TRPM7 channels mediate spontaneous Ca2+ fluctuations in growth plate chondrocytes that promote bone development

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Science Signaling  09 Apr 2019:
Vol. 12, Issue 576, eaaw4847
DOI: 10.1126/scisignal.aaw4847

Ca2+ fluctuations promote growth plate chondrogenesis

In the growth plates of long bones, ordered arrays of chondrocytes proliferate, mature, secrete cartilage matrix, and then undergo apoptosis. The cartilage matrix is subsequently replaced with trabecular bone. Because Ca2+ signaling is implicated in chondrogenesis in vitro, Qian et al. performed Ca2+ imaging of live chondrocytes in slices of embryonic mouse femurs. Growth plate chondrocytes generated spontaneous Ca2+ fluctuations that depended on the cation channel TRPM7. Experiments in bone slices and in cultured metatarsal bones in which Trpm7 was conditionally knocked out indicated that Trpm7-mediated Ca2+ fluctuations were required for the proper development of chondrocytes and bone outgrowth. Furthermore, chondrocyte-specific knockout of Trpm7 in mice caused defects in chondrocyte Ca2+ fluctuations, growth plate morphology, and bone outgrowth.

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