Fig. 3
From: Pulmonary midkine inhibition ameliorates sepsis induced lung injury
Targeted abrogation of midkine in the lung tissue ameliorated acute lung injury in CLP model. a Immunofluorescence staining of GFP of lung tissue in control mouse (WT), mouse transduced with vehicle AAV (AAV. Veh) and mouse transduced with AAV carrying midkine RNAi sequence (AAV.RNAi.MK, n = 6 in each group). Lower panel showed immunohistochemistry staining of midkine in lung tissue in WT, AAV.Veh and AAV.RNAi.MK group (n = 6 in each group). b Midkine and ACE protein levels in lung tissue determined by Western blots in control mouse (WT), mouse transduced with vehicle AAV (AAV.Veh) and mouse transduced with AAV carrying midkine RNAi sequence (AAV.RNAi.MK) (n = 6 in each group). c Immunohistochemistry staining of midkine in lung tissue of control mouse (WT) and mouse transduced with AAV midkine RNAi (AAV.RNAi.MK) with sham operation (upper panel), and the respective group mouse with CLP (lower panel) (n = 6 in each group). d H&E staining of control mouse (WT), mouse transduced with vehicle AAV (AAV.Veh) and mouse transduced with AAV carrying midkine RNAi sequence (AAV.RNAi.MK) in CLP vs. sham mouse were shown. Quantitative assessment by lung histopathological score was presented (n = 6). e BALF analysis from control mouse (WT), mouse transduced with vehicle AAV (AAV.Veh) and mouse transduced with AAV carrying midkine RNAi (AAV.RNAi.MK) in CLP vs sham mouse were shown (n = 6). Cell counts (upper left), TNF-α in BALF (upper right), protein contents in BALF (lower left) and lung wet/dry ratio (lower right) were shown (n = 6 in each group). f ACE hydrolytic activity determined by FAPGG in control mouse (WT), mouse transduced with vehicle AAV (AAV.Veh) and mouse transduced with AAV with midkine RNAi (AAV.RNAi.MK) in CLP vs. sham mouse was shown (left). ACE activity was measured at indicated time point. Angiotensin I was added to lung homogenization and the converted angiotensin II was determined (right) (n = 6 in each group)