The Calcium Component of Gonadotropin-Releasing Hormone-Stimulated Luteinizing Hormone Subunit Gene Transcription Is Mediated by Calcium/Calmodulin-Dependent Protein Kinase Type II | Zendy

Daniel J. Haisenleder | Zendy; Heather A. Ferris | Zendy; Margaret A. Shupnik | Zendy

Open Access

The Calcium Component of Gonadotropin-Releasing Hormone-Stimulated Luteinizing Hormone Subunit Gene Transcription Is Mediated by Calcium/Calmodulin-Dependent Protein Kinase Type II

Author(s) -

Daniel J. Haisenleder,

Heather A. Ferris,

Margaret A. Shupnik

Publication year - 2003

Publication title -

endocrinology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.674

H-Index - 257

eISSN - 1945-7170

pISSN - 0013-7227

DOI - 10.1210/en.2002-0013

Subject(s) - camk , endocrinology , medicine , gonadotropin releasing hormone , calcium , calmodulin , voltage dependent calcium channel , ibmx , calcium channel , gonadotropic cell , biology , calcium in biology , protein kinase a , chemistry , luteinizing hormone , kinase , microbiology and biotechnology , forskolin , hormone , autophosphorylation , stimulation

Calcium influx plays a critical role in GnRH regulation of rat LH subunit gene transcription, but the site(s) of action are undefined. We investigated the potential of GnRH acting through calcium to activate calcium/calmodulin-dependent protein kinase type II (Ca/CaMK II) in mouse gonadotrope-derived LβT2 cells. GnRH stimulated Ca/CaMK II β subunit activity 3-fold 2 min after treatment and returned to control values by 45 min. The Ca/CaMK II response to GnRH was blocked by administration of the Ca/CaMK II-specific inhibitor, KN-93. The calcium channel activator Bay K 8644 stimulated a 3-fold increase in Ca/CaMK II activity, similar to GnRH. Blocking calcium influx with nimodipine or depleting intracellular calcium storage pools with thapsigargin each resulted in a partial suppression of GnRH-induced activation of Ca/CaMK II, and in combination, completely suppressed the Ca/CaMK II response to GnRH. KN-93 and nimodipine also suppressed α-subunit and LHβ promoter responses to GnRH by 40–60%. LHβ promoter constructs containing either proximal or proximal and distal GnRH-responsive regions were sensitive to inhibition. These data show for the first time that Ca/CaMK II activation plays an important role in the transmission of GnRH signals from the plasma membrane to the LH subunit genes.

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