Ask about this productRelated genes to: POSTN antibody
- Gene:
- POSTN NIH gene
- Name:
- periostin
- Previous symbol:
- -
- Synonyms:
- OSF-2, PN, periostin
- Chromosome:
- 13q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-02-10
- Date modifiied:
- 2016-04-05
Related products to: POSTN antibody
Related articles to: POSTN antibody
- Chronic heart failure (HF) remains a global health challenge due to the lack of therapies that effectively disrupt the pathological fibro-inflammatory networks driving disease progression. While current nanomedicine strategies often target intracellular pathways in isolated cell types, they overlook the multicellular crosstalk central to HF. Here, we develop scalably synthesized Prussian blue (PB) nanoparticles that selectively intercept the CCL2-CCR2 chemokine axis, a key pathway in fibroblast-macrophage communication. Single-nucleus RNA sequencing of murine and human failing hearts identifies a conserved pro-fibroinflammatory cardiac fibroblast subpopulation (POSTN CCL2) that recruits CCR2 macrophages via CCL2 secretion. PB nanoparticles exhibit ultrahigh affinity (K = 1.11 × 10 m) for free CCL2, inducing conformational distortion in its N-terminal domain via specific C≡N interface interactions with CRS1 residues, thereby blocking CCR2 engagement, a mechanism distinct from conventional nanomaterials. Although ineffective in monocultures, PB nanoparticles robustly improve cardiac function and remodeling in murine and translational porcine pressure-overload HF models, reducing left ventricular end-diastolic volume by 56.2% and fibrosis by 40.5%, while selectively depleting CCR2 macrophages without systemic immunosuppression. Supported by scalable production (> 100 g/batch), long-term stability, and biosafety, this work establishes a cell communication-targeting nanomedicine strategy for network-driven diseases like HF. - Source: PubMed
Publication date: 2026/04/24
Chen BoWei GaoZeng GuoweiLi HaoyuWu RongrongYan HongyuZhou ZijieLuo KaiZhang XiaoyangLi CongHuang LongmingCheng LingyanZhang XinjieZheng JinghaoShi BozhongCai XiaojunHe Xiaomin - Muscle fibrosis is a key pathological feature of Duchenne muscular dystrophy (DMD) and is closely associated with disease progression. Fibroadipogenic progenitors (FAPs) are major contributors to fibrosis, yet the precise mechanisms remain unclear. To investigate FAP dynamics and lineage specification, we generated dual-reporter mice (PRURD2) by crossing D2.B10-Dmdmdx/J (D2-mdx) mice with FAP and brown/beige adipose tissue (BAT) reporter lines. Corresponding control mice (PRURDBA) were established on the DBA/2J background. At 12 months, heart, diaphragm, and tibialis anterior (TA) muscles were collected for histological analysis. FAPs were isolated via FACS and subjected to single-cell RNA sequencing. PRURD2 mice exhibited increased fibrosis across all muscles compared to controls ( < 0.01) and a significant rise in PDGFRα-GFP + FAPs ( < 0.05). UMAP clustering identified 11 distinct FAP subpopulations, with the fibrosis-associated CD55 cluster enriched in PRURD2 mice. Pseudotime analysis showed lineage progression from progenitor clusters toward the fibrogenic CD55 cluster. CellChat analysis indicated increased interactions in PRURD2 mice involving fibrosis-related pathways like COLLAGEN, TGF-β, WNT, NOTCH, and ANGPTL. Additionally, fibrosis-related signaling pathways such as THY1, TWEAK, EPHA, EPHB, and SEMA6 showed increased interactions among FAP clusters in PRURD2 mice. Differential gene expression analysis revealed top upregulated genes including , , and . PRURD2 mice develop severe fibrosis in skeletal and cardiac muscle, driven by FAP-induced signaling pathways and genes. This model is valuable for understanding muscle fibrosis in DMD and developing anti-fibrotic therapies. - Source: PubMed
Publication date: 2026/04/24
Fusagawa HiroyoriLau JustinSharma SankalpLiu MengyaoSamimi YusefFranchet-Schaer GabrielFang AshleyFusagawa MinamiKim HubertFeeley Brian TLiu Xuhui - High serum periostin is linked to an increased risk of osteoporotic fractures in postmenopausal women. However, the relationships between serum periostin and bone microarchitecture, particularly muscle mass, and muscle function remain unclear. This study aims to investigate the relationships between serum periostin and bone mineral density, bone microarchitecture, muscle mass and function, falls, and fractures in community-dwelling Chinese postmenopausal women. - Source: PubMed
Publication date: 2026/04/07
Gong YiyiWu YushuoMa XiaosenCui LijiaLi XiangPang QianqianChi YueJiajue RuizhiLiu WeiWang OuLi MeiXing XiaopingZhang ZaizhuYu WeiJiang YanXia Weibo - Therapeutic mesenchymal stromal cells (MSCs) promote healing in severe injuries like skin burns. However, expansion on stiff culture surfaces activates MSCs into scar-promoting myofibroblasts. We previously introduced 'mechanical memory' to describe how MSCs primed on scar-stiff surfaces retain myofibroblast traits even after switching to softer, skin-like surfaces. Now, we identify mechanisms and factors that suppress myofibroblast activation during priming in soft cultures. These 'soft memory' factors are poised to preserve MSC regenerative features while preventing fibrogenesis. Mechanically primed MSCs were compared via RNA- and ATAC-sequencing to co-analyze gene transcription and chromatin accessibility. Highly accessible promoters of genes upregulated after soft priming, which retained this pattern after transitioning to stiff surfaces, were enriched for HOXA11 transcription factor binding motifs. Knocking down HOXA11 increased osteogenic gene expression in soft-primed MSCs and reduced anti-fibrotic factors, including the transcription factor SALL1, which suppresses pro-fibrotic genes like Postn, Col8a1, Grem2, Thbs1, Thbs2, and Gata6. We identify GATA6 as a keeper of stiff-induced myofibroblast memory after switching to soft surfaces. Manipulating the SALL1-GATA6 circuit yielded therapeutic MSCs that suppressed fibrosis in a hypertrophic skin-scarring animal model. Therefore, controlling myofibroblast memory could improve MSC-based organ repair therapies. - Source: PubMed
Publication date: 2026/04/22
Younesi Fereshteh SadatMiller Andrew EDiao LiGuo XinyingAndonian NatalieKarimizadeh ElhamBarker Thomas HHinz Boris - Esophageal cancer (EC) is a common gastrointestinal cancer with the highest mortality. Studies have suggested that macrophages play a key role in cancer progression. Increasing evidence reveals that periostin (POSTN) is associated with the physiological and pathological processes in EC. However, the upstream mechanisms of POSTN on EC cell oncogenic properties and macrophages are still vague. - Source: PubMed
Publication date: 2026/04/22
Ding HaoLiu GuanchuRan XingqiangYang BoFu Maoyong