LRRC15 Antibody
- Known as:
- LRRC15 Antibody
- Catalog number:
- 36589
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- LRRC15 Antibody
Related genes to: LRRC15 Antibody
- Gene:
- LRRC15 NIH gene
- Name:
- leucine rich repeat containing 15
- Previous symbol:
- -
- Synonyms:
- LIB
- Chromosome:
- 3q29
- Locus Type:
- gene with protein product
- Date approved:
- 2003-04-25
- Date modifiied:
- 2015-08-27
Related products to: LRRC15 Antibody
Related articles to: LRRC15 Antibody
- Type II diabetes mellitus (T2DM) is one of the most prevalent diseases in the United States and is associated with diabetic foot ulcers (DFU) and their impaired, often chronic, wound healing. The T2DM mouse model with dysfunctional leptin receptor (db/db) has been used in basic and translational studies of wound healing due to its systemic phenotypes (hyperphagia, hypometabolism, obesity, T2DM) and its notable delayed skin wound healing. However, a characterization of the temporal cellular dynamics of the db/db wound healing model has not been performed, nor has the model been systematically compared to human DFUs. We performed the first comprehensive single-cell, multi-omic analysis of dermal cells in diabetic (db/db) compared to non-diabetic (ND) mice across three time points ranging from the inflammatory to the delayed proliferative and resolution phases of healing. Single-cell transcriptomics were uniquely linked to their corresponding cells' surface protein expressions of cell-specific receptors, including immune cells (CD45) such as neutrophils (CD11b, Ly6G), monocytes/macrophages (CD11b, F4/80, CD11c, Ly6C) and T lymphocytes (CD3, CD4), and dermal cells such as endothelial cells (CD31) and fibroblasts (CD26, CD140a), and showed high concordance between protein cell markers and their gene expressions in major cell types. Differential multi-omic analyses characterized two neutrophil ( Ly6G , Ly6G ), three monocyte/macrophage (F4/80 CD11b , Ly6c CD11b , CD11c CD11b ) and three fibroblast ( CD26 , CD140a , CD26 ) subtypes showing dysregulated dynamics across the time course of healing in db/db vs ND mice. Notably, NETotic Ly6G neutrophils and phagocytic F4/80 CD11b macrophage subtypes were drastically up-regulated in diabetic wounds. Differential cell-cell communication analyses revealed striking differences in crosstalk dynamics between fibroblast, macrophage and neutrophil subtypes in the early phase of healing, and ligand-receptor interactome analyses identified CD44 as the hub of dysregulated immune cell interactions in diabetic wounds, implicating cell adhesion, migration and inflammatory pathways, especially those mediated by ICAM1. Inhibition of CD44 using blocking antibodies in primary macrophages from db/db mice and via intradermal injections in db/db mice significantly normalized the early wound immune dysfunction, in part by inhibiting ICAM1 and reversing the excessive neutrophil influx into diabetic wounds. A new integrated dataset of single-cell human chronic wound studies revealed similar CD44-mediated immune cell dysfunctions in diabetic vs non-diabetic foot ulcers, pointing to CD44 as a promising therapeutic target for T2DM-associated chronic wounds. - Source: PubMed
Publication date: 2026/04/29
Wietecha Mateusz SPang JingboKang MiyaHafedi AvinWalsdorf SamanthaKeiser ShalynMaienschein-Cline MarkKoh Timothy J - Pneumonia remains a leading cause of global mortality. Conventional diagnostic approaches frequently fail to distinguish microbial colonization from true infection in the lower respiratory tract, complicating clinical decision-making and contributing to antibiotic overuse. Improved diagnostic strategies are urgently needed. In this prospective, single-center study, deep sputum specimens were collected from patients with respiratory colonization (n = 17) and infectious pneumonia (n = 27) admitted to the neurosurgical ICU of Huashan Hospital. Metagenomic next-generation sequencing (mNGS) and metatranscriptomic profiling were performed to characterize both the pulmonary microbiota and the host immune response. These features were subsequently integrated to construct a diagnostic model. Microbial community profiling revealed reduced alpha diversity and enrichment of metabolically active pathogenic taxa in the infection group, consistent with a dysbiotic state permissive to invasion. In contrast, the colonization group demonstrated a more balanced microbial ecosystem. Transcriptomic analyses identified 2232 differentially expressed host genes between the two groups. The colonization group showed marked activation of the Wnt, MAPK, chemokine, and focal adhesion pathways, which are functionally implicated in epithelial barrier maintenance and early immune homeostasis. A multi-omics diagnostic model incorporating seven gene features (ANKRD52, ZC3HAV1L, SERPINE3, CDPF1, ZNF720, TAGLN3, and LRRC15) achieved a discrimination between colonization and infection (AUC = 0.951 in the training cohort; 0.875 in the validation set). By jointly analyzing the pulmonary microbiome and host transcriptome, this study provides insight into host-microbe interactions distinguishing colonization from infection and presents a predictive model with potential clinical relevance. - Source: PubMed
Publication date: 2026/04/03
