CD138 Mouse-Mono
- Known as:
- CD138 Mouse-Mono
- Catalog number:
- 413881F
- Product Quantity:
- 6ml
- Category:
- -
- Supplier:
- Nichereion
- Gene target:
- CD138 Mouse-Mono
Related genes to: CD138 Mouse-Mono
- 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: CD138 Mouse-Mono
Related articles to: CD138 Mouse-Mono
- Most research on idiopathic pulmonary fibrosis (IPF) has focused on the interplay among fibroblasts, the immune system and epithelial cells. There is growing evidence that microvascular dysfunction also plays a role in disease progression, but large human translational studies are lacking. In this research, we aim to identify a proteomic signature of microvascular instability and assess the impact of current therapeutics on the microvasculature. - Source: PubMed
Publication date: 2026/09/10
Csordas David JMa Shwu-FanHuang YongReceveur BrodyStrickland EmmaCucuzzella Lily CPugashetti Janelle VuLee Cathryn TPodolanczuk Anna JMartinez Fernando JAdegunsoye AyodejiOldham Justin MNoth ImreKim John SPeirce Shayn M - Syndecans (SDCs) 1-4 are a family of transmembrane heparan sulfate proteoglycans (HSPGs) that regulate cell-cell communication, adhesion, extracellular matrix organization, and signaling pathways involved in tumor biology. In prostate cancer (PCa), accumulating evidence suggests that SDCs contribute to tumor progression, therapeutic resistance, and interactions within the tumor microenvironment. However, their specific, stage-dependent roles remain incompletely understood. This review provides an integrated synthesis of current experimental and clinical evidence on SDC1-SDC4 in PCa, complemented by exploratory analyses of publicly available transcriptomic, genomic, and proteomic datasets. In contrast, copy-number alteration (CNA) strata dichotomized by the mean for SDC1, SDC2, and SDC4 showed differences in progression-free interval. Specific CNA subclasses and relationships between CNA values and SDC mRNA or protein abundance could not be determined. Proteomic pseudotime analysis further suggested that SDC4 expression increases during PCa progression, supporting its potential involvement in advanced disease. We discuss the regulation and modulation of SDCs by androgen deprivation therapy (ADT), enzymatic shedding, integrin-mediated signaling, extracellular matrix interactions, lipid signaling pathways, and microRNA networks. In particular, SDC1-microRNA interactions may influence PCa cell proliferation, cellular senescence, epithelial-mesenchymal transition (EMT), and intracellular signaling pathways. Overall, this review highlights SDCs as context-dependent regulators of PCa biology with potential relevance as biomarkers or therapeutic targets. However, clinical translation will require independent validation, standardized assays, compartment-resolved analyses, and mechanistic confirmation. - Source: PubMed
Publication date: 2026/09/04
Machado Ranyelison SilvaTamura Rodrigo EsakiGötte MartinOnyeisi Jessica Oyie Sousa - Chronic endometritis (CE) is a persistent inflammatory condition of the endometrium associated with infertility. Current diagnosis relies on histopathological markers like CD138, which may not fully assess the functional state of the endometrial microenvironment. This study aimed to investigate whether the endometrial microbiome test (EMT) combined with personalized therapy could improve pregnancy outcomes in infertile women undergoing IVF, compared with standard management based on CD138 results. - Source: PubMed
Publication date: 2026/08/26
He FangPeng E'NuoLin JiaoMao ZhuoLu XiaoweiXu HuiGuo LeiZou YangyunWang JingLu SijiaHuang Xianghong - 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 - Early antithrombin (AT) depletion after trauma may result from thrombin-related consumption, vascular leakage, and systemic protein loss. We examined the biomarker profile associated with early AT depletion and whether reduced AT activity identifies an adverse early injury phenotype. - Source: PubMed
Publication date: 2026/09/09
Matsumoto HironoriKan AkihitoTakezawa MitsuakiTanabe TsunenoriAnnen SuguruMukai NaokiOhshita MuneakiNakabayashi YukiKikuchi SatoshiTakeba JunSato Norio