Ask about this productRelated genes to: CD44 antibody
- Gene:
- CD44 NIH gene
- Name:
- CD44 molecule (Indian blood group)
- Previous symbol:
- MIC4, MDU2, MDU3
- Synonyms:
- IN, MC56, Pgp1, CD44R, HCELL, CSPG8
- Chromosome:
- 11p13
- Locus Type:
- gene with protein product
- Date approved:
- 1989-06-30
- Date modifiied:
- 2019-04-23
Related products to: CD44 antibody
Related articles to: CD44 antibody
- Gut microbiota may affect the development of autoimmune (type 1) diabetes by differential potency of intestinal species to induce endotoxin tolerance (ET). However, where ET impinges on immune mechanisms underlying autoimmune diabetes is yet incompletely understood. We investigated the effects of lipopolysaccharide (LPS) from E. coli and B. vulgatus, two common intestinal species dominating either in low- or high-incidence countries, on activation and chemoattraction of islet-specific T cells in non-obese diabetic (NOD) mice. Intraperitoneal (i.p.) injection of E. coli LPS induced costimulatory ligands CD40, CD80 and CD86 on both conventional and cross-presenting (XCR1+) dendritic cells (DC) and islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP)-reactive islet-specific T cells in the pancreatic lymph node. In comparison to mice not primed with E. coli LPS or primed with B. vulgatus LPS, the second injection of E. coli LPS lowered the frequency of IGRP-reactive T cells and CD80 expression on DC subsets, as well as CD44 and CD69 activation markers and the CXCR3 chemokine receptor on IGRP-reactive T cells. In islets, expression of chemokine CXCL10 accentuated, and insulitis became more severe in mice primed with B. vulgatus LPS. Our results provide mechanistic insight into how ET affects islet autoimmunity and suggest that physiological exposure to E. coli LPS may benefit in moderating autoimmune diabetes. - Source: PubMed
Silojärvi Satu MLeino Linda A APöysti Sakari AHänninen Arno L M - This study explores a surface modification strategy that mimics the native cellular environment through the layer-by-layer assembly of natural polyelectrolytes. Specifically, we developed a multilayer matrix composed of 10 alternating layers of chitosan (a polycation) and hyaluronic acid (a polyanion), seeded with Wharton's jelly mesenchymal stem cells (WJ-MSCs) derived from human umbilical cords. These cells are attractive for cartilage regeneration due to their accessibility, robust differentiation potential, and low immunogenicity. WJ-MSCs were cultured on the multilayer films at a density of 3000 cells/cm in standard growth medium. Positive controls included cells on multilayer films supplemented with transforming growth factor-beta (TGF-β), while negative controls were cells cultured on glass in standard medium. Cell morphology, proliferation, matrix formation, and expression of key chondrogenic markers were assessed. The WJ-MSCs adhered well, exhibited fibroblast-like morphology, and expressed characteristic MSC markers (CD44, CD90, CD73) while lacking hematopoietic markers (CD34, CD45), as defined by ISCT guidelines. The chitosan-hyaluronic acid (CHI-HA) films supported spontaneous chondrogenic differentiation, as demonstrated by upregulation of chondrogenic genes and proteins, and positive staining for chondroitin sulfate. Notably, chondrogenic differentiation on CHI-HA films enhanced the immunomodulatory profile of WJ-MSCs, as shown by upregulation of IL-10 and selective modulation of TLR expression. Despite increased TNF-α, this was attributed to TGF-β signaling rather than inflammation. Overall, CHI-HA films promoted both chondrogenic and immunoregulatory functions, offering a promising platform for cartilage tissue engineering. - Source: PubMed
Publication date: 2026/04/08
Basso RashaGhamrawi AhedAasar BayanGhassa KhoderShakik NourKaram MarioEl-Hajjar LayalKaram MarcNassar AlineHaddad LaraEl-Sabban MarwanNasr ZeinaHarmouch Chaza - Extracellular matrix (ECM) disorder was considered as the result of fibrosis, but it is recently recognized that fibrotic ECM initiates a self-reinforcing circuit and contributes to development of fibrosis. Versican, an ECM component, participates in cell-ECM interaction and ECM regeneration. In pleura, versican is primarily derived from pleural mesothelial cells (PMCs). However, the role and mechanism of versican in pleural fibrosis remained unknown. In this study, versican and versican-mediated pleural viscoelasticity was found elevated in both human and murine pleural fibrotic tissues. Versican knockdown by shRNA prevented increases of viscoelasticity as well as pleural fibrosis. High level of versican and viscoelasticity promoted mesothelial to mesenchymal transition (MesoMT) in PMCs. Mechanistically, increased viscoelasticity induced pleural fibrosis through CD44/USP10/Smad4 mechanotransduction pathway. In conclusion, these results revealed that excessive versican in fibrotic pleural ECM enhanced ECM viscoelasticity, and consequently promoted progression of pleural fibrosis. - Source: PubMed
