Fig. 4: SPRY4 causes heterotopic bone formation of BM-MSCs in vivo. | Cell Death & Disease

Fig. 4: SPRY4 causes heterotopic bone formation of BM-MSCs in vivo.

From: SPRY4 is responsible for pathogenesis of adolescent idiopathic scoliosis by contributing to osteogenic differentiation and melatonin response of bone marrow-derived mesenchymal stem cells

Fig. 4

BM-MSCs were infected with lentivirus to silence or overexpress SPRY4. After pre-induction for 3 days, cells were loaded on scaffold materials and implanted into NOD/SCID mice for 10 weeks (n = 6 for each group). a, b Osteoids formed in SPRY4-silenced xenografts (LV-shSPRY4-1 and LV-shSPRY4-2) and control xenografts (LV-NC) were detected by HE staining (a), and osteoid area fractions were quantified by Image J (b). c, d Osteoids formed in SPRY4-overexpressed xenografts (lenti-SPRY4) and vector control xenografts (lenti-NC) were detected by HE staining (c), and osteoid area fractions were quantified by Image J (d). e, f Collagen deposition in SPRY4-silenced xenografts (LV-shSPRY4-1 and LV-shSPRY4-2) and control xenografts (LV-NC) were detected by Masson staining (e), and colour intensity was quantified by Image J (f). g, h Collagen deposition in SPRY4-overexpressed xenografts (lenti-SPRY4) and vector control xenografts (lenti-NC) were detected by Masson staining (g), and colour intensity was quantified by Image J (h). Scaffolds without cell loading were implanted as negative controls, and femurs from mice were used as positive controls for histological analysis

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