ArticleCell death & disease2021
Secreted KIAA1199 promotes the progression of rheumatoid arthritis by mediating hyaluronic acid degradation in an ANXA1-dependent manner.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 35 citations in OpenAlex.
- KIAA1199 aggravates sepsis-induced lung injury by promoting complement activation.Communications biology · 2026Article
- Extracellular matrix remodeling in the pathogenesis and therapeutic strategies of rheumatoid arthritis.Clinical and experimental medicine · 2026Review
- CEMIP promotes gefitinib resistance in lung cancer with EGFR-mutation possibly through forming a stable complex CEMIP/c-MYC.BBA advances · 2026Article
- Advances in Intra-Articular Injection Hydrogel Drug Delivery Systems in the Treatment of Rheumatoid Arthritis.Pharmaceutics · 2025Review
- CEMIP Maintains Vascular Contractility by Controlling PP1c-MLC20 Cascade in SMCs.Circulation research · 2025Article
- Hyaluronidases as Targets for the Treatment of Neurological Diseases.Proteoglycan research · 2025Article
- circ_0002970 promotes fibroblast-like synoviocytes invasion and the inflammatory response through Hippo/YAP signaling to induce CTGF/CCN1 expression in rheumatoid arthritis.Arthritis research & therapy · 2025Article
- The crucial role of CEMIP in cancer metastasis: Mechanistic insights and clinical implications.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Review
- Article
- New molecules indispensable for hyaluronan degradation, HYBID (CEMIP/KIAA1199) and TMEM2 (CEMIP2): Differential roles in physiological and pathological non-neoplastic conditions.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2025Review
- Adaptor protein CEMIP reduces the chemosensitivity of small cell lung cancer via activation of an SRC-YAP oncogenic module.Acta pharmacologica Sinica · 2024Article
- Epidermal keratinocytes regulate hyaluronan metabolism via extracellularly secreted hyaluronidase 1 and hyaluronan synthase 3.The Journal of biological chemistry · 2024Article
- Glycobiology in osteoclast differentiation and function.Bone research · 2023Review
- Identification of MYH9 as a key regulator for synoviocyte migration and invasion through secretome profiling.Annals of the rheumatic diseases · 2023Article
- Aggrecan and Hyaluronan: The Infamous Cartilage Polyelectrolytes - Then and Now.Advances in experimental medicine and biology · 2023Article
- Research on the biological mechanism and potential application of CEMIP.Frontiers in immunology · 2023Review
- Article
- CEMIP, a Promising Biomarker That Promotes the Progression and Metastasis of Colorectal and Other Types of Cancer.Cancers · 2022Review
- Expression and regulation of recently discovered hyaluronidases, HYBID and TMEM2, in chondrocytes from knee osteoarthritic cartilage.Scientific reports · 2022Article
- Hyaluronidase 1 deficiency decreases bone mineral density in mice.Scientific reports · 2022Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In inflamed joints, enhanced hyaluronic acid (HA) degradation is closely related to the pathogenesis of rheumatoid arthritis (RA). KIAA1199 has been identified as a hyaladherin that mediates the intracellular degradation of HA, but its extracellular function remains unclear. In this study, we found that the serum and synovial levels of secreted KIAA1199 (sKIAA1199) and low-molecular-weight HA (LMW-HA, MW < 100 kDa) in RA patients were significantly increased, and the positive correlation between them was shown for the first time. Of note, treatment with anti-KIAA1199 mAb effectively alleviated the severity of arthritis and reduced serum LMW-HA levels and cytokine secretion in collagen-induced arthritis (CIA) mice. In vitro, sKIAA1199 was shown to mediate exogenous HA degradation by attaching to the cell membrane of RA fibroblast-like synoviosytes (RA FLS). Furthermore, the HA-degrading activity of sKIAA1199 depended largely on its adhesion to the membrane, which was achieved by its G8 domain binding to ANXA1. In vivo, kiaa1199-KO mice exhibited greater resistance to collagen-induced arthritis. Interestingly, this resistance could be partially reversed by intra-articular injection of vectors encoding full-length KIAA1199 instead of G8-deleted KIAA119 mutant, which further confirmed the indispensable role of G8 domain in KIAA1199 involvement in RA pathological processes. Mechanically, the activation of NF-κB by interleukin-6 (IL-6) through PI3K/Akt signaling is suggested to be the main pathway to induce KIAA1199 expression in RA FLS. In conclusion, our study supported the contribution of sKIAA1199 to RA pathogenesis, providing a new therapeutic target for RA by blocking sKIAA1199-mediated HA degradation.
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