TY - JOUR
T1 - Post-transcription regulation of mRNA and hormone synthesis and release at the anterior pituitary gland
T2 - Information derived from the recovery of pituitary gonadotrope cell function after therapy with a GnRH agonist
AU - D'Occhio, M. J.
AU - Challen, G. A.
AU - Braga, D. P.A.F.
AU - Aspden, W. J.
AU - Trigg, T. E.
PY - 2000
Y1 - 2000
N2 - This review presents a summary of post-transcription regulation of mRNAs with a focus on the anterior pituitary gland. The control of gene transcription and production of mRNAs is the predominant form of regulation of hormone synthesis. However, post-transcription regulation of mRNAs provides another level of control of hormone synthesis. Examples of how hormone synthesis can be controlled at the level of MRNA include MRNA nuclear export and subcellular localization, MRNA stability and turnover, and regulation of MRNA translation. The gonadotrope cells of the anterior pituitary have multiple internal effector systems and provide an ideal model cell to study post-transcription regulation of mRNAs. Gonadotrope cells are stimulated to release LH and FSH by hypothalamic GnRH that binds to GnRH receptors. GnRH receptors are coupled to G-proteins and second messenger signaling pathways that involve cAMP and IP3. These signaling pathways are associated with the release of LH and FSH and transcription of mRNAs for LH and FSH. The stability of these mRNAs can be influenced by androgens, estrogens and progestagens. Therapy with a GnRH agonist leads to desensitization of gonadotrope cells to GnRH and a depletion of cellular stores of LH and FSH mRNAs, and content of LH and FSH. After discontinuation of therapy with GnRH agonist, levels of LH and FSH mRNAs return to normal some time before LH and FSH content and secretion are restored. This is indicative of post-transcription regulation of LH and FSH mRNAs. Future studies on post-transcription regulation of mRNAs will provide new molecular insights into how gonadotrope cells balance and integrate stimulation by GnRH with feedback modulation by the gonads.
AB - This review presents a summary of post-transcription regulation of mRNAs with a focus on the anterior pituitary gland. The control of gene transcription and production of mRNAs is the predominant form of regulation of hormone synthesis. However, post-transcription regulation of mRNAs provides another level of control of hormone synthesis. Examples of how hormone synthesis can be controlled at the level of MRNA include MRNA nuclear export and subcellular localization, MRNA stability and turnover, and regulation of MRNA translation. The gonadotrope cells of the anterior pituitary have multiple internal effector systems and provide an ideal model cell to study post-transcription regulation of mRNAs. Gonadotrope cells are stimulated to release LH and FSH by hypothalamic GnRH that binds to GnRH receptors. GnRH receptors are coupled to G-proteins and second messenger signaling pathways that involve cAMP and IP3. These signaling pathways are associated with the release of LH and FSH and transcription of mRNAs for LH and FSH. The stability of these mRNAs can be influenced by androgens, estrogens and progestagens. Therapy with a GnRH agonist leads to desensitization of gonadotrope cells to GnRH and a depletion of cellular stores of LH and FSH mRNAs, and content of LH and FSH. After discontinuation of therapy with GnRH agonist, levels of LH and FSH mRNAs return to normal some time before LH and FSH content and secretion are restored. This is indicative of post-transcription regulation of LH and FSH mRNAs. Future studies on post-transcription regulation of mRNAs will provide new molecular insights into how gonadotrope cells balance and integrate stimulation by GnRH with feedback modulation by the gonads.
KW - Anterior pituitary gland
KW - Desensitization
KW - Downregulation
KW - GnRH agonist
KW - MRNA stability
KW - Ovarian follicular growth
KW - Post-transcription regulation
UR - http://www.scopus.com/inward/record.url?scp=0034443690&partnerID=8YFLogxK
U2 - 10.5016/1806-8774.2000v2p91
DO - 10.5016/1806-8774.2000v2p91
M3 - Review article
AN - SCOPUS:0034443690
SN - 1806-8774
VL - 2
SP - 91
EP - 112
JO - Annual Review of Biomedical Sciences
JF - Annual Review of Biomedical Sciences
ER -