Ask about this productRelated genes to: HABP2 antibody
- Gene:
- HABP2 NIH gene
- Name:
- hyaluronan binding protein 2
- Previous symbol:
- -
- Synonyms:
- HABP, PHBP, HGFAL, FSAP
- Chromosome:
- 10q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 1996-11-15
- Date modifiied:
- 2014-11-19
Related products to: HABP2 antibody
Related articles to: HABP2 antibody
- Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by synovial inflammation, cartilage degradation, and bone erosion. The diseases also involves pathological changes in the surrounding fascial tissues that lead to persistent pain. Current clinical treatments rely primarily on non-steroidal anti-inflammatory drugs and analgesics, which often have limited efficacy and potential side effects. Manual acupuncture (MA), a traditional therapeutic modality, has shown promising effects in alleviating RA-related symptoms. However, the underlying mechanisms remain largely unclear. Fibroblasts, which are known for their mechanosensitivity and immunomodulatory functions, may play a crucial role in mediating the therapeutic effects of acupuncture. In this study, we demonstrated that MA significantly ameliorated pathological changes in joint-associated fascia in a murine model of adjuvant-induced arthritis with minimal impact on bone and cartilage morphology. Post-acupuncture analysis revealed the upregulation of extracellular matrix (ECM)-related genes and proteins, such as fibromodulin, collagen I, and hyaluronan synthase 2, along with increased expression of mechanosensitive molecules, including Piezo1, Ras homolog family member A (RhoA), and Yes-associated protein 1 (YAP1). Moreover, local changes were observed in the expression of fibroblast-associated markers including Fibroblast Growth Factor 2 (FGF-2), Fibroblast Growth Factor 7 (FGF-7), Fibroblast-Specific Protein 1 (FSP-1), Cannabinoid Receptor 2 (CB2), and Proliferating Cell Nuclear Antigen (PCNA). Notably, selective ablation of fibroblasts in the acupoint area via recombinant adeno-associated virus -mediated apoptosis significantly attenuated the analgesic effect of acupuncture, accompanied by reduced collagen fiber deposition, decreased mast cell degranulation, and downregulation of ECM components and regulatory molecules, such as Hyaluronan Binding Protein 2 (HABP2) and CB2. In conclusion, the study findings suggest that acupuncture alleviates RA-induced pathological and pain responses by activating fibroblasts in the fascial tissue. This mechanotransduction process likely involves the downstream modulation of cannabinoid receptors and ECM-related proteins, including hyaluronic acid and collagen. - Source: PubMed
Publication date: 2026/01/22
Tu Shi-WeiKawanokuchi JunTakagi KenLiu Yang-YangLi Jun-YiDeng Kai-YuanLi Yan-WeiYao Kai-FangChen Zhi-HanFan Ze-ZhiXu Zhi-FangSa Yu-PingLin Xiao-WeiWang Shen-JunFang Yu-XinLiu XiaMa NingGuo Yi - Factor VII activating protease (FSAP) can be activated by damaged or necrotic cells and plays a role in coagulation and inflammation. - Source: PubMed
Publication date: 2026/01/12
Peng MengyuanLin TianjiaoZhu QingyunLi AngPan Xinting - Recurrent pregnancy loss (RPL), also termed recurrent spontaneous abortion, is defined as the failure of ≥2 consecutive pregnancies before 20 weeks of gestation. Approximately 5% of pregnant couples experience RPL. The hyaluronan-binding protein 2 () gene is involved in coagulation and plays an important role during pregnancy. In >50% of RPLs, the etiology remains unexplained. We collected 765 blood samples from 388 female RPL patients and 377 healthy female controls. To investigate the relationships between polymorphisms and RPL, we examined six variants (rs3832698 A>del, rs10885478 G>A, rs932650 T>C, rs7923349 G>T, rs1157916 G>A, and rs2240879 T>C) to clarify their association with RPL risk. The rs2240879 CC genotype was significantly associated with an increased RPL risk ( = 0.028). In haplotype analysis, the combination of rs3832698 del and rs2240879 T (del-T) was associated with elevated risk ( = 0.043); this risk persisted in combinations with additional polymorphisms (rs3832698 A>del, rs10885478 G>A, rs932650 T>C, rs7923349 G>T; del-A-T-T, < 0.001; rs3832698 A>del, rs10885478 G>A, rs932650 T>C, rs7923349 G>T, rs1157916 G>A, rs2240879 T>C; del-A-C-T-G-T, = 0.024). The rs3832698 and rs1157916 genotypes were significantly associated with prothrombin time ( = 0.020 and = 0.012, respectively). We identified associations between polymorphisms and RPL; rs2240879 was linked to an increased RPL risk. Additionally, rs3832698 was associated with an altered prothrombin time. These findings suggest that represents a biomarker for RPL susceptibility. - Source: PubMed