Publication date: 2026/04/23
Jia Zi-HengHe Xin-LiangCui Xiao-LinLi QianCheng Pei-PeiZhao Li-QinYe Shu-YiHu Shi-HeLian Chen-YueZhang He-DeLiang Li-MeiSong Lin-JieYu FanXiong LiangXiang FeiWang XiaorongWang MengDai XiyongYe HongMa Wan-Li - Despite serving as a radical alternative to surgery for inoperable colorectal hepatic metastases patients, thermal ablation faces local tumor progression rates up to 25% from residual tumors, seriously compromising treatment efficacy and survival of patients. We constructed hyaluronic acid (HA)-modified nanoparticles as carriers for the hydrophobic necrosis-avid agent I-hypericin (I-Hyp), enabling tumor necrosis-targeted radiotherapy. I-Hyp was synthesized via iodogen-catalyzed electrophilic substitution and loaded into amphiphilic block copolymer hyaluronan-b-poly(ε-caprolactone) (HA-PCL) using dialysis, yielding HA-PCL@(I-Hyp) nanoparticles (HP-NPs). HP-NPs were characterized in terms of size, stability, and drug release. Biodistribution and antitumor efficacy were evaluated in rodent models (nude mice and SRG rats bearing HT-29 subcutaneous tumors) with residual tumors induced by incomplete microwave ablation. HP-NPs showed 84.32% encapsulation efficiency, a uniform spherical shape with a hydrodynamic diameter of 75.66 nm, and rapid cytosolic degradation, enabling the release of I-Hyp in necrotic regions. After intravenous injection into animals with residual tumors, HP-NPs accumulated in tumor tissue through the enhanced permeability and retention effect and CD44/HA receptor-ligand interactions. The released I-Hyp remained selectively in necrotic areas, delivering localized β-radiation to the surrounding residual tumor tissue and significantly inhibiting tumor growth via induction of apoptosis. In conclusion, HP-NPs enable targeted radiotherapy to residual tumor tissue after ablation for colorectal metastases by leveraging necrosis avidity and CD44-mediated HA endocytosis, effectively reducing post-ablation tumor progression. This nanoplatform shows potential for clinical translation in colorectal metastasis treatment. - Source: PubMed
Publication date: 2025/11/07
Bao HanWang NingZhu XiaowenChen SongWang YangHan XiangjunZhong Hongshan - Melanoma is a highly aggressive skin cancer with biologically distinct subtypes. Acral melanoma (AM), a rare but particularly aggressive form, often presents with lymph node (LN) metastasis at diagnosis. Despite its clinical severity, the mechanisms underlying its metastatic behavior remain unclear. Emerging studies suggest the tumor microenvironment as a key driver of metastatic niche formation, but its specific role in AM progression is not well characterized. To investigate the role of the tumor microenvironment in AM progression, we performed single-cell RNA sequencing (scRNA-seq) on tumor tissues and matched adjacent normal samples from treatment-naïve AM patients, comparing cases with (LN) and without (LN) lymph node metastasis. Key transcriptomic findings were validated by immunofluorescence staining. Functional relevance was tested by conducting in vitro and in vivo assays. An independent validation cohort was employed to confirm key observations and evaluate prognostic associations. Our results reveal preferential SPP1 signaling pathways, including autocrine amplification within secreted phosphoprotein (SPP) 1 macrophages and their interactions with S100A8 melanoma cells via the SPP1-CD44 axis. S100A8 melanoma cells emerged as the predominant malignant subpopulation in LN metastatic tumors (56.3% versus 34.7% in non-metastatic cases). Clinically, elevated SPP1 expression emerged as an independent predictor of poor overall survival. In vivo, anti-SPP1 therapy induced a macrophage phenotype switch and significantly reduced tumor burden. Together, these findings indicate that LN AM is characterized by an SPP1 macrophage-driven immunosuppressive microenvironment and highlight the SPP1-CD44 axis as a promising therapeutic target for limiting AM dissemination. - Source: PubMed
Publication date: 2026/04/22
Liang YaoZheng YuliCai ZhimouShi ZhangruiShen MaoqiaYu RuixinWang FangCao XiaolongXu Rui