Fig 1: Protein aggregation in renal proximal tubules after angiotensin II treatment. Angiotensin was administered to rats to increase cellular protein turnover in proximal tubules, and aggregation-prone protein content was analyzed by immunohistochemistry. Angiotensin II was elevated by either infusion from subcutaneous minipumps or by adrenalectomy with glucocorticoid substitution. (A) Representative example of the RPL22/27 immunostaining in the kidney cortex from a control and angiotensin II (AngII)-treated rats, as indicated. PT denotes proximal tubules, while DT marks distal tubules and connecting tubules. (B) Similar RPL22/27 staining in sections from dexamethasone-treated adrenalectomized rats (ADX) and from similar rats with aldosterone and dexamethasone coadministration (ADX+Aldo). (C) Micrographs comparing keratin 5 immunoreactivity in renal cortex from control and angiotensin II-treated rats. (D) Immunolabeling for ataxin-3 in the angiotensin II versus vehicle administration model, as indicated. (E) Similar staining in model of dexamethasone-corrected adrenalectomy with and without angiotensin II administration (ADX+AngII), as indicated.