NDLI: Prokineticin 2 is a catabolic regulator of osteoarthritic cartilage destruction in mouse

Content Provider	Springer Nature : BioMed Central
Author	Yang, Jiye Shin, Youngnim Kim, Hwee-Jin Kim, Hyo-Eun Chun, Jang-Soo
Abstract	Background Our preliminary study indicates that the multi-functional protein, prokineticin 2 (Prok2), is upregulated in osteoarthritic (OA) chondrocytes as a target of the hypoxia-inducible factor (HIF)-2α. This study aims to elucidate the potential roles of Prok2 in OA. Methods Prok2 expression was assessed through microarray analysis in chondrocytes and confirmed via immunostaining in OA cartilage. Experimental OA was induced through destabilization of the medial meniscus (DMM). Functions of Prok2 were assessed by adenoviral overexpression, intra-articular (IA) injection of recombinant Prok2 (rProk2), and knockdown of Prok2 in joint tissues. We also explored the potential utility of Prok2 as an OA biomarker using enzyme-linked immunosorbent assay (ELISA). Results HIF-2α upregulated Prok2, one of the prokineticin signaling components, in OA chondrocytes of mice and humans. Adenoviral overexpression of Prok2 in chondrocytes and cartilage explants, as well as the application of rProk2, led to an upregulation of matrix metalloproteinase (MMP)3 and MMP13. Consistently, the overexpression of Prok2 in joint tissues or IA injection of rProk2 exacerbated cartilage destruction and hindpaw mechanical allodynia induced by DMM. However, the knockdown of Prok2 in joint tissues did not significantly affect DMM-induced cartilage destruction. Additionally, despite being a secreted protein, the serum levels of Prok2 in OA mice and human OA patients were found to be below the range detected by ELISA. Conclusion The upregulation of Prok2 exacerbates OA cartilage destruction and hindpaw mechanical allodynia. However, its knockdown is not sufficient to inhibit experimental OA and Prok2 is not a potential candidate serum biomarker of OA.
Related Links	https://arthritis-research.biomedcentral.com/counter/pdf/10.1186/s13075-023-03206-4.pdf
Ending Page	13
Page Count	13
Starting Page	1
File Format	HTM / HTML
ISSN	14786362
DOI	10.1186/s13075-023-03206-4
Journal	Arthritis Research & Therapy
Issue Number	1
Volume Number	25
Language	English
Publisher	BioMed Central
Publisher Date	2023-12-06
Access Restriction	Open
Subject Keyword	Rheumatology Orthopedics Prokineticin Chondrocytes Osteoarthritis Matrix-degrading enzymes Mechanical allodynia Biomarker
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology Rheumatology
Journal Impact Factor	4.4/2023
5-Year Journal Impact Factor	4.9/2023

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