1999
DOI: 10.1530/jrf.0.1170379
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Inhibition of ovulation by tyrosine kinase inhibitors in the in vitro perfused rat ovary

Abstract: did not ovulate and showed low secretion of progesterone and oestradiol. Addition of LH + 3-isobutyl-1-methylxanthine resulted in a marked stimulation of steroid release, and ovulations occurred in all ovaries (9.0 \ m=+-\ 0.9; mean \ m=+-\ sem). The protein tyrosine kinase inhibitors, genistein and tyrphostin A25, significantly inhibited ovulation at the higher concentrations tested (3.0 \m=+-\0.3at 100 \g=m\molgenistein l \m=-\1; 5.8 \ m=+-\ 1.0 at 500 \g=m\mol tyrphostin A25 l \ m=-\ 1) but no effect was se… Show more

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Cited by 8 publications
(7 citation statements)
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References 7 publications
(9 reference statements)
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“…Action TKs blockers demonstrated, that TKs can inhibit progesterone, estradiol, but not IGF-I and PGF-2 alpha output by mammalian granulosa nad whole ovarian follicles (Makarevich et al, 1997), although other studies did not confirm the involvement of TK signaling pathways in control of synthesis of mammalian ovarian steroids, plasminogen activator or prostaglandins (Matousek et al, 1999). In chicken ovaries, TKs was shown to suppress release of estradiol and argininevasotocin, but not progesterone and testosteron (Sirotkin and Grossmann, 2003).…”
Section: Protein Kinases Control Release Of Hormones By Ovarian Cellsmentioning
confidence: 95%
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“…Action TKs blockers demonstrated, that TKs can inhibit progesterone, estradiol, but not IGF-I and PGF-2 alpha output by mammalian granulosa nad whole ovarian follicles (Makarevich et al, 1997), although other studies did not confirm the involvement of TK signaling pathways in control of synthesis of mammalian ovarian steroids, plasminogen activator or prostaglandins (Matousek et al, 1999). In chicken ovaries, TKs was shown to suppress release of estradiol and argininevasotocin, but not progesterone and testosteron (Sirotkin and Grossmann, 2003).…”
Section: Protein Kinases Control Release Of Hormones By Ovarian Cellsmentioning
confidence: 95%
“…4). Effect of pharmacological activators or blockers of PKs showed, that PKA, PKG, MAPKs, PI3K/Akt, CDKs, TKs, and ALK can both promote (in some cases also suppress) ovarian granulosa cell proliferation (Makarevich et al, , 2004bTamura et al, 2004;Sirotkin andGrossmann, 2003, 2006;Wang and Tsang, 2007), although the ability of TK-dependent intracellular signaling to stimulate ovarian folliculogenesis and ovulation is reported too (Matousek et al, 1999). The cAMP/PKAdependent intracellular mechanisms can either inhibit (Peluso, 2006;Graves and Lawrence, 1996;Hsueh et al, 1996;Hillier and Tetsuka, 1997), stimulate (Cheadle et al, 2008;Viegas et al, 2008) or not influence (Dupont et al, 2008) follicular cell proliferation, but other PKs are involved predominantly in promotion of ovarian cell cycle.…”
Section: Protein Kinases Control Ovarian Cell Proliferationmentioning
confidence: 99%
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“…Different caspase inhibitors (dissolved in Me 2 SO) diluted in 0.15 M NaCl solution or vehicle solution for the respective inhibitors (15 g/ ovary) were injected into the ovarian bursal cavity in a volume of 60 l. Only animals with the swelling of bursa and no visible leakage of the injected fluids were included in the study (n ϭ 3 rats/treatment group). The intrabursal route of administration has been utilized in various in vivo studies to deliver different drugs to the ovary (31)(32)(33). After the completion of the injection procedure, ovaries were returned to the abdominal cavity and the abdominal wall was sutured with absorbable suture and the skin with the surgical clips.…”
Section: A Pgf 2␣ -Induced Luteal Tissue Apoptosis In the Buffalo Comentioning
confidence: 99%
“…In recent years, evidence has begun to accumulate that, NGF and its receptors trkA and p75 have important roles in sexual development [8], folliclular development and ovulation [14][15][16]. In mammals, throughout the functional lifespan of the ovary, the process of follicle recruitment, follicular development and ovulation, secretion of steroid hormones is cyclic a n d d e p e n d s o n t h e c y c l i c s e c r e t i o n o f gonadotropins from the pituitary [17].…”
Section: T O D a T E B E S I D E S N G F B R A I N -D E R I V E Dmentioning
confidence: 99%