Fibrocyte Phenotype of ENTPD1+CD55+ Cells and Its Association with Pain in Osteoarthritic Synovium

Author:

Tsuchiya Maho1,Ohashi Yoshihisa1,Fukushima Kensuke1,Okuda Yusei2ORCID,Suto Arisa2ORCID,Matsui Takashi23ORCID,Kodera Yoshio23,Sato Masashi4,Tsukada Ayumi1,Inoue Gen1ORCID,Takaso Masashi1,Uchida Kentaro15ORCID

Affiliation:

1. Department of Orthopaedic Surgery, Kitasato University School of Medicine, Sagamihara 252-0374, Japan

2. Department of Physics, School of Science, Kitasato University, Sagamihara 252-0373, Japan

3. Center for Disease Proteomics, School of Science, Kitasato University, Sagamihara 252-0373, Japan

4. Department of Immunology, Kitasato University School of Medicine, Sagamihara 252-0374, Japan

5. Research Institute, Shonan University of Medical Sciences, Chigasaki 253-0083, Japan

Abstract

Osteoarthritis (OA) is a prevalent degenerative joint disorder characterized by cartilage erosion, structural changes, and inflammation. Synovial fibroblasts play a crucial role in OA pathophysiology, with abnormal fibroblastic cells contributing significantly to joint pathology. Fibrocytes, expressing markers of both hematopoietic and stromal cells, are implicated in inflammation and fibrosis, yet their marker and role in OA remain unclear. ENTPD1, an ectonucleotidase involved in purinergic signaling and expressed in specific fibroblasts in fibrotic conditions, led us to speculate that ENTPD1 plays a role in OA pathology by being expressed in fibrocytes. This study aimed to investigate the phenotype of ENTPD1+CD55+ and ENTPD1−CD55+ synovial fibroblasts in OA patients. Proteomic analysis revealed a distinct molecular profile in ENTPD1+CD55+ cells, including the upregulation of fibrocyte markers and extracellular matrix-related proteins. Pathway analysis suggested shared mechanisms between OA and rheumatoid arthritis. Correlation analysis revealed an association between ENTPD1+CD55+ fibrocytes and resting pain in OA. These findings highlight the potential involvement of ENTPD1 in OA pain and suggest avenues for targeted therapeutic strategies. Further research is needed to elucidate the underlying molecular mechanisms and validate potential therapeutic targets.

Funder

Uehara Memorial Foundation

Nakatomi Foundation

SRL, Inc

Kitasato University Research Grant

All Kitasato Project Study

Patients’ Association of Kitasato University School of Medicine

Publisher

MDPI AG

Reference50 articles.

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