Anti - Mouse, CD138 Clone MI15
- Known as:
- Anti - Mouse, CD138 Clone MI15
- Catalog number:
- 61-0108-2
- Product Quantity:
- 0.2mL
- Category:
- -
- Supplier:
- Genemed
- Gene target:
- Anti - Mouse CD138 Clone MI15
Related genes to: Anti - Mouse, CD138 Clone MI15
- Gene:
- SDC1 NIH gene
- Name:
- syndecan 1
- Previous symbol:
- SDC
- Synonyms:
- CD138, syndecan, SYND1
- Chromosome:
- 2p24.1
- Locus Type:
- gene with protein product
- Date approved:
- 1991-03-18
- Date modifiied:
- 2014-11-19
Related products to: Anti - Mouse, CD138 Clone MI15
Related articles to: Anti - Mouse, CD138 Clone MI15
- Acute respiratory distress syndrome (ARDS) has a high clinical mortality rate and continues to draw research attention regarding its mechanisms and potential treatments. Disruption of the endothelial barrier is a primary pathological feature, and glycocalyx degradation is a key factor contributing to this disruption. Human umbilical cord mesenchymal stem cells (hucMSCs) exhibit strong anti-inflammatory and immunomodulatory effects, making their application in ARDS treatment an area of increasing interest. Proteomic screening identified Cxcl12 as a protein secreted by hucMSCs. In male C57 mice and cell models, lipopolysaccharide (LPS) was used to induce injury, followed by interventions with hucMSCs or hucMSCs with silenced Cxcl12 to assess glycocalyx-related proteins SDC-1, HS, and the repair marker EXT-1. To evaluate downstream signaling, the CXCR4 receptor was inhibited and related indicators were examined. Silencing Cxcl12 reduced the therapeutic effect of hucMSCs on LPS-induced glycocalyx damage. Inhibition of CXCR4 also weakened the effect of Cxcl12. These findings indicate that hucMSCs alleviate LPS-induced glycocalyx damage in pulmonary vascular endothelial cells by secreting Cxcl12, which activates the downstream receptor CXCR4, providing a therapeutic effect for ARDS. - Source: PubMed
Publication date: 2026/04/16
Cui JinfengPeng ZhenyiChen YuanyuanLiu WeiChen QiuwenWang XiaozhiWang TaoHuang XiaoSun Ting - Peritoneal fibrosis (PF) is a serious complication in patients undergoing peritoneal dialysis (PD). Heparanase (HPA) may drive the progression of PF by promoting inflammation and tissue remodeling. This study aimed to evaluate HPA expression in peritoneal dialysate from end-stage renal disease (ESRD) patients receiving PD and to assess the correlation between HPA and fibrosis markers in PF. Peritoneal dialysate samples from ESRD patients were collected to measure HPA, syndecan-1 (SDC-1), and fibrosis markers. To further investigate the regulatory role of HPA in PF, a mouse model was established. Then mice were divided into four groups (n = 6 per group): control, PF, PF + HPSEi, and PF + Bailing groups. Tissue samples were collected for the detection of HPA, SDC-1, and fibrosis markers using RT-qPCR and Western blot. Fibrosis was evaluated via H&E and Masson staining. In peritoneal dialysate from 104 participants, HPA levels were positively correlated with SDC-1 (r = 0.617), TGF-β (r = 0.413), fibronectin (r = 0.278), and collagen I (r = 0.276). HPA (β = 0.0024), SDC-1 (β = 0.0572), TGF-β (β = 0.4358), and collagen I (β = 0.0023) were positively correlated with dialysis duration (all p < 0.05). Additionally, HPA was associated with high peritoneal transport function (p = 0.043). In mouse tissues, HPA inhibitor treatment downregulated TGF-β1, α-SMA, collagen I, and SDC-1, while upregulated E-cadherin expression and reducing tissue fibrosis. These effects were similar to those observed in the Bailing treatment group (all p < 0.05). HPA is positively correlated with SDC-1 and fibrosis markers. Inhibition of HPA attenuates PF, potentially through the HPA/SDC-1/TGF-β axis. - Source: PubMed
Wang JinLiu LipingHuang ShitaoHuang ZhongyaSun YiboYu YangZhao XueZeng Xiuqin - This randomized, double-blind, placebo-controlled trial investigated the effects of extract (CLE) supplementation on vascular, redox-inflammatory biomarkers, and neuropathy symptoms in adults with type 2 diabetes mellitus (T2DM). - Source: PubMed
Publication date: 2026/04/15
Viudes Drielly RodriguesMateus Alanna RamalhoSilva Cristina Antonialido Carmo Franco Maria - To investigate the mechanism by which NOD-like receptor heat protein domain-associated protein 3 (NLRP3) activation mediates coronary endothelial dysfunction at different stages of Kawasaki disease (KD). - Source: PubMed
Zheng RonghaoYue JingChen QianjunXie JingWen LintaoDuan NanaShang JianpingZhu SongbaiHuang LiZou YangSong XiaoxiangWu XiaolinFeng Qihua - Understanding of pulmonary gas exchange measurements in divers at sea is incomplete. In this study, arterial blood gases (ABGs) were measured in SCUBA divers breathing compressed air and pedalling at depths of 15 or 40 m in seawater (msw). In breath-hold divers (BHDs), ABGs were obtained before, at 15, 25 or 40 msw, and at the surface before breathing. Lung ultrasound was also performed in both groups before, at 15 msw, and after all the dives. Blood syndecan-1 (SDC-1) and heparan sulfate (HS) were also measured. Among 10 SCUBA divers (one female; ages 32-57), PaO increased at depth as predicted. Among 12 BHDs (three female, ages 33-62), PaO rose at depth and decreased on surfacing; two participants at 15 msw and one at 25 msw did not develop bottom hyperoxaemia. Lung ultrasound was normal at 15 msw, while interstitial oedema or pleural irregularities were found after surfacing in most SCUBA divers and BHDs. In SCUBA divers, significant post-dive increases occurred in SDC-1 and HS; in BHDs, a significant increase was found in HS after the 15 and 25 msw dives, while SDC-1 increased after all depths. Compared with warm-freshwater experiments, ABG values in SCUBA divers were similar, while in BHDs relative hypoxaemia at depth was less common. Elevated levels of glycocalyx markers were consistent with endothelial stress, possibly providing a mechanism for fluid to accumulate in the pulmonary interstitium and explaining the ultrasound abnormalities. KEY POINTS: The understanding of lung-environment interactions during open-sea diving remains limited. We integrated underwater and surface arterial blood gases, lung ultrasound and endothelial glycocalyx markers (syndecan-1, heparan sulfate) to quantify gas-exchange perturbations and lung stress in SCUBA and breath-hold divers (BHDs). SCUBA: arterial oxygen (PaO) increased at depth and returned to baseline at the surface; BHDs: PaO increased at depth (except in three participants), then values fell to hypoxaemia on surfacing. Post-dive lung ultrasound showed subclinical interstitial oedema - from focal B-lines to diffuse patterns - and pleural irregularities more marked after deeper dives and in BHDs than in SCUBA. Circulating glycocalyx markers increased post-dive, consistent with endothelial stress. - Source: PubMed
Publication date: 2026/04/13
Paganini MatteoGiacon Tommaso AntonioMrakic-Sposta SimonaMartani LucaCialoni DaniloZucchi LorenzoMaffei VincenzoCifali RosarioMarmo MarianoCamporesi Enrico MMoon Richard EBosco Gerardo