Thyroid hormones stimulate renal expression of CFTR

CFTR is a multifunctional protein of the ATP binding cassette family that may contribute to overall electrolyte homeostasis by acting as a chloride channel in the kidney. In renal tissues CFTR does not exists only in its full-length form, but also as a kidney-specific, truncated splice variant, TNR-CFTR. In this study we show that both forms of CFTR are regulated by thyroid hormones in rat renal tissue. Four groups of male rats were used: control, hypothyroid, hypothyroid with T-4 treatment and hyperthyroid rats. The hypothyroid rats showed a decrease of both CFTR and TNR-CFTR mRNAs (44%, and 49%, respectively, n=5; p < 0.05) and proteins (30% and 37%, respectively, n=5, p < 0.05) expressions, compared to control group. In hyperthyroid rats, a significant increase in both CFTR and TRN-CFTR mRNAs expressions (43% and 95%, n=5; p < 0.05) and proteins (250% and 38%, respectively, n=5, p < 0.05) was observed when compared to control group. Treatment of immortalized rat proximal tubule cells (IRPTC) with T-3 (10(-7)M) produced also an increase of CFTR mRNA expression (95%, n=5, p < 0.05). Analysis of the promoter region of CFTR transfected to IRPTC showed that T-3 (10(-7) M) stimulates the CFTR promoter (38%, n=4, p < 0.05). Copyright (c) 2007 S. Karger AG, Basel.