Membrane initiated steroid signaling

AB - It is well known that many of the actions of estrogen in the central nervous system are mediated via intracellular receptor/transcription factors that interact with steroid response elements on target genes. However, there now exists compelling evidence for membrane steroid receptors for estrogen in hypothalamic and other brain neurons. It is not well understood how estrogen signals via membrane receptors, and how these signals influence not only membrane excitability but also gene transcription in neurons. Indeed, it has been known for some time that estrogen can rapidly alter neuronal activity within seconds, indicating that some cellular effects can occur via membrane-delimited events. In addition, estrogen can affect second messenger systems including calcium mobilization and a plethora of kinases to alter cell signaling. Therefore, this review considers our current knowledge of rapid membrane-initiated and intracellular signaling by estrogen in the brain, and the nature of receptors involved and how they contribute to homeostatic functions.

RNA from SIGCs was isolated using the RNAzol isolation system following the manufacturer's instructions (Biotecx, Houston, TX). For reverse transcriptase-polymerase chain reaction (RT-PCR) analysis, 2 μg of total RNA was converted to first-strand cDNA with SuperScript II RNaseH − reverse transcriptase and oligo-dT primer (Life Technologies, Gaithersburg, MD). PCR was performed using 20% of the RT reaction product as template with primers specific for the ligand binding domain of the nuclear PR. The sense primer was identical to that described by Park and Mayo [ 28 ] (5′-GATGACCAGATAACTCTCAT-3′) and the antisense primer (5′-GTGAAAGAGAGAGGCTTC-3′) ends at position 2763 (accession L16922; [ 6 ]). The alpha chains of the GABA A receptor were detected using the primer pairs and protocol of Liu and Burt [ 29 ].

A 2014 study showed that a factor XIIa inhibitory antibody provides thromboprotection in extracorporeal circulation without increasing bleeding risk. [21] Experiments on neonatal animals showed that ECMO treatment can lead to apoptosis of enterocytes, damage of the intestinal mucosal barrier and bacterial translocation. This might explain greater severity of systemic inflammatory response syndrome in neonates. [22] ECMO has also seen its use on cadavers as being able to increase the viability rate of transplanted organs . [23]

AB - Background: We demonstrated that E2 conjugated to BSA (E2BSA) induces a rapid membrane-initiated inhibition of LH secretion followed hours later by a slight increase in LH secretion. Whether these actions of E2BSA are restricted to the pituitary gland and whether the membrane-initiated pathway of E2BSA contributes to the up-regulation of the number of GnRH receptors during the positive feedback effect of E2 were evaluated here. We have shown that the suppression of LH secretion induced by E2 and E2BSA is the result of a decreased responsiveness of the pituitary gland to GnRH. In this study we further tested the ability of E2BSA to decrease the responsiveness of the pituitary gland to GnRH under the paradigm of the preovulatory surge of LH induced by : For the first experiment GnRH and LH secretions were determined in samples of pituitary portal and jugular blood, respectively, in ewes treated with 12 mg E2BSA. In the second experiment, the number of GnRH receptors was quantified in ewes 12 h after administration of 25 micrograms E2 (the expected time for the increase in the number of GnRH receptors and the positive feedback effect of E2 in LH secretion) or 12 mg E2BSA. In the third experiment, the preovulatory-like surge of LH was characterized in ewes injected with 25 micrograms E2 alone or followed 8 h later (before the beginning of the LH surge) with 60 mg : a) the decrease in LH secretion induced by E2BSA was not accompanied by changes in the pulsatile pattern of GnRH, b) E2BSA increased the number of GnRH receptors, and c) the presence of E2BSA in E2-treated ewes delayed the onset, reduced the length, and decreased the amount of LH released during the preovulatory surge of : a) the rapid suppression of LH secretion induced by E2BSA is mediated only via a direct action on the pituitary gland, b) E2 acting via a membrane-initiated pathway contributes to increase the number of GnRH receptors and, c) administration of E2BSA near the beginning of the pre-ovulatory surge of LH delays and reduces the magnitude of the surge.

Membrane initiated steroid signaling

membrane initiated steroid signaling

AB - Background: We demonstrated that E2 conjugated to BSA (E2BSA) induces a rapid membrane-initiated inhibition of LH secretion followed hours later by a slight increase in LH secretion. Whether these actions of E2BSA are restricted to the pituitary gland and whether the membrane-initiated pathway of E2BSA contributes to the up-regulation of the number of GnRH receptors during the positive feedback effect of E2 were evaluated here. We have shown that the suppression of LH secretion induced by E2 and E2BSA is the result of a decreased responsiveness of the pituitary gland to GnRH. In this study we further tested the ability of E2BSA to decrease the responsiveness of the pituitary gland to GnRH under the paradigm of the preovulatory surge of LH induced by : For the first experiment GnRH and LH secretions were determined in samples of pituitary portal and jugular blood, respectively, in ewes treated with 12 mg E2BSA. In the second experiment, the number of GnRH receptors was quantified in ewes 12 h after administration of 25 micrograms E2 (the expected time for the increase in the number of GnRH receptors and the positive feedback effect of E2 in LH secretion) or 12 mg E2BSA. In the third experiment, the preovulatory-like surge of LH was characterized in ewes injected with 25 micrograms E2 alone or followed 8 h later (before the beginning of the LH surge) with 60 mg : a) the decrease in LH secretion induced by E2BSA was not accompanied by changes in the pulsatile pattern of GnRH, b) E2BSA increased the number of GnRH receptors, and c) the presence of E2BSA in E2-treated ewes delayed the onset, reduced the length, and decreased the amount of LH released during the preovulatory surge of : a) the rapid suppression of LH secretion induced by E2BSA is mediated only via a direct action on the pituitary gland, b) E2 acting via a membrane-initiated pathway contributes to increase the number of GnRH receptors and, c) administration of E2BSA near the beginning of the pre-ovulatory surge of LH delays and reduces the magnitude of the surge.

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