Calcineurin and Akt expression in hypertrophied bladder in STZ-induced diabetic
Authors Liu G, Li M, Daneshgari F
Submitted By Firouz Daneshgari on 2/22/2012
Status Published
Journal Experimental and molecular pathology
Year 2012
Date Published 4/1/2012
Volume : Pages 92 : 210 - 216
PubMed Reference 22305959
Abstract Diabetes causes significant increases in bladder weight but the natural history
and underlying mechanisms are not known. In this study, we observed the temporal
changes of detrusor muscle cells (DMC) and the calcineurin (Cn) and Akt
expressions in detrusor muscle in the diabetic rat. Male Sprague-Dawley rats
were divided into 3 groups: streptozotocin-induced diabetics, 5% sucrose-induced
diuretics, and age-matched controls. The bladders were removed 1, 2, or 9weeks
after disease induction and the extent of hypertrophy was examined by bladder
weights and cross sectional area of DMC. Cn and Akt expression were evaluated by
immunoblotting. Both diabetes and diuresis caused significant increases in
bladder weight. The mean cross sectional areas of DMC were increased in both
diabetic and diuretic animals 1, 2, or 9weeks after disease induction. The
expression levels of both the catalytic A (CnA) and regulatory B (CnB) subunits
of Cn were increased at 1 and 2weeks, but not at 9weeks. Expression of Akt was
similar among control, diabetic, and diuretic rat bladder at all time points. In
conclusion, diabetes and diuresis induce similar hypertrophy of detrusor muscle
during the first 9weeks, indicating that bladder hypertrophy in the early stage
of diabetes is in response to the presence of increased urine output in
diabetes. Our results suggest that the Cn, but not the Akt signaling pathway may
be involved in the development of bladder hypertrophy.

Investigators with authorship
Firouz DaneshgariCase Western Reserve