| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Department of Zoology, University of Hong Kong, Pokfulam Road, Hong Kong SAR, People’s Republic of China
(Requests for offprints should be addressed to A O L Wong; Email: olwong{at}hkucc.hku.hk)
Growth hormone (GH) is known to stimulate luteinizing hormone (LH) release via paracrine interactions between somatotrophs and gonadotrophs. However, it is unclear if LH can exert a reciprocal effect to modulate somatotroph functions. Here we examined the paracrine effects of LH on GH gene expression using grass carp pituitary cells as a cell model. LH receptors were identified in grass carp somatotrophs and their activation by human chorionic gonadotropin (hCG) increased ‘steady-state’ GH mRNA levels. Removal of endogenous LH by immunoneutralization using LH antiserum inhibited GH release and GH mRNA expression. GH secretagogues, including gonadotrophin releasing hormone (GnRH), pituitary adenylate cyclase-activating polypeptide (PACAP) and apomorphine, were effective in elevating GH mRNA levels but these stimulatory actions were blocked by LH antiserum. In pituitary cells pretreated with actinomycin D, the half-life of GH mRNA was not affected by hCG but was enhanced by LH immunoneutralization. Treatment with LH antiserum also suppressed basal levels of mature GH mRNA and primary transcripts. hCG increased cAMP synthesis in carp pituitary cells and hCG-induced GH mRNA expression was mimicked by forskolin but suppressed by inhibiting adenylate cyclase and protein kinase A. Similarly, the stimulatory actions of hCG and forskolin on GH mRNA expression were blocked by inhibiting Janus kinase 2 (JAK2) and MAP kinase (MAPK), including P42/44MAPK and P38 MAPK. These results suggest that LH is essential for the maintenance of GH release, GH gene expression, and somatotroph responsiveness to GH-releasing factors. The paracrine actions of LH on GH mRNA expression are mediated by a concurrent increase in GH gene transcription and GH mRNA turnover, probably through JAK2/MAPK coupled to the cAMP-dependent pathway.
This article has been cited by other articles:
|
|
 |
|
  M. Lasa, B. Gil-Araujo, M. Palafox, and A. Aranda Thyroid Hormone Antagonizes Tumor Necrosis Factor-{alpha} Signaling in Pituitary Cells through the Induction of Dual Specificity Phosphatase 1 Mol. Endocrinol., February 1, 2010; 24(2): 412 - 422. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Q. Jiang, W. K. W. Ko, E. A. Lerner, K. M. Chan, and A. O. L. Wong Grass carp somatolactin: I. Evidence for PACAP induction of somatolactin-{alpha} and -{beta} gene expression via activation of pituitary PAC-I receptors Am J Physiol Endocrinol Metab, August 1, 2008; 295(2): E463 - E476. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Q. Jiang, M. He, X. Wang, and A. O. L. Wong Grass carp somatolactin: II. Pharmacological study on postreceptor signaling mechanisms for PACAP-induced somatolactin-{alpha} and -{beta} gene expression Am J Physiol Endocrinol Metab, August 1, 2008; 295(2): E477 - E490. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. H. Sze, H. Zhou, Y. Yang, M. He, Y. Jiang, and A. O. L. Wong Pituitary Adenylate Cyclase-Activating Polypeptide (PACAP) as a Growth Hormone (GH)-Releasing Factor in Grass Carp: II. Solution Structure of a Brain-Specific PACAP by Nuclear Magnetic Resonance Spectroscopy and Functional Studies on GH Release and Gene Expression Endocrinology, October 1, 2007; 148(10): 5042 - 5059. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. Huo, G. Fu, X. Wang, W. K. W. Ko, and A. O. L. Wong Modulation of Calmodulin Gene Expression as a Novel Mechanism for Growth Hormone Feedback Control by Insulin-like Growth Factor in Grass Carp Pituitary Cells Endocrinology, September 1, 2005; 146(9): 3821 - 3835. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
