S100A9 monoclonal antibody (M13), clone 1C22
- Known as:
- S100A9 mab (anti-) (M13), clonality 1C22
- Catalog number:
- H00006280-M13
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Abno
- Gene target:
- S100A9 monoclonal antibody (M13) clone 1C22
Related genes to: S100A9 monoclonal antibody (M13), clone 1C22
- Gene:
- ADH5P4 NIH gene
- Name:
- ADH5 pseudogene 4
- Previous symbol:
- ADH5B
- Synonyms:
- bA707M13.2
- Chromosome:
- 6q12
- Locus Type:
- pseudogene
- Date approved:
- 2003-11-26
- Date modifiied:
- 2019-01-18
- Gene:
- ARHGAP42 NIH gene
- Name:
- Rho GTPase activating protein 42
- Previous symbol:
- TMEM133
- Synonyms:
- FLJ32810, GRAF3, AD031
- Chromosome:
- 11q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2010-04-28
- Date modifiied:
- 2017-11-20
- Gene:
- C1QTNF12 NIH gene
- Name:
- C1q and TNF related 12
- Previous symbol:
- C1QDC2, FAM132A
- Synonyms:
- MGC105127, CTRP12, ADIPOLIN
- Chromosome:
- 1p36.33
- Locus Type:
- gene with protein product
- Date approved:
- 2005-09-27
- Date modifiied:
- 2018-11-15
- Gene:
- CD163 NIH gene
- Name:
- CD163 molecule
- Previous symbol:
- -
- Synonyms:
- M130, MM130, SCARI1
- Chromosome:
- 12p13.31
- Locus Type:
- gene with protein product
- Date approved:
- 2000-01-18
- Date modifiied:
- 2016-10-05
- Gene:
- CEACAMP6 NIH gene
- Name:
- carcinoembryonic antigen related cell adhesion molecule pseudogene 6
- Previous symbol:
- CGM13
- Synonyms:
- -
- Chromosome:
- 19q13.2
- Locus Type:
- pseudogene
- Date approved:
- 1994-11-04
- Date modifiied:
- 2016-01-14
Related products to: S100A9 monoclonal antibody (M13), clone 1C22
Related articles to: S100A9 monoclonal antibody (M13), clone 1C22
- Renal interstitial fibrosis is a key pathological feature associated with the progression of chronic kidney disease (CKD) progression. Macrophages play a central role in renal inflammation and fibrosis, and the S100 calcium binding protein A8/A9 (S100A8/A9) protein that they express participates in the immune response as an important regulatory inflammatory factor. Therefore, this study aimed to investigate the role of S100A8/A9 in M2-driven macrophage-to-myofibroblast transition (MMT) during progressive fibrosis in patients with CKD. We analyzed renal biopsy tissues from patients with CKD, constructed S100A9 overexpression and macrophage-specific knockdown mouse models, and developed an in vitro transforming growth factor β1 (TGF-β1)-induced MMT cell model. Our results revealed that S100A8/A9 was significantly upregulated in fibrotic kidneys and was mainly expressed in CD68/F4/80 macrophages with an MMT phenotype. Further experiments demonstrated that S100A9 knockdown significantly reduced renal interstitial fibrosis, collagen deposition, and tissue damage in mice with unilateral ureteral obstruction (UUO), and inhibited MMT. Conversely, S100A9 overexpression exacerbated the fibrotic phenotype. Moreover, both in vitro and in vivo, knockdown of S100A9 or pharmacological inhibition with the S100A8/A9 inhibitor paquinimod blocked the activation of the toll-like receptor 4 (TLR4)/ myeloid differentiation primary response gene 88 (MyD88)/ nuclear factor kappa-B (NF-κB) signaling pathway, reduced M2 macrophage polarization, and attenuated MMT. These findings suggest that S100A8/A9 may drives M2 macrophage-mediated MMT via the TLR4/NF-κB pathway, thereby promoting renal fibrosis. Therefore, targeting S100A8/A9 may represent a promising approach for the treatment of renal fibrosis in CKD. - Source: PubMed
Publication date: 2026/04/16
Chen XulongZha WeiweiShen JiangwenLi LinFu YanfangTian PuXunZheng BingxuanLi Cheng - Acute ulcerative colitis elevates the risk of plaque rupture in patients with atherosclerosis, potentially triggering acute cardiovascular events. Clinical treatment strategies capable of simultaneously alleviating colitis and stabilizing atherosclerotic plaques are still lacking. Extracellular traps have been observed within atherosclerotic plaques in patients with myocardial ischemia. Given the crucial role of macrophages in the formation and progression of plaques, whether macrophage extracellular traps (METs) significantly contribute to the stability of atherosclerotic (AS) plaques during acute inflammation remains unclear. Curcumin exhibits lipid-lowering and anti inflammatory properties; however, its potential to stabilize AS plaques under inflammatory conditions and its specific effects on METs have yet to be elucidated. This study aims to investigate whether curcumin can stabilize atherosclerotic plaques in an acute inflammatory state and to explore its underlying mechanisms. Curcumin treatment significantly reduced the necrotic core of unstable plaques and increased collagen content in atherosclerotic mice with ulcerative colitis, thereby markedly stabilizing the plaques. Curcumin inhibited TLR4 activity and the production of inflammatory cytokines, including TNF-α, IL-6, IL-1β, S100A8, and S100A9. It also suppressed PAD4 activation, leading to decreased formation of macrophage extracellular traps (METs) and downregulated expression of collagen-degrading matrix metalloproteinase 9 (MMP9). Our findings suggested that curcumin enhances the stability of atherosclerotic plaques under acute inflammatory conditions by attenuating METs formation and reducing inflammation through suppression of TLR4/PAD4, shedding new light on its anti-atherosclerotic mechanism and providing a novel treatment for inflammatory comorbidity. - Source: PubMed
