Fig. 3: Deletion of PP2A in LepR+ MSCs inhibited proliferation and hypertrophic differentiation of POC in embryonic stage. | Communications Biology

Fig. 3: Deletion of PP2A in LepR+ MSCs inhibited proliferation and hypertrophic differentiation of POC in embryonic stage.

From: PP2A in LepR+ mesenchymal stem cells contributes to embryonic and postnatal endochondral ossification through Runx2 dephosphorylation

Fig. 3

Sections of E18.5 distal femur from Lepr-cre; Ppp2r1afl/fl mice were subjected to immunostaining. a–d Immunohistochemistry (IHC) and immunofluorescence reveal that LepR+ MSCs express Ppp2r1a and unphosphorylated (Y307) PP2AC in POC. a LepR IHC. b Ppp2r1a IHC. c Double immunofluorescence of LepR and Ppp2r1a. d Unphosphorylated (Y307) PP2AC IHC. e Illustration of conditional knockout of Ppp2r1a in LepR+ MSCs. IHC reveals successful deletion of Ppp2r1a in LepR+ MSCs in POC. IHC reveals that deletion of Ppp2r1a in LepR+ MSCs leads to decreased expression of Ki67 (f) and hypertrophic markers, such as Runx2, Osterix, collagen X, MMP13 and alkaline phosphatase (g), and increased expression of Perilipin (h) in POC at E18.5. The rectangle box shows magnified picture. HZ = Hypertrophic zone; POC = Primary ossification center; ColX =collagen X; ALP = alkaline phosphatase. Scale bar, 100 μm.

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