TY - JOUR
T1 - Intestinal Na+/Ca2+ exchanger protein and gene expression are regulated by 1,25(OH)2D3 in vitamin D-deficient chicks
AU - Centeno, Viviana
AU - Picotto, Gabriela
AU - Pérez, Adriana
AU - Alisio, Arturo
AU - Tolosa De Talamoni, Nori
N1 - Funding Information:
This work was supported by grands from FONCYT [PICT2005-32464], CONICET [PIP 2005-2006] and SECYT (UNC) (Dr. Nori Tolosa de Talamoni). Prof. Dr. Nori Tolosa de Talamoni and Dr. Gabriela Picotto are Members of Investigator Career from the Consejo Nacional de Investigaciones Científicas y Tecnológicas (CONICET). Dr. Viviana Centeno is a Postdoctoral Fellow from Secretaria de Ciencia y Técnica, Universidad Nacional de Córdoba (SECYT-UNC).
PY - 2011/5/15
Y1 - 2011/5/15
N2 - The role of 1,25(OH)2D3 on the intestinal NCX activity was studied in vitamin D-deficient chicks (-D) as well as the hormone effect on NCX1 protein and gene expression and the potential molecular mechanisms underlying the responses. Normal, -D and -D chicks treated with cholecalciferol or 1,25(OH)2D3 were employed. In some experiments, -D chicks were injected with cycloheximide or with cycloheximide and 1,25(OH)2D3 simultaneously. NCX activity was decreased by -D diet, returning to normal values after 50 IU daily of cholecalciferol/10 days or a dose of 1 μg calcitriol/kg of b.w. for 15 h. Cycloheximide blocked NCX activity enhancement produced by 1,25(OH)2D3. NCX1 protein and gene expression were diminished by -D diet and enhanced by 1,25(OH)2D3. Vitamin D receptor expression was decreased by -D diet, effect that disappeared after 1,25(OH)2D3 treatment. Rapid effects of 1,25(OH)2D3 on intestinal NCX activity were also demonstrated. The abolition of the rapid effects through addition of Rp-cAMPS and staurosporine suggests that non genomic effects of 1,25(OH)2D3 on NCX activity are mediated by activation of PKA and PKC pathways. In conclusion, 1,25(OH)2D3 enhances the intestinal NCX activity in -D chicks through genomic and non genomic mechanisms.
AB - The role of 1,25(OH)2D3 on the intestinal NCX activity was studied in vitamin D-deficient chicks (-D) as well as the hormone effect on NCX1 protein and gene expression and the potential molecular mechanisms underlying the responses. Normal, -D and -D chicks treated with cholecalciferol or 1,25(OH)2D3 were employed. In some experiments, -D chicks were injected with cycloheximide or with cycloheximide and 1,25(OH)2D3 simultaneously. NCX activity was decreased by -D diet, returning to normal values after 50 IU daily of cholecalciferol/10 days or a dose of 1 μg calcitriol/kg of b.w. for 15 h. Cycloheximide blocked NCX activity enhancement produced by 1,25(OH)2D3. NCX1 protein and gene expression were diminished by -D diet and enhanced by 1,25(OH)2D3. Vitamin D receptor expression was decreased by -D diet, effect that disappeared after 1,25(OH)2D3 treatment. Rapid effects of 1,25(OH)2D3 on intestinal NCX activity were also demonstrated. The abolition of the rapid effects through addition of Rp-cAMPS and staurosporine suggests that non genomic effects of 1,25(OH)2D3 on NCX activity are mediated by activation of PKA and PKC pathways. In conclusion, 1,25(OH)2D3 enhances the intestinal NCX activity in -D chicks through genomic and non genomic mechanisms.
KW - Calcitriol
KW - Chicks
KW - Intestinal cells
KW - NCX activity
KW - NCX1 expression
KW - Vitamin D deficiency
UR - http://www.scopus.com/inward/record.url?scp=79955057541&partnerID=8YFLogxK
U2 - 10.1016/j.abb.2011.03.011
DO - 10.1016/j.abb.2011.03.011
M3 - Article
AN - SCOPUS:79955057541
SN - 0003-9861
VL - 509
SP - 191
EP - 196
JO - Archives of Biochemistry and Biophysics
JF - Archives of Biochemistry and Biophysics
IS - 2
ER -