Publication date: 2025/12/07
Lee Jeong YongKim Young RanKo Eun JuPark Hyeon WooLee Jae HyunHong Seung HoShin Ji EunAhn Eun HeeKim Ji HyangKim Nam Keun - The deep fascia, traditionally regarded as a passive structural tissue, is now recognized as a metabolically and biologically active structure where biochemical signals and biomechanical forces interact to influence proprioception, pain, force transmission, and adaptation to mechanical load. In this study, the convergence point between Angiotensin II (Ang II) signaling via its receptor, Angiotensin type 1 receptor (AT1R), and the mechanosensor Yes-associated protein (YAP) was investigated in human fascial fibroblasts. The presence of angiotensin II (Ang II) receptors was confirmed in fibroblasts from the deep fascia, with the AT1 receptor being the most prevalent subtype. Short-term exposure to Ang II (15-30 min) caused YAP dephosphorylation and its translocation to the nucleus, indicating YAP activation. Notably, prolonged Ang II treatment (7 days) significantly increased the expression of fibrosis-related genes, including collagen types I and III (, ), and hyaluronan binding protein 2 (). This gene expression was decreased by pretreatment with the AT1R antagonist irbesartan or the YAP inhibitor verteporfin. Additionally, Ang II promoted fibroblast proliferation/migration, key features of fibrotic progression, through AT1R-dependent pathways. These findings show that Ang II acts as both a biochemical and biomechanical signal in the deep fascia, activating YAP signaling and promoting fibrotic remodeling. Our results uncover a new Ang II-YAP pathway in fascial fibroblasts, offering potential targets for therapy in fibrosis and related conditions involving the deep fascia. - Source: PubMed
Publication date: 2025/11/17
Caroccia BrasilinaCaputo IlariaBertoldi GiovanniFavaro ValentinaAngelini AndreaBenetti AndreaPetrelli LuciaDi Battista PieroPiazza MariaRuggieri PietroDe Caro RaffaeleStecco CarlaPirri Carmelo - As a continuation of Part I on the structure and regulation of factor VII-activating protease (FSAP), this narrative review synthesizes mechanistic, translational, and limited clinical evidence to delineate FSAP's roles at the interface of coagulation and fibrinolysis. Current evidence indicates that FSAP enhances thrombin generation primarily via proteolytic inactivation of tissue factor pathway inhibitor (TFPI), whereas direct activation of factor VII (FVII) by FSAP appears weak or context-restricted. Beyond plasma proteins, FSAP can upregulate tissue factor (TF) in human macrophages, while platelet-related effects remain insufficiently substantiated. On the fibrinolytic axis, FSAP indirectly accelerates clot lysis by converting single-chain urokinase (scuPA) to its active two-chain form (tcuPA) and, less efficiently, by processing tissue-type plasminogen activator (tPA); in addition, selective cleavage of fibrinogen Aα and Bβ chains remodels clot architecture, yielding thinner fibers with higher density and increased susceptibility to proteolysis. Collectively, the data position FSAP as a context-sensitive modulator of thrombin generation and fibrin turnover. Key gaps include isoform specificity, in vivo cellular targets, and the quantitative contribution of the FSAP-TFPI and FSAP-fibrinogen-urokinase/tPA axes in human pathophysiology, which warrant focused mechanistic and clinical studies. - Source: PubMed
Publication date: 2025/11/03
Schachta IgaŻekanowska EwaStyczyński JanMurawska JoannaLattanzi SimonaAlexandre Andrea MSłomka Artur