Figure 5.
Figure 5. Intratumoral PDGFR-β+ cells selectively up-regulate RGS-5. (A) Immunoreactivity of anti–PDGFR-β antibodies in normal pancreatic islets and (C) RIP1-Tag5 tumors is compared to RGS-5 in situ hybridization signals in islets (B) and tumors (D; for all frozen sections, original magnification × 10). (E) RNA from normal islets (1 pool of 200 islets), angiogenic islets (3 pools of 10 angiogenic islets), and tumors (12 independent tumor samples) was analyzed for the expression of known pericyte markers (PDGFR-β, desmin, αSMA) and for VEGFR2 as a marker for endothelial cells. (F) Western blot analysis of pools of islets and RT5 tumors. (G) Relative expression of RGS-5 in normal islets, angiogenic islets, and tumors is shown. Expression levels in panels E and G were normalized to HPRT.

Intratumoral PDGFR-β+cells selectively up-regulate RGS-5. (A) Immunoreactivity of anti–PDGFR-β antibodies in normal pancreatic islets and (C) RIP1-Tag5 tumors is compared to RGS-5 in situ hybridization signals in islets (B) and tumors (D; for all frozen sections, original magnification × 10). (E) RNA from normal islets (1 pool of 200 islets), angiogenic islets (3 pools of 10 angiogenic islets), and tumors (12 independent tumor samples) was analyzed for the expression of known pericyte markers (PDGFR-β, desmin, αSMA) and for VEGFR2 as a marker for endothelial cells. (F) Western blot analysis of pools of islets and RT5 tumors. (G) Relative expression of RGS-5 in normal islets, angiogenic islets, and tumors is shown. Expression levels in panels E and G were normalized to HPRT.

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