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פותח על ידי קלירמאש פתרונות בע"מ -
Pituitary Adenylate Cyclase Activating Polypeptide and Neuropeptide Y
Year:
2002
Source of publication :
Neuroendocrinology
Authors :
בונפיל, דוד
;
.
Volume :
75
Co-Authors:

Gal Gura, Helena Safariana, Zvi Naor, Zvi Yaron

Departments of Zoology and Biochemistry, and The Norman and Rose Lederer Chair of Experimental Biology, Tel-Aviv University, Tel Aviv, Israel

Facilitators :
From page:
164
To page:
174
(
Total pages:
11
)
Abstract:

There is ample information on the hypophysiotropic function of pituitary adenylate cyclase-activating polypeptide (PACAP) and neuropeptide Y (NPY) in fish as in mammals, although evidence as to their direct effects on gonadotropic cells is scarce. We have previously reported that NPY and PACAP38 augment gonadotropinreleasing hormone (GnRH)-induced expression of glycoprotein · (·) subunit gene in the teleost fish, tilapia. The aim of the present study was to elucidate possible direct effects of these peptides on gonadotropin subunit gene expression in culture of tilapia pituitary cells, as well as the transduction pathways involved. Both NPY and PACAP38 (0.001–10 nM) increased the level of phosphorylated extracellular signal-regulated kinase (pERK) dosedependently, reaching a peak at 0.1 and 0.01 nM, respectively. Inhibition of protein kinase C (PKC) by GF109203X (GF; 0.01–10 nM) suppressed NPY-stimulated pERK levels and its effect on · and luteinizing hormone (LH) ß subunit mRNA levels. However, NPY had no effect on follicle stimulating hormone (FSH) ß mRNA levels. NPY-elevated ·, LHß mRNA and pERK levels were also attenuated by inhibition of protein kinase A (PKA) with H89 (0.01– 10 nM). Exposure of the cells to the MAPK kinase (MEK) inhibitor (PD98059; PD 10, 25 and 50 ÌM) completely blocked NPY-induced ERK activity. In addition, this inhibitor abated the · and LHß mRNA responses to NPY. Similar experiments conducted to elucidate PACAP38 signaling revealed that PACAP38 (0.01 nM) elevated all threegonadotropin subunit gene expression via both PKCERK and PKA-ERK cascades. It is suggested that both NPY and PACAP38 act directly on gonadotropes to elevate gonadotropin subunit gene expression. Whereas the expression of · and LHß subunit genes is regulated by both NPY and PACAP, the effect on the FSHß transcript is elicited only by PACAP38. NPY and PACAP38 stimulatory actions are mediated via protein kinase C (PKC) and protein kinase A (PKA), converging at the MEK-ERK cascade. These findings represent one of the fine tuning levels that differentially regulates gonadotropin subunit gene expression

Note:
Related Files :
Fishes
Gonadotropins
neuropeptide
Pituitary adenylate cyclase-activating polypeptide
Protein Kinases
עוד תגיות
תוכן קשור
More details
DOI :
Article number:
0
Affiliations:
Database:
גוגל סקולר
Publication Type:
מאמר
;
.
Language:
אנגלית
Editors' remarks:
ID:
39197
Last updated date:
02/03/2022 17:27
Creation date:
03/02/2019 13:16
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Scientific Publication
Pituitary Adenylate Cyclase Activating Polypeptide and Neuropeptide Y
75

Gal Gura, Helena Safariana, Zvi Naor, Zvi Yaron

Departments of Zoology and Biochemistry, and The Norman and Rose Lederer Chair of Experimental Biology, Tel-Aviv University, Tel Aviv, Israel

Pituitary Adenylate Cyclase Activating Polypeptide and Neuropeptide Y Regulation of Gonadotropin Subunit Gene Expression in Tilapia: Role of PKC, PKA and ERK

There is ample information on the hypophysiotropic function of pituitary adenylate cyclase-activating polypeptide (PACAP) and neuropeptide Y (NPY) in fish as in mammals, although evidence as to their direct effects on gonadotropic cells is scarce. We have previously reported that NPY and PACAP38 augment gonadotropinreleasing hormone (GnRH)-induced expression of glycoprotein · (·) subunit gene in the teleost fish, tilapia. The aim of the present study was to elucidate possible direct effects of these peptides on gonadotropin subunit gene expression in culture of tilapia pituitary cells, as well as the transduction pathways involved. Both NPY and PACAP38 (0.001–10 nM) increased the level of phosphorylated extracellular signal-regulated kinase (pERK) dosedependently, reaching a peak at 0.1 and 0.01 nM, respectively. Inhibition of protein kinase C (PKC) by GF109203X (GF; 0.01–10 nM) suppressed NPY-stimulated pERK levels and its effect on · and luteinizing hormone (LH) ß subunit mRNA levels. However, NPY had no effect on follicle stimulating hormone (FSH) ß mRNA levels. NPY-elevated ·, LHß mRNA and pERK levels were also attenuated by inhibition of protein kinase A (PKA) with H89 (0.01– 10 nM). Exposure of the cells to the MAPK kinase (MEK) inhibitor (PD98059; PD 10, 25 and 50 ÌM) completely blocked NPY-induced ERK activity. In addition, this inhibitor abated the · and LHß mRNA responses to NPY. Similar experiments conducted to elucidate PACAP38 signaling revealed that PACAP38 (0.01 nM) elevated all threegonadotropin subunit gene expression via both PKCERK and PKA-ERK cascades. It is suggested that both NPY and PACAP38 act directly on gonadotropes to elevate gonadotropin subunit gene expression. Whereas the expression of · and LHß subunit genes is regulated by both NPY and PACAP, the effect on the FSHß transcript is elicited only by PACAP38. NPY and PACAP38 stimulatory actions are mediated via protein kinase C (PKC) and protein kinase A (PKA), converging at the MEK-ERK cascade. These findings represent one of the fine tuning levels that differentially regulates gonadotropin subunit gene expression

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