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. 2022 Jun 29;37(8):1545–1561. doi: 10.1002/jbmr.4616

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© 2022 The Authors. Journal of Bone and Mineral Research published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research (ASBMR).

This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

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Fig. 6 — Loss of Bmpr1a in Pdgfra‐derived progenitors impairs bone healing. (A) Experimental design. Bmpr1a ^fl/fl (control) and Pdgfra ^CreERT ;Bmpr1a ^fl/fl mice were induced with TMX at days 7 and 1 before fracture, day 0 and day 1 post‐fracture. Tibial fractures were induced at d0 and calluses were harvested at d14 and d21 post‐fracture. (B) Histomorphometric quantification of callus, cartilage, and bone volumes at d14 and d21 post‐fracture in Bmpr1a ^fl/fl control and Pdgfra ^CreERT ;Bmpr1a ^fl/fl mutant mice (in black and orange, respectively) (n = 6–7 animals per group). (C) Longitudinal callus sections from Pdgfra ^CreERT ;Rosa ^mTmG ;Bmpr1a ^+/+ control (left) and Pdgfra ^CreERT ;Rosa ^mTmG ;Bmpr1a ^fl/fl mutant (right) mice at d14 post‐fracture stained with SO (callus delimited by a black dotted line). High magnifications of boxed areas of cartilage (1 and 3) and bone (2 and 4) show Pdgfra‐derived cells in cartilage and bone. (D) Quantification of GFP+ signal normalized on total GFP+ and Tomato+ signal in cartilage and bone. n = 4–5 animals per group, each dot represents a single animal. Exact p value calculated with two‐sided Mann‐Whitney test, values represent median and interquartile range. Scale bars: low magnification = 1 mm, high magnification = 200 μm. b = bone; bm = bone‐marrow; d0 = day 0; SO = Safranin O; TMX = tamoxifen.