Fu ZhangfanSun YuhanYao HaijunLiu QihuiZhang QiranHu JinZhou YangJiang NingAi JingwenJin JialinZhang Wenhong - Microplastics are emerging contaminants that pose health risks. They can cause hepatic lipid interventions, but the underlying mechanisms require investigation. This study assessed the retention of polypropylene microplastics in mouse liver and determined the intercorrelations between hepatic lipid fluctuations and transcriptomic changes. Microplastic-induced liver dysfunction was confirmed by the variations of transamination, cholesterol metabolism, biotransformation, and redox state. Chronic high-dose treatment induced distinct pathological changes, including regional fibrotic remodeling and ultrastructural mitochondrial abnormalities. Raman biospectra of liver slice proposed vital peaks of 1060, 1132, 1168, 1340, 1446, 1618, and 1670 cm, representing the liver biomolecule landscapes. Transcriptomic changes were mainly involved in mRNA transcription, multicellular organism development, various stimuli response, cell differentiation, and lipid metabolic process. Microplastic exposure dosage exerted more profound effects than exposure duration on gene expressions of oxidation-reduction process, signal transduction, and lipid metabolism. WGCNA analysis proposed 47 hub genes involved gene expression orchestration, cell fate monitor, and mitochondria translation modulation. Nine differentially expressed genes associated with lipid biomarkers were related to mitochondria transcription ( and ), cell differentiation , and ), lipid catabolism ( and ) and tRNA methyltransferase (), and Raman peak at 1670 cm intimately connected with aggregated forms of protein. Our findings suggested that polypropylene microplastics could change the liver molecular landscape and induce lipid metabolism disorders and transcriptomic changes in mitochondrial protein translation and expression regulation, highlighting their significant consequences in nutrient and energy imbalance. - Source: PubMed
Publication date: 2025/10/29
Wang MiaoWang JingSun XinglinZhang KenaGao JingXu XiaoyingWu JiaruiTao FangfangZhang DayiLiu Mingying - Immune checkpoint inhibitors show insufficient efficacy against pancreatic ductal adenocarcinoma (PDAC). The tumor microenvironment (TME) has a remarkable influence on responsiveness to cancer immunotherapy. The aim of this study was to investigate immunosuppressive characteristics of TME in PDAC tissues. The flow cytometry (FCM) of PDAC surgical specimens revealed that the profile of tumor-infiltrating leukocytes was classified into myeloid cell- and T-cell-dominant subtypes; the myeloid subtype was associated with poorer patient outcomes. Myeloid-derived suppressor cells (MDSCs) showed the highest hazard ratio among various myeloid cell types. Single-cell RNA sequencing and FCM revealed that most MDSCs, but not lymphocytes, in PDAC tissues characteristically express CD74. Macrophage migration inhibitory factor (MIF), a CD74 ligand, was highly expressed in cancer-associated fibroblasts (CAFs) and cancer cells. Spatial transcriptomics demonstrated that the MIF-CD74 myeloid cell interaction was recognized in CAF-dominant areas in PDAC tissue. CAFs expressing immune suppressor molecules such as MFAP5 and LRRC15 were consistent with MIF CAFs. Furthermore, MIF CAFs enhanced the migratory activity of MDSCs and promoted MDSC induction and activation. In the murine model, MDSCs were significantly increased in MIF-expressing PDAC tumors, as were CD74 M-MDSCs per M-MDSC, confirming in vivo interaction between CD74 and MIF. MDSCs play a crucial role in creating an immunosuppressive TME in PDAC; the MIF-CD74 axis drives interactions between MDSCs and CAFs. - Source: PubMed
Publication date: 2026/02/20
Fukuda HironoriArai KosukeHashimoto EriSekine KeisukeArai YasuhitoHiraoka NobuyoshiHirata AyaYamashita MakikoNarumi KentaKikuchi AyakaSawai EriSawada YuriaSunami AyanaMizoguchi YukihiroSadahiro RyoichiAikawa YukikoHenmi YasukoOkumura GenkiSugiyama EriTakahashi MamiShibata TatsuhiroNishito YukariMizuno HideakiNara SatoshiEsaki MinoruKoyama ShoheiKitano ShigehisaYoshida TeruhikoOchiai AtsushiTsunoda HiroyukiAoki Kazunori - Joint function is impaired by disuse, as well as overuse. However, the underlying mechanisms remain unclear. Here, we elucidate the mechanisms of synovial and cartilage changes using a minimized mechanical stress (MMS) mouse model by combining knee joint immobilization and unloading. In this model, synovitis appeared by day 3, followed by subsequent fibrosis leading to joint contracture within two weeks. In contrast, articular cartilage degeneration developed gradually after the synovial alterations. Notably, synovial changes were attenuated by discontinuation of joint immobilization, while cartilage changes improved after discontinuation of joint immobilization and loading. Bulk RNA sequencing (RNA-seq) analyses supported the transcriptomic alterations for synovitis, fibrosis, and cartilage degeneration, and identified ten cytokines associated with cartilage changes. Single-cell RNA-seq (scRNA-seq) further identified distinct subsets in the MMS synovium: Lrrc15 myofibroblasts and Mmp9 macrophages, expressing many of these cytokines. Histological examination showed that MMS initially induced macrophage proliferation, while macrophage depletion by intra-articular administration of clodronate liposomes inhibited MMS-induced synovitis, fibrosis and cartilage degeneration, accompanied by a marked reduction in the MMS-distinct subsets. Our findings identified MMS-induced alterations in synovial cells and their roles in joint phenotype, suggesting that joint motion and mechanical loading contribute to the regulation of joint homeostasis. - Source: PubMed
Publication date: 2026/02/09
Ishikura HisatoshiOkada HiroyukiKin YotaChijimatsu RyotaHiguchi JunyaMiyahara JunyaTachibana NaohiroNagata KoseiTerashima AsukaYano FumikoOmata YasunoriSeki MasahideSuzuki YutakaBaron RolandTanaka SakaeSaito Taku