Key result
ACE2 inhibits ALI-induced pulmonary apoptosis in vivo partially by suppressing miR-4262 and upregulating Bcl-2.
Why the study?
The mechanisms by which ACE2 suppresses apoptosis of pulmonary endothelial cells during acute lung injury are not completely understood.
Population
Bleomycin-induced mouse model for acute lung injury
Comparison
ACE2 treatment and miR-4262 antisense vs no ACE2 treatment
Design
Preclinical experimental study
Authors
Loading...
Should not change ALI practice; hypothesis-generating for ACE2/miR-4262 axis pending human validation.
ACE2 protects against acute lung injury by suppressing miR-4262, thereby preventing the downregulation of the anti-apoptotic protein Bcl-2 in pulmonary endothelial cells.
Bao et al. (2015) studied Acute lung injury (ALI). ACE2 and miR-4262 antisense vs. Without ACE2 / miR-4262 mimics was evaluated on Apoptosis of pulmonary cells and severity of ALI. ACE2 inhibited ALI-induced apoptosis of pulmonary cells in vivo partially through suppression of miR-4262 and upregulation of Bcl-2 protein.
Synapse has enriched 4 closely related papers on similar clinical questions. Consider them for comparative context: