Fig 1.
Change of kidneys in ischemic AKI.
(A) Renal function in C57BL/6 mice renal ischemia reperfusion creatinine and blood urea nitrogen (BUN) evaluated. (B) Kidney sections were subjected to PAS-staining and histological changes were scored. ATN injury scores for PAS-stained kidney sections showed increased tubular injury in ischemic AKI. *p < 0.05 at each time point compared to control.
Fig 2.
Changes of serum cytokine in ischemic AKI.
Inflammatory cytokines, interleukin (IL)-6, tumor necrosis factor alpha (TNF-α) by protein, and monocyte chemoattractant protein-1 (MCP-1) were measured. *p < 0.05 at each time point compared to control.
Fig 3.
Change of the lungs in ischemic AKI.
(A) Neutrophil infiltration in the lungs was evaluated in ischemic AKI (S1 Fig). (B) Immunoblot of BCL-2-associated X protein (Bax), and B cell leukemia/lymphoma 2 (Bcl-2) were measured. Bax/Bcl-2 ratio in the lungs was identified in ischemic AKI. (C) Receptor for advanced glycation end products (RAGE), marker to reflect pneumocyte I injury in ischemic AKI. (D) Total protein changes in BAL in ischemic AKI. *p < 0.05 at each time point compared to control.
Fig 4.
Change of lung tight-junction protein in ischemic AKI.
Alveolar permeability barrier tight-junction proteins were measured by immunoblot. Claudin-4, claudin-18, and JAMA-1. *p < 0.05 at each time point compared to control.
Fig 5.
Change of SP-A and SP-D in ischemic AKI.
SP-A and SP-D in serum changed significantly in ischemic AKI. SP-A and SP-D in the lungs showed no changes in ischemic AKI. SP-A and SP-D in the kidneys were significantly different in AKI than in the sham. *p < 0.05 at each time points compared to control.
Fig 6.
Presence of SP-A and SP-D in the lung of sham and AKI.
Immunohistochemical localization of SP-A and SP-D in experimental animal lung. The immunohistochemistry showed the expression of SP-A and SP-D in ischemic AKI.
Fig 7.
Schematic of AKI and lung crosstalk.