(c) 2012 Elsevier Inc. All rights reserved.”
“The objective

FK506 chemical structure of the present study was to evaluate the effects of ghrelin on the concentrations of estrogen (E-2) and progesterone (P-4) in serum and the mRNA expression of estrogen receptor beta (ER beta) and progesterone receptor (PRA+B) in ovary in rats during estrous cycle. Adult female Sprague Dawley rats were intracerebroventricularly (i.c.v.) injected with 3 nmol ghrelin during the estrous cycle, and sacrificed 15 min later. Blood samples and ovaries were collected. The concentrations of serum E-2 and P-4 were measured by radioimmunoassay, while the amount of ER beta and PRA+B mRNA was assessed by real-time quantitative PCR. Our studies showed that ghrelin could significantly reduce the serum concentration of E-2 throughout the estrous cycle (P < 0.05), the serum level of P-4 (P < 0.05), and the amount of ER beta mRNA during metestrus (P < 0.05). Meanwhile, the amount of PRA+B mRNA was only reduced during diestrus (P < 0.05). Overall, our present findings provide the first

evidence that i.c.v. injection of ghrelin could reduce the serum concentration of E-2 and www.selleckchem.com/HDAC.html P-4 and the level of ER beta and PRA+B mRNA expression, supporting the role of ghrelin in reproduction.”
“Besides their role in cardiac repolarization, human ether-a-go-go-related gene potassium (hERG) channels are expressed in several tumor cells including rhabdomyosarcoma cells. JQ1 The channels foster cell proliferation. Ubiquitously expressed AMP-dependent protein kinase (AMPK) is a serine-/threonine kinase, stimulating energy-generating and inhibiting energy-consuming processes thereby helping cells survive periods of energy depletion. AMPK has previously been shown to regulate Na+/K+ ATPase, Na+/Ca2+ exchangers, Ca2+ channels and K+ channels. The present study

tested whether AMPK regulates hERG channel activity. Wild type AMPK (alpha 1 beta 1 gamma 1), constitutively active (gamma R70Q)AMPK (alpha 1 beta 1 gamma 1(R70Q)), or catalytically inactive (alpha K45R)AMPK (alpha 1(K45R)beta 1 gamma 1) were expressed in Xenopus oocytes with hERG. Tail currents were determined as a measure of hERG channel activity by two-electrode-voltage clamp. hERG membrane abundance was quantified by chemiluminescence and visualized by immunocytochemistry and confocal microscopy. Moreover, hERG currents were measured in RD rhabdomyosarcoma cells after pharmacological modification of AMPK activity using the patch clamp technique. Coexpression of wild-type AMPK and of constitutively active (gamma R70Q)AMPK significantly downregulated the tail currents in hERG-expressing Xenopus oocytes. Pharmacological activation of AMPK with AICAR or with phenformin inhibited hERG currents in Xenopus oocytes, an effect abrogated by AMPK inhibitor compound C. (gamma R70Q)AMPK enhanced the Nedd4-2-dependent downregulation of hERG currents.