Apoptosis of bovine granulosa cells: Intracellular pathways and differentiation

Follicular atresia in granulosa and theca cells occurs by apoptosis through weak hormonal stimulation. We have previously proposed an in vitro model to study this process by inducing apoptosis in BGC-1, a bovine granulosa cell line, and in primary cultures from ovaries with or without corpus luteum...

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Bibliographic Details
Published in:Acta histochemica 2017-06, Vol.119 (5), p.462-470
Main Authors: Carou, M.C., Cruzans, P.R., Maruri, A., Farina, M.G., Fiorito, C.D., Olea, G., Lombardo, D.M.
Format: Article
Language:English
Subjects:
3β-HSD
Animals
Apoptosis
Apoptosis - drug effects
Apoptosis - physiology
bcl-2-Associated X Protein - genetics
BGC-1
Bovine granulosa cells
Cattle
Cell Differentiation - drug effects
Cell Differentiation - physiology
Cell Line
Cells, Cultured
Differentiation
Enzyme Activation - drug effects
Female
Gene Expression Regulation, Developmental - drug effects
Genes, bcl-2 - genetics
GnRH analogs
Gonadotropin-Releasing Hormone - analogs & derivatives
Gonadotropin-Releasing Hormone - metabolism
Granulosa Cells - cytology
Granulosa Cells - drug effects
Leuprolide - pharmacology
Mitochondria - drug effects
Mitochondria - metabolism
Oligopeptides - pharmacology
Ovary - cytology
Ovary - metabolism
Phospholipase D - metabolism
Signal Transduction
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Summary:Follicular atresia in granulosa and theca cells occurs by apoptosis through weak hormonal stimulation. We have previously proposed an in vitro model to study this process by inducing apoptosis in BGC-1, a bovine granulosa cell line, and in primary cultures from ovaries with or without corpus luteum (CPGB+ and CPGB−, respectively), with different doses of gonadotropin releasing hormone (GnRH) analogs (leuprolide acetate (LA) as agonist and antide as antagonist). BGC-1 represent immature granulosa cells, whereas CPGB represent different degrees of luteinization. Our aim was to evaluate the intracellular pathways involved in the GnRH regulation of apoptosis in BGC-1. Treatment with LA 100nM but not with antide led to an increase in BAX over BCL-2 expression, showing antagonism of antide. All treatments inhibited phospholipase-D (PLD) activity compared to control, implying agonist behavior of antide. Progesterone in vitro production and 3β-hydroxysteroid dehydrogenase (3β-HSD) expression revealed different degrees of luteinization: BGC-1 were immature, whereas CPGB+ were less differentiated than CPGB−. We concluded that LA-induced apoptosis in BGC-1 occurs by activation of the mitochondrial pathway and by inhibition of PLD activity and that antide might work both as an antagonist of the intrinsic pathway and as an agonist of the extrinsic protection pathway by inhibiting PLD activity.
ISSN:0065-1281
1618-0372
DOI:10.1016/j.acthis.2017.04.010