(A) An in vivo parabiosis platform allowed for the conjoining of the circulatory systems of two mice in the context of miR-210 +/+ (WT) and miR-210 −/− (KO) partners. One-week post-surgery, mouse pairs were exposed to chronic hypoxia (10% O2) for 3 weeks to induce endogenous miR-210 up-regulation. (Red arrows denote comparison groups.) (B-D) As assessed by RT-qPCR in plasma (B, N=8,7,9,8 mice) and in CD31+/CD45− lung endothelial cells (D, N=12,11,10,12 mice), while miR-210 expression was negligible in KO-KO pairs, extracellular miR-210 level in KO partners of KO-WT pairs was increased to comparable level as WT-WT pairs whereas intracellular miR-210 in those mice was readily detected but still less than that of WT partners and WT-WT pairs. Extracellular miR-210 in plasma was found to be co-immunoprecipitated specifically in the presence of α-Argonaute 2 (AGO2) as compared with control IgG (C, N=4 mice/group). (E) By in situ staining of miR-210 (red), its target proteins ISCU1/2 (grey, pointed out by red arrows), and the endothelial marker CD31 (green), miR-210 expression in the KO partners of KO-WT pairs was detected specifically in pulmonary arteriolar endothelium (yellow, micrograph inset), accompanied by a reciprocal decrease in ISCU1/2 expression in these miR-210-positive cells, as compared with KO-KO pairs (N=6 mice/group, average of N=10–12 vessels/mice. Scale bar denotes 50 μm.). (F-H) In parallel, there was no significant difference of endothelin-1 content in plasma (F, N=4 mice/group), nitrate and nitrite content in lungs (G, N=5 mice/group) or inflammatory cytokine IL-6 content in plasma (H, N=4 mice/group) between KO partners of KO-WT pairs with KO-KO pair. (Data are presented as mean ± SEM. In x-axes of (B,D,E,F,G,H) bold font denotes parabionts being studied, whereas regular font denotes partner parabionts. Mann Whitney U test for C,F,G,H and one-way ANOVA with post-hoc Bonferroni testing were performed for other panels.)