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. Author manuscript; available in PMC: 2014 Apr 1.
Published in final edited form as: Cancer Res. 2013 Jan 30;73(7):2333–2344. doi: 10.1158/0008-5472.CAN-12-3086

Figure 2.

Figure 2

TGFβ mediates the tropism of BM-hMSCs to gliomas through TGF-β receptors on BM-hMSCs

(A) and (E). Expression of TGFβIIR (A) or CD105 (E) in BM-hMSCs by western blots. α-tubulin is internal control.

(B) In vitro migration of BM-hMSCs in which TGF-β receptors were knocked down toward CM of U87. Error bars, SDs.

(C) Homing of GFP-labeled BM-hMSCs-TGFβRII-kd (two independent shRNAs, #4 and #7) to U87 tumor. The scale bars, 500μm.

(D) Quantitative assessments of homing of BM-hMSCs. Error bars, SEs.

(F) Homing of BM-hMSC-CD105-kd to U87 tumors. Scale bars, 500μm.

(G) Quantitative assessments of localization of BM-hMSCs. Error bars, SEs.

(H) (I) (J) Lamellipodia formation was examined in BM-hMSCs-parental, -scramble, and -TGFβRII-kd with or without TGF-β. (H) Representative pictures of cells at scratch sites at 10x of magnification. (I) Representative pictures of cells at the edge of the scratch. Scale bars, 50μm. Arrows, lamellipodia. (J) Quantitative assessments of cell with lamellipodia. Error bars, SDs.