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Bone marrow-derived CD34-positive (CD34+) endothelial progenitor cells (EPCs) has unique functions in the mechanism of compensatory lung growth (CLG). The content of this study is mainly to describe the effect of microRNA (miR)-155 in the mechanisms of EPCs and CLG. Our study found that transfection of miR-155 mimic could promote EPC proliferation, migration and tube formation, while transfection of miR-155 inhibitor had the opposite effect. It was also found that transfection of pc-JARID2 inhibited EPC proliferation, migration and tube formation, while transfection of si-JARID2 had the opposite effect. miR-155 can target and negatively regulate JARID2 expression. Overexpression of JARID2 weakened the promoting effects of miR-155 mimic on EPC proliferation, migration, and tubular formation, while silencing JARID2 weakened the inhibitory effects of miR-155 inhibitors on EPC proliferation, migration, and tubular formation. Transplantation of EPCs transfected with miR-155 mimic into the left lung model effectively increased lung volume, total alveolar number, diaphragm surface area, and lung endothelial cell number, while transplantation of EPCs co-transfected with miR-155 mimic and pc-JARID2 reversed this phenomenon. Overall, we found that miR-155 activates CD34+ EPC by targeting negative regulation of JARID2 and promotes CLG.

骨髓来源的CD34阳性（CD34+）内皮祖细胞（endothelial progenitor cells，EPCs）在代偿性肺生长（compensatory lung growth，CLG）的调控机制中具有独特功能。本研究旨在阐明微小RNA（microRNA，miR）-155在内皮祖细胞及代偿性肺生长机制中的作用。研究发现，转染miR-155模拟物可促进内皮祖细胞的增殖、迁移及管形成能力，而转染miR-155抑制剂则产生相反效应。同时，转染pc-JARID2可抑制内皮祖细胞的增殖、迁移及管形成能力，转染si-JARID2则呈现相反作用。进一步证实，miR-155可靶向负调控JARID2的表达。过表达JARID2会削弱miR-155模拟物对内皮祖细胞增殖、迁移及管形成的促进作用，而沉默JARID2则可减弱miR-155抑制剂对内皮祖细胞增殖、迁移及管形成的抑制效应。将转染miR-155模拟物的内皮祖细胞移植入左肺模型后，可有效提升肺容积、肺泡总数、膈肌表面积及肺内皮细胞数量；而共转染miR-155模拟物与pc-JARID2的内皮祖细胞移植则可逆转上述现象。综上，本研究证实miR-155通过靶向负调控JARID2激活CD34+内皮祖细胞，进而促进代偿性肺生长。