent carotid and femoral ultrasound to detect atheromatous plaques. Compared with controls, AD showed increased circulating Th2 (CCL13, ST2, IL-13), innate (IL-6, IL-18), Th1 (IFN-γ), and Th17 (IL-17RA) markers, together with cardiovascular-related proteins including CCL19, FGF21, HGF, and P-selectin, with enrichment of atherosclerosis-related pathways. In AD, plaques were associated with higher LDL receptor, CDH5, transferrin receptor, CCL19, and CCL25, and lower IGFBP-2 levels, which also correlated with atherosclerosis burden. A composite proteomic score showed good discrimination of plaques (AUC 0.94) and outperformed traditional cardiovascular risk factors. Proteomic profiles and plaque-associated proteins differed markedly from psoriasis. These findings identify a disease-specific systemic proteomic signature in AD linked to early atherosclerosis and highlight circulating biomarkers with potential relevance for cardiovascular risk stratification. - Source: PubMed
Publication date: 2026/09/09
Berna-Rico EmilioNeria FernandoGómez-de la Fuente EnriquePérez-García BibianaAranda Carlos JAbbad-Jaime de Aragón CarlotaPerez-Bootello JavierDomínguez-López RaquelMonge DianaDavo-Mogica MariaBlauvelt AndrewGonzález-Cantero Álvaro - Fibroblasts are mesenchymal cells in the healthy vascular adventitia. In atherosclerosis, single-cell sequencing datasets suggest fibroblasts are abundant in plaques. However, their identity, origin, and fate during plaque progression remain unclear, which we aim to unravel here. - Source: PubMed
Publication date: 2026/09/09
Li GuanliangAsselberghs Sebastiaan E JYu BaixueFeng CongMendez Paul-LennardKasakovski DimitriGoossens PieterAckermans Tia MTillie Renée J H AGijbels Marion JTemmerman LieveXu HeDonners Marjo M P CKheder Dlzar AMaryam SidrahJin HanXue ChenyiHayat SikanderConklin Austin CRomanoski Casey EGiacca MauroMiller Clint LReilly Muredach PChen MingKramann RafaelMees BarendBaker Andrew HSluimer Judith C - Intestinal ischemia/reperfusion (I/R) disrupts the gut vascular barrier (GVB), causing bacterial translocation and organ injury. Dexmedetomidine can protect the GVB, but its clinical use is limited by dose‑dependent cardiorespiratory depression. To address this, we develop reactive oxygen species (ROS)‑responsive nanoparticles for targeted intestinal delivery and evaluate the efficacy and mechanism of dexmedetomidine‑loaded nanoparticles (Dex‑NPs) against intestinal I/R‑induced GVB damage. We observe that GVB disruption in clinical and experimental specimens is associated with reduced expression of Claudin5 and VE‑cadherin. Dex‑NPs preferentially accumulate in the ischemic intestine and release the drug upon ROS stimulation. Low‑dose Dex‑NPs (dexmedetomidine 5 µg/kg) confer GVB and hepatic protection comparable to high‑dose free dexmedetomidine, without detectable acute cardiorespiratory depression under the conditions tested. Mechanistically, dexmedetomidine inhibits histone deacetylase (HDAC), enhances H3K27 acetylation, and upregulates T-cell factor 4 (TCF4, encoded by TCF7L2), which directly binds and activates CLDN5 and CDH5 promoters, thereby restoring Claudin5/VE‑cadherin expression and GVB integrity; TCF4 knockdown largely abolishes these protective effects. In summary, ROS‑responsive Dex‑NPs enable low‑dose dexmedetomidine to preserve GVB integrity and mitigate post‑I/R liver injury via HDAC inhibition and TCF4 upregulation, circumventing dose‑limiting toxicity and suggesting TCF4 as a potential therapeutic target in oxidative stress‑associated gut endothelial barrier dysfunction. - Source: PubMed
Publication date: 2026/09/08
Zhang Hu-FeiShen Jian-TongZhang Hua-HuaGao Si-QiWang Ji-AoWang Yue-LingLi Mei-LingLiu Zi-MengZhang Yi-NanLi YanZhang Xu-Yu - 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