Rat Anti-Mouse CD90 Thy-1
- Known as:
- Rat Antibody toMouse CD90 Thy-1
- Catalog number:
- 128-10059-1
- Product Quantity:
- 500
- Category:
- -
- Supplier:
- Ray Biotech
- Gene target:
- Rat Anti-Mouse CD90 Thy-1
Related genes to: Rat Anti-Mouse CD90 Thy-1
- Gene:
- THY1 NIH gene
- Name:
- Thy-1 cell surface antigen
- Previous symbol:
- -
- Synonyms:
- CD90
- Chromosome:
- 11q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2015-07-22
Related products to: Rat Anti-Mouse CD90 Thy-1
Related articles to: Rat Anti-Mouse CD90 Thy-1
- Long-term exposure to ambient particulate matter ≤2.5 μm in aerodynamic diameter (PM2.5) has been associated with optic neuropathy and retinal neurodegeneration, but experimental evidence remains limited. We assessed two certified environmental particulate reference materials in primary mouse retinal cells and after repeated ocular-surface exposure in mice. For the in vitro analyses, technical replicate wells were first averaged within each independent cell isolation, and each experimental condition was then normalized to the corresponding control from the same biological replicate. Particulate exposure produced condition-dependent changes in 2',7'-dichlorofluorescin diacetate (DCFDA) fluorescence and ATP-dependent viability, with statistically significant effects concentrated in selected retinal glial-cell conditions. After within-experiment normalization and multiplicity adjustment, direct comparisons did not demonstrate a statistically significant protective effect of α-tocopherol or N-acetylcysteine on particulate-associated responses, and retinal glial-cell coculture did not significantly improve RGC survival relative to monoculture. In postnatal mice, topical particulate administration was associated with inner retinal thinning and lower RGC-marker-positive cell counts. In adult Thy1-CFP mice, neither sample-specific nor post hoc pooled within-mouse comparisons with contralateral saline-treated eyes were statistically significant. A separate post hoc exploratory between-animal comparison showed fewer CFP-positive cells in pooled particulate-treated eyes than in independent bilateral-saline controls (mean difference, -14.4 cells; 95% CI, -28.1 to -0.7; P = 0.040). These findings support cellular and retinal susceptibility under the conditions used, but they do not establish particle transport to the retina, a causal oxidative mechanism, or quantitative risk from ambient PM2.5 exposure in humans. - Source: PubMed
Publication date: 2026/08/26
Chen WanjingIizuka YokoMabuchi FumihikoYoshizawa SatokoMuramatsu TomokoKashiwagi Kenji - The ventral hippocampus (vHPC) itself or its input pathways can directly influence behaviors related to anxiety and depression. Cofilin 1, as a member of the actin-depolymerizing factor/cofilin (ADF/cofilin) family, participates in dendritic spine remodeling, thereby influencing depression-like behaviors. - Source: PubMed
Publication date: 2026/09/04
Yu Zong-HaoChen GengGe Ming-JunZhang Zhen-QiangShen Jun-XianPan ChuanHan FeiLu Ya-PingXu Hui - Vascular plasticity is a crucial biological asset enabling our bodies to rapidly adapt to infections and acute inflammation. However, repeated insults during chronic disease can result in these vascular adaptations becoming irreversible, thereby driving disease progression and fibrosis. This study aimed to understand if phenotypic changes in endothelial cell (EC) identity could be indicative of progressive fibrosis and thereby offer diagnostic and therapeutic opportunities for patients with metabolic dysfunction-associated steatotic liver disease (MASLD). We integrated high-resolution imaging, proteomic and transcriptomic analysis which collectively highlighted a central role for endothelial-to-mesenchymal transition (EndMT)-induced EC plasticity in the derivation of 'fibrosis-associated' EC (FAEC). We demonstrated that: 1) full spectrum flow cytometry can provide new opportunities to categorize and phenotype EC subpopulations, 2) two distinct EndMT-derived FAEC subpopulations expanded during fibrogenesis; THY1.2+ICAM1+ and TAGLN+MCAM+ EC that displayed unique immunomodulatory and metabolic phenotypes, 3) TAGLN+ FAEC are a conserved, pro-fibrotic cell type that arose at early stages of MASLD, and 4) increased hepatic expression of TAGLN was significantly associated with detrimental patient outcomes at all stages of liver disease. This study paves the way for the development of FAEC-specific diagnostic and therapeutic approaches to tackle progressive fibrotic disease. - Source: PubMed
