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. Author manuscript; available in PMC: 2012 Feb 15.
Published in final edited form as: Cancer Cell. 2011 Feb 15;19(2):257–272. doi: 10.1016/j.ccr.2011.01.020

Figure 2. A significant portion of gastric CAFs originate from the bone marrow.

Figure 2

(A) EGFP (lower panel) or RFP (upper panel) expression and co-staining for αSMA and DAPI in stomachs of WT or 12 and 18-month mice with H. felis infection (arrows indicate αSMA and GFP or RFP co-expression) after UBC-GFP- or αSMA-RFP-labeled BMT.

(B) FACS of freshly isolated gastric MF from WT mice with double-labeled BMT after 18 months of H. felis infection.

(C) FACS data on BM cell contribution to the tumor microenvironment in WT, IL-1β, and H. felis infected WT mice harboring gastritis or dysplasia. Green: non-αSMA+ BM-derived cells, red: αSMA+ BM-derived cells, grey: all non-BM-derived cells. (*=p< 0,05)

(D, E) Endogenous RFP and GFP expression in stomach of 18 months H. felis infected WT mice after UBC-GFP/αSMA-RFP- double-labeled BM transplantation

(F) Endogenous RFP and GFP expression in in vitro culture of isolated MF from stomachs of 18 months H. felis infected WT mice after UBC-GFP/αSMA-RFP- double-labeled BM transplantation

(G) Gene expression data after FACS sorting of GFP(−) and GFP(+) CAFs from a BM-transplanted H. felis-infected IL-1β mouse. qRT-PCR for expression of GFP, CXCL1, CCL5, SSP1, CXCR4, MMP9, IL-6, IL-1β, SDF-1α, and TNFa (copies are calculated per 10000 copies of GAPDH, *=p<0.05 compared to all other cells).

All data are represented as mean +/− SEM. (See also Figure S2 and Table S1)