Figure 1: Inhibition of phospho-p38 MAPK in ALDO systemic GC-A KO mice. | Scientific Reports

Figure 1: Inhibition of phospho-p38 MAPK in ALDO systemic GC-A KO mice.

From: Natriuretic peptide receptor guanylyl cyclase-A pathway counteracts glomerular injury evoked by aldosterone through p38 mitogen-activated protein kinase inhibition

Figure 1

(a) Immunohistochemical study for phopho-p38 MAPK in glomeruli. Left panel shows a glomerulus in uninephrectomized, aldosterone-infused and high salt diet-fed (ALDO) wild-type mice. Right panel shows a glomerulus in ALDO systemic GC-A KO mice. Arrows, phospho-p38 MAPK-positive cells. Scale bar, 50 μm. (b) Time course of systolic blood pressure in ALDO wild-type mice, ALDO wild-type mice with FR167653, ALDO systemic GC-A KO mice, and ALDO systemic GC-A KO mice with FR167653. (c) Time course of albuminuria in these four groups. (d) Light microscopic analyses were performed at 4 weeks after aldosterone administration, stained with periodic acid-Schiff. In juxtamedullary glomeruli, ALDO systemic GC-A KO mice showed segmental sclerosis with glomerular hypertrophy. Treatment with FR167653 improved these changes. Scale bar, 50 μm. (e) Glomerular cross-sectional area and (f) mesangial area in juxtamedullary glomeruli at 4 weeks. (g) Histological examination of tubules and interstitial fibrosis by Masson’s trichrome-staining at 4 weeks. ALDO systemic GC-A KO mice exhibited tubular dilatation with protein cast deposition. These change were ameliorated by FR167653. Scale bar, 50 μm. n = 5, each. Mean ± SEM. ††p < 0.01 vs. ALDO wild-type mice. *p < 0.05, **p < 0.01 vs. ALDO systemic KO mice. WT, wild-type mice; KO, systemic GC-A knockout mice.

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