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MICRORNA‐150 REGULATES SURFACTANT SECRETION VIA P2X7 RECEPTORS
Author(s) -
Weng Tingting,
Mishra Amarjit,
Guo Yujie,
Wang Yang,
Su Lijing,
Liu Lin
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.612.26
Subject(s) - secretion , purinergic receptor , microbiology and biotechnology , microrna , receptor , pulmonary surfactant , hek 293 cells , chemistry , cell , biology , gene , endocrinology , extracellular , biochemistry
P2X7 receptor (P2X7R) is a purinergic ion‐channel receptor. Previously, we found that the activation of P2X7R in alveolar type I cells could activate the surfactant secretion in alveolar epithelial type II cells. In this study, we determined whether miRNAs regulate P2X7R‐mediated surfactant secretion. We first used a dual‐luciferase assay to screen the regulation of P2X7R 3′‐UTR activity by miR‐150, miR‐186, miR‐204 and miR‐211. We found that miR‐150 is a regulator of P2X7R in lung epithelial cells. The miR‐150 regulation could be disrupted by site mutation of mature miR‐150 or mutation of P2X7R 3′‐UTR at miR‐150 binding sites. MiR‐150 expression level in alveolar type II cells was much higher than alveolar type I cells, which was inversely correlated with the P2X7R protein level. Adenovirus expressing miR‐150 significantly downregulated the P2X7R protein expression in E10 cells. Furthermore, pre‐treatment of E10 cells with adenovirus expressing miR‐150 disrupted the surfactant secretion stimulated by E10 cell conditioned media. Our study is the first of its kind to demonstrate that miR‐150 regulates P2X7R mediated surfactant secretion (supported by NIH grants R01 HL‐083188).