Publication date: 2026/09/01
Gkantsinikoudi ChristinaDignam Joshua PKumar RajuJokl ElliotRana MeenakshiLi WenhaoSamus MarynaLandi StephanieAthwal Varinder SKendall Timothy JRot AntalFallowfield Jonathan APiper Hanley KarenAlazawi WilliamDufton Neil P - The pathobiology of multiple myeloma is influenced by cells of the bone marrow, but whether tumor support is organized in a spatially-defined tumor microenvironment (TME) remains unclear. Using spatial transcriptomics and imaging mass cytometry, we show that myeloma cells initially exist as scattered cells throughout the marrow, yet with disease evolution condense into a spatially-defined TME. Dense tumor nodules contain a cellular ecosystem distinct from the surrounding marrow, enriched for macrophages, conventional dendritic cells, and CD8⁺ T cells, as well as endothelial cells and THY1⁺ mesenchymal stromal cells. Conversely, neutrophil lineage cells are absent from this TME but interact with scattered myeloma cells outside of dense nodules. Presence of the dense tumor architecture at diagnosis confers a worse prognosis, emphasizing the relevance of spatial organization of the bone marrow. Together, these findings define a discrete spatial and cellular myeloma TME, that provides spatially-guided insights into patient stratification and disease pathobiology. - Source: PubMed
Publication date: 2026/09/01
Koops MarnixBertamini LucaPapazian NatalieKorst CharlotteBudai Mátyás JánosHoogenboezem Remco MSanders Mathijs Avan der Holt Bronnovan Duin MarkBroijl AnnemiekBalogh PéterZweegman SonjaRaaijmakers Marc Hgpvan de Donk Niels W C JKellermayer ZoltánSonneveld PieterCupedo Tom - Pulmonary fibrosis (PF) is a progressive and fatal lung disorder driven by abnormal fibroblast activation and excessive extracellular matrix (ECM) deposition, leading to structural and functional decline. Existing therapies can slow progression but fail to interrupt fibrotic remodeling. Here, we engineered HUCMSC-Lipo, an inhalable biomimetic formulation fusing human umbilical cord mesenchymal stem cell (HUCMSC) membranes with artificial phospholipids, with formulation parameters systematically optimized using a Bayesian optimization (BO) framework to ensure structural stability and nebulization compatibility. HUCMSC-Lipo maintained membrane functionality and structural integrity for effective nebulized delivery. We successfully established a non-human primate (NHP) PF model and innovatively developed a multidimensional evaluation framework. Utilizing a range of methods, including but not limited to positron emission tomography/computed tomography (PET/CT) molecular imaging with radiolabeled fibroblast activation protein (FAP) inhibitors, we confirmed that HUCMSC-Lipo suppressed fibrotic progression and restored pulmonary function by targeting the regulation of fibroblast activation. Mechanistically, THY-1 enrichment in HUCMSC-Lipo bound integrin receptors to block the FAK/PI3K signaling cascade and restore fibroblast mechanosensitivity, fundamentally turning off the pathological activation "switch" in fibroblasts. Our work presents an inhalable biomimetic formulation that combines therapeutic efficacy with synthetic accessibility, offering a mechanism-targeted approach to PF treatment with strong clinical translatability. - Source: PubMed
Publication date: 2026/08/04
Zhao FangyuSun YigeWang HaoranHou DayongZhang RuiXia WenjingZhang YongchenLi LuyaoZhao XueqiWang KaiqiPan WenwenWang JiannanWang KaiYang LiliChen WeiLi XinNong ChunyangLu HuiyingZhang YiZhang ZhaoyangWu LinaHan ZhaoguoTang Ben-ZhongSun Xilin