CD11b
- Known as:
- CD11b
- Catalog number:
- 10-211-C025
- Product Quantity:
- 0.025 mg
- Category:
- -
- Supplier:
- Exbio
- Gene target:
- CD11b
Related genes to: CD11b
- Gene:
- ITGAM NIH gene
- Name:
- integrin subunit alpha M
- Previous symbol:
- CR3A, CD11B
- Synonyms:
- MAC-1, CD11b
- Chromosome:
- 16p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1988-08-05
- Date modifiied:
- 2019-04-23
Related products to: CD11b
Related articles to: CD11b
- Lactic acid metabolism and neutrophil extracellular traps (NETs) are critical immune regulators, yet their specific crosstalk in systemic lupus erythematosus (SLE) and lupus nephritis (LN) pathogenesis remains poorly understood. Here, by integrating bulk and single-cell RNA sequencing (scRNA-seq) analyses, we identified and as pivotal upregulated genes in SLE, demonstrating robust diagnostic value (AUC >0.7) supported by reliable nomogram models. Additional analysis of a human LN renal biopsy dataset (GSE32591) showed increased ITGAM and TKT in LN glomerular samples, supporting their renal relevance. Regulatory network analyses suggested potential molecular interactions involving these genes with specific microRNAs (e.g., hsa-miR-142-5p-ITGAM and hsa-miR-1-3p-TKT), while scRNA-seq analysis suggested cell-type-associated expression patterns, with donor-level analysis showing higher TKT expression in monocytes from SLE patients. To translate these computational insights into biological relevance, we conducted rigorous validations. In an apoptotic cell-induced LN mouse model, we confirmed renal injury, increased ITGAM and TKT protein expression, and enrichment of TKT in CD14 monocyte-lineage cells. Crucially, targeted pharmacological inhibition of TKT using oxythiamine significantly mitigated disease progression in LN mice. Oxythiamine treatment not only restored renal function and attenuated tissue fibrosis but also reprogrammed aberrant lipid metabolism and cellular proliferation. Oxythiamine treatment was further associated with reduced ITGAM expression and lower renal Cit-H3 levels, consistent with an attenuation of NET-associated inflammatory activity. Together, our integrated multi-omics and data indicate that TKT is closely linked to immunometabolic remodeling in experimental lupus nephritis, accompanied by alterations in lactate accumulation, ITGAM expression, and NET-associated inflammatory activity. These findings support TKT-associated metabolic remodeling as a potential therapeutic avenue that warrants further mechanistic investigation in LN. - Source: PubMed
Publication date: 2026/07/01
Zhu LitongLin TaoyanCheong Lai YeeChui An Ying ChristyChan Tak MaoYap Desmond Y H - MicroRNAs have been widely demonstrated to participate in the pathogenesis of cerebrovascular diseases. In this study, an in vitro cellular oxygen-glucose deprivation/reoxygenation (OGD/R) model was established in mouse BV2 microglial cells, and differentially expressed microRNAs (DEMs) were screened by small RNA sequencing. The significant downregulation of miR-714 during OGD/R process was confirmed and its effects was verified by CCK-8 and apoptosis assays. MSC-derived exosomes (MSC-exo) were used to transport miR-714, and the mRNA expression level and cellular uptake of miR-714 were detected by qRT-PCR and fluorescence microscopy, respectively. The effects of MSC-exo-miR-714 on the proliferation and apoptosis of OGD/R BV2 cells were evaluated by CCK-8, Annexin V-FITC/PI double staining and TUNEL assays. In addition, bioinformatics analysis was performed to predict the target genes of miR-714. qRT-PCR and Western blotting were used to verify the regulatory effects of MSC-exo-miR-714 on ITGAM (integrin subunit alpha M) at mRNA and protein levels. The potential anti-inflammatory mechanism was further explored using gene enrichment analysis and Western blotting. The results showed that MSC-exo-miR-714 could significantly promote proliferation, inhibit apoptosis, and reduce protein expression of IL-6, IL-1β, TNF-α, NF-κB, and p-NF-κB in OGD/R-injured BV2 cells by directly targeting ITGAM. In conclusion, miR-714 is significantly down-regulated under in vitro OGD/R injury and serves as a key regulator in BV2 microglial injury. MSC-exo-miR-714 protects glial cells against OGD/R damage in vitro by directly targeting ITGAM and inhibiting inflammatory signaling. These findings are limited to the in vitro setting, and further in vivo validation is required. - Source: PubMed
