Prolactin restores branchial mitochondrion-rich cells expressing Na+/Cl- cotransporter in hypophysectomized Mozambique tilapia.

Hypophysectomy and hormone replacement therapy were conducted to investigate the regulation of branchial mitochondrion-rich cell (MRC) recruitment and hormone receptor expression in euryhaline tilapia (Oreochromis mossambicus). Gene expression and immunolocalization of Na(+)/Cl(-) cotransporter (NCC) and Na(+)/K(+)/2Cl(-) cotransporter (NKCC) were used as markers for freshwater (FW)- and seawater (SW)-type MRCs, respectively. In FW fish, hypophysectomy resulted in a significant drop in plasma osmolality, an effect associated with a marked reduction of NCC gene expression and the disappearance of MRCs with apical-NCC immunoreactivity. In contrast, hypophysectomy in SW fish did not impact plasma osmolality, NKCC, or Na(+), K(+)-ATPase(alpha1) gene expression, or the recruitment of MRCs with basolateral-NKCC. Hypophysectomized fish in SW exhibited reduced mRNA levels of prolactin (PRL) receptor 1 and growth hormone (GH) receptor in the gill; GH receptor expression was also reduced following hypophysectomy in FW. PRL replacement therapy restored NCC gene expression and the appearance of MRCs with apical NCC in both FW and SW; there was no interaction of PRL with cortisol. In FW, cortisol modestly stimulated NKCC mRNA levels, while no effect of GH was evident. In SW, no clear effects of hormone replacement on gene expression of NKCC, Na(+), K(+)-ATPase(alpha1), or hormone receptors were detected. Taken together, the essential nature of PRL to survival of Mozambique tilapia in FW is derived, at least in part, from its ability to stimulate the recruitment of MRCs that express NCC, while recruitment of SW-type MRCs does not require pituitary mediation in this euryhaline tilapia.