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. Author manuscript; available in PMC: 2014 Aug 1.
Published in final edited form as: Arterioscler Thromb Vasc Biol. 2013 May 23;33(8):10.1161/ATVBAHA.112.301068. doi: 10.1161/ATVBAHA.112.301068

Fig. 2.

Fig. 2

Transplantation of eNOS deficient recipients with bone marrow (BM) from wild type (WT) donors does not confer eNOS expression on vascular endothelium. (A) Table of BM transplanted chimeras used in the present study, outlining mouse BM donors/recipients and sites of eNOS expression at 6–8 weeks post-transplant. (B) Representative flow cytometry data (histograms) evidencing ≥ 90% conversion of BM recipients’ blood (peripheral leukocytes) to the donor phenotype (CD45.1 or CD45.2) prior to use in nitrite and blood pressure experiments (representative experiment of n=340+). (C) Representative western blot of aortic homogenates from WT mice (n=2, lanes 1–2), eNOS−/− mice (n=3, lanes 4–6), WT recipients of WT marrow (WT→WT; n=3, lanes 8–10), and eNOS deficient recipients of WT marrow (WT→eNOS−/−, n=2, lanes 12–13). (D) eNOS mRNA in aortas and blood (all cellular components) of C57Bl/6J (WT) compared to eNOS deficient (eNOS−/−) mice. Ratios of eNOS/β-actin mRNA are given as mean ± SEM for each group (n=2 per group). nd denotes nondetectable at 40 cycles. (E) Cross-transplantation of eNOS−/− mice with WT marrow does not give rise to eNOS mRNA expression in aortas (BC+/EC+: n=2, BC−/EC+: n=3, BC+/EC−: n=5, BC−/EC−: n=3). (F, G) Expression of (F) cyclooxygenase-1 (COX-1) and (G) cyclooxygenase-2 (COX-2) mRNA in aortas of cross-transplanted chimeras is similar between groups (BC+/EC+: n=3, BC−/EC+: n=2, BC+/EC−: n=4, BC−/EC−: n=3). BC+/EC+ (globally competent for eNOS), BC−/EC+ (deficient of blood eNOS), BC+/EC− (deficient of vascular eNOS) and BC−/EC− (globally deficient of eNOS). Ratios of β-actin mRNA are given as mean ± SEM for each group. nd denotes non-detectable eNOS mRNA at 40 cycles.