Publication date: 2026/07/15
Yang Xiao-XiaWang Yong-JieXue Ai-YingXue XiaSun De-Qing - Percutaneous coronary intervention, such as stenting, restores coronary perfusion after myocardial ischemia but also induces ischemia-reperfusion (I/R) injury, in part driven by innate immune activation. Here, we identified Toll-like receptor 7 (TLR7), an endosomal sensor of single-stranded RNA, as a key mediator of postischemic inflammation. Genetic deletion or pharmacologic inhibition of TLR7 with enpatoran reduced inflammation and myocardial infarction (MI) size and improved cardiac function 24 hours after I/R in mice. Single-nucleus RNA sequencing demonstrated coordinated induction of TLR7-responsive inflammatory endothelial and myeloid cell programs, including increased endothelial ITGAM expression and leukocyte adhesion. TLR7/8 activation promoted ITGAM-dependent endothelial-leukocyte interactions under shear stress, whereas ITGAM blockade reduced immune cell infiltration and limited MI injury. These findings identify the TLR7-ITGAM signaling axis as a central driver of endothelial-leukocyte crosstalk in myocardial I/R injury and support TLR7 inhibition as a promising therapeutic strategy to mitigate ischemic MI after percutaneous coronary intervention. - Source: PubMed
Publication date: 2026/07/14
Li YijiaYang YangPark ChanheeRen BoyangLi RuoxingShetty AmolWilliams BrittneyLi ZiyiZou LinChao Wei - Volatile anesthetics, particularly sevoflurane, have demonstrated cardioprotective properties during cardiac surgery. However, their immunomodulatory mechanisms at the molecular level remain unclear. Given the close relationship between cardiac injury and immune responses, understanding how anesthetic agents influence immune-related pathways may provide new insights into perioperative myocardial protection. This study aimed to explore the immunological and molecular mechanisms underlying the effects of sevoflurane anesthesia on cardiomyocytes in patients undergoing coronary artery bypass grafting (CABG). Gene expression data (GSE4386) from myocardial tissues of CABG patients anesthetized with sevoflurane or propofol were analyzed. Differentially expressed genes (DEGs) were identified using R software, followed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses. Protein-protein interaction networks were constructed to identify key immune-associated hub genes. A total of 211 DEGs were identified. Functional enrichment revealed that these genes were predominantly associated with immune and inflammatory processes, including leukocyte activation, cytokine-cytokine receptor interaction, neutrophil extracellular trap formation, and chemokine signaling pathways. Hub genes such as ITGAM, PTPRC, TYROBP, TLR2, and TLR4 were identified as central immune regulators potentially mediating the cardioprotective and immunomodulatory effects of sevoflurane. Sevoflurane anesthesia may confer myocardial protection after CABG by modulating immune-related signaling pathways and inflammatory gene expression. These findings highlight the immunoregulatory potential of volatile anesthetics, providing novel perspectives for immune-targeted strategies in perioperative cardiac management. - Source: PubMed
Publication date: 2026/06/03
Liu WeimingLiu Mengyuan - Blood-based biomarkers are increasingly recognized as promising tools for the diagnosis and monitoring of neurodegenerative diseases, offering a minimally invasive alternative to cerebrospinal fluid (CSF) testing. We evaluated the analytical performance and clinical utility of the Olink Target 48 Neurodegeneration panel, a novel multiplex proteomic platform based on the proximity extension assay (PEA) technology, in a large, clinically diverse dementia cohort. - Source: PubMed
Publication date: 2026/07/11
Bentivenga Giuseppe MarioMammana AngelaBaiardi SimoneVittoriosi EricaMastrangelo AndreaRuggeri EdoardoVargiu Claudia MarinaPolischi BarbaraStanzani-Maserati MichelangeloRizzo GiovanniPantieri RobertaRaggi AlbertoCapellari SabinaParchi Piero