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Publication : RSPO2 defines a distinct undifferentiated progenitor in the tendon/ligament and suppresses ectopic ossification.

First Author  Tachibana N Year  2022
Journal  Sci Adv Volume  8
Issue  33 Pages  eabn2138
PubMed ID  35984875 Mgi Jnum  J:343449
Mgi Id  MGI:7332316 Doi  10.1126/sciadv.abn2138
Citation  Tachibana N, et al. (2022) RSPO2 defines a distinct undifferentiated progenitor in the tendon/ligament and suppresses ectopic ossification. Sci Adv 8(33):eabn2138
abstractText  Ectopic endochondral ossification in the tendon/ligament is caused by repetitive mechanical overload or inflammation. Tendon stem/progenitor cells (TSPCs) contribute to tissue repair, and some express lubricin [proteoglycan 4 (PRG4)]. However, the mechanisms of ectopic ossification and association of TSPCs are not yet known. Here, we investigated the characteristics of Prg4-positive ((+)) cells and identified that R-spondin 2 (RSPO2), a WNT activator, is specifically expressed in a distinct Prg4(+) TSPC cluster. The Rspo2(+) cluster was characterized as mostly undifferentiated, and RSPO2 overexpression suppressed ectopic ossification in a mouse Achilles tendon puncture model via chondrogenic differentiation suppression. RSPO2 expression levels in patients with ossification of the posterior longitudinal ligament were lower than those in spondylosis patients, and RSPO2 protein suppressed chondrogenic differentiation of human ligament cells. RSPO2 was induced by inflammatory stimulation and mechanical loading via nuclear factor kappaB. Rspo2(+) cells may contribute to tendon/ligament homeostasis under pathogenic conditions.
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