Publication date: 2026/04/16
Li XintongQiu TianleWei YingxueLi QiuruiQiu JingwenDu Ronghui - Ocular rosacea (OR) is a chronic inflammatory disease of the ocular surface frequently associated with meibomian gland dysfunction (MGD), with limited therapeutic options and an underexplored pathophysiology. Here, we uncover the pivotal role of mineralocorticoid receptor (MR) pathway overactivation in driving MGD and OR. Analysis of eyelid tissues from OR patients revealed increased MR expression and altered local corticosteroid metabolism, associated with inflammation, fibrosis, and impaired meibocyte renewal. Using a transgenic rat model overexpressing human MR, we demonstrate that MR overactivation initiates subclinical MGD and, with aging or ultraviolet-B exposure, drives a full OR-like phenotype characterized by gland dropout, oxidative and mitochondrial stress, immune infiltration, epithelial barrier disruption, and secondary corneal damage. Cross-species transcriptomic integration of rat, human MGD, and rosacea datasets identified a conserved MR-dependent gene signature, highlighting S100A9 as a specific downstream target and biomarker of MR activation. Local pharmacological MR antagonism suppressed S100A9 expression. These findings establish MR overactivation as a unifying pathogenic driver of MGD and OR and identify MR blockade as a promising therapeutic strategy, with S100A9 as a candidate biomarker for patient stratification and treatment monitoring. - Source: PubMed
Publication date: 2026/04/16
Zhu LinxinYesilirmak NiluferRodrigues-Braz DanielaGélizé EmmanuelleLheure CoralieMorel XavierBourges Jean-LouisJaisser FrédéricZhao MinBehar-Cohen Francine - Myelodysplastic neoplasms (MDSs) are clonal disorders characterized by ineffective hematopoiesis, dysplasia, and a risk of transformation into acute myeloid leukemia. MDS is also associated with a higher incidence of osteoporosis, suggesting a complex interplay between hematopoiesis, the bone marrow (BM) microenvironment, and bone homeostasis. Targeting inflammation has emerged as a promising therapeutic strategy, particularly in lower risk MDS. Tasquinimod (TASQ) is a small-molecule inhibitor of the inflammatory alarmin S100A9, blocking its interaction with TLR4 and RAGE receptors. We investigated the efficacy of TASQ in modulating inflammation and improving disease phenotype using in vitro and in vivo MDS models. Immunofluorescence staining of human BM identified neutrophils and macrophages as primary S100A9 sources. Exposure of mesenchymal stromal cells (MSCs) to S100A9 induced Toll-like receptor 4 (TLR4) downstream signaling, resulting in increased expression of IRAK1, NF-κB-p65, interleukin-1β (IL-1β), IL-18, caspase 1, and PD-L1. These effects were effectively abolished by TASQ. Additionally, TASQ restored the disturbed MSC-mediated hematopoietic support, as demonstrated by increased numbers of cobblestone area-forming cells and colony-forming units. In NHD13 MDS mice, TASQ (30 mg/kg, 12 weeks) improved hemoglobin and red blood cell counts, but exerted no effect in wild-type (WT) mice. Additionally, TASQ improved bone microarchitecture by increasing trabecular number and bone volume, likely a result of reduced osteoclast activity. Our findings suggest that TASQ mitigates inflammasome activation in the MDS BM, improving erythropoiesis and bone health. These results provide a necessary preclinical basis for clinical trials in lower risk MDS patients, in whom anemia and osteoporosis often coexist. - Source: PubMed
Publication date: 2026/04/14
Wobus ManjaWeidner HeikeWehner RebekkaBaumann Anna-LenaMöbus KristinBalaian EkaterinaTörngren MarieVahtola ErikEriksson HelenaWinter SusannPlatzbecker UweChavakis TriantafyllosHofbauer Lorenz ChristianRauner MartinaBornhäuser MartinSockel Katja - Aging is the most important risk factor for Parkinson's disease (PD). S100A9, a calcium-binding protein, is closely related to a variety of aging-related diseases, but its role in the pathogenesis of PD is still unclear. This study aims to investigate the role of S100A9 in aging-related mechanisms in PD. C57BL/6J mice were intraperitoneally injected with 1-methyl-4-phenyl-1,2,3, 6-tetrahydropyridine (MPTP; 15 mg/kg four times daily), followed by Paquinimod (a S100A9 inhibitor; 7 mg/kg, once a day for 7 days after model establishment, totaling 8 doses). We found that MPTP induced significant motor deficits and dopaminergic nerve damage, accompanied by up-regulation of p21 expression, down-regulation of Lamin B1 expression, and significant increases in SASP factors such as MMP9, IL-1α, IL-1β, and IL-6. Treatment with recombinant S100A9 protein induced senescence-like molecular alterations and reduced expression of mitochondrial biogenesis-associated genes in astrocytes in vitro. Inhibition of S100A9 effectively improved movement disorders, restore TH-positive fiber density, reduce the expression of cell senescence markers and SASP factors, and up-regulate mitochondrial function-related genes. Studies have shown that S100A9 plays a key bridge between aging and neurodegeneration in PD. Inhibition of S100A9 may be a potential therapeutic strategy to alleviate cell senescence and mitochondrial damage in PD. - Source: PubMed
Publication date: 2026/04/13
Tan Lu-LuMa Xiao-YuXia Yi-MengLi TingLi Ming-AnWu JianNie XinHuang Shu-BingCui ChunZhao Wei-JiangQiao Chen-MengShen Yan-Qin