Steady-state concentrations of mRNA encoding two inhibitors of protein kinase C in ovine luteal tissue.
Prostaglandin F2 alpha (PGF2 alpha) decreases secretion of progesterone from the corpus luteum in domestic ruminants. However, it is less effective during the early part of the oestrous cycle (Louis et al., 1973) and at the time of maternal recognition of pregnancy (Silvia and Niswender, 1984; Lacroix and Kann, 1986). Decreased luteal responsiveness may be due to failure of PGF2 alpha to activate fully its normal second messenger system, protein kinase C (PKC). Alternatively, increased resistance of the corpus luteum to PGF2 alpha might be attributable to greater concentrations of recently identified biological inhibitors of PKC. These possibilities were addressed by measuring steady-state concentrations of mRNA encoding PGF2 alpha receptor and two inhibitors of PKC, protein kinase C inhibitor-1 (PKCI-1) and kinase C inhibitor protein-1 (KCIP-1, brain 14-3-3 protein), in corpora lutea collected from ewes on days 4, 10 and 15 of the oestrous cycle (n = 5 per day) and day 15 of pregnancy (n = 7). There were no differences in mean concentrations of mRNA encoding PGF2 alpha receptor among the groups. However, concentrations of mRNA encoding both inhibitors of PKC were higher (P < 0.01) on day 4 of the oestrous cycle compared with the other groups. Treatment of ewes with a luteolytic dose of PGF2 alpha, which activates PKC, did not change concentrations of mRNA encoding either PKCI-1 or KCIP-I up to 24 h later. Luteal expression of mRNA encoding the PKC inhibitors and PGF2 alpha receptor was also examined in ewes treated with oestradiol in vivo for 16 h in the midluteal phase. High concentrations of oestradiol in serum (20 and 70 pg ml-1) did not influence quantities of any of the mRNAs examined. Therefore, an increase in PKC inhibitors may be involved in resistance of the corpus luteum to PGF2 alpha during the early part of the oestrous cycle but does not appear to mediate the increased resistance of the corpus luteum to PGF2 alpha during maternal recognition of pregnancy. Neither PGF2 alpha nor oestradiol affected steady-state concentrations of mRNAs encoding PKCI-1 or KCIP-I.
Juengel
J L
JL
Animal Reproduction and Biotechnology Laboratory, Colorado State University, Fort Collins 80523, USA.
Melner
M H
MH
Clapper
J A
JA
Turzillo
A M
AM
Moss
G E
GE
Nett
T M
TM
Niswender
G D
GD
D048948:14-3-3 Proteins; D000818:Animals; D001345:Autoradiography; D003338:Corpus Luteum / Q000187:drug effects / Q000378:metabolism*; D015237:Dinoprost / Q000494:pharmacology; D004791:Enzyme Inhibitors; D004958:Estradiol / Q000097:blood / Q000494:pharmacology; D004971:Estrus / Q000378:metabolism; D005260:Female; D009419:Nerve Tissue Proteins / Q000235:genetics; D011247:Pregnancy; D011374:Progesterone / Q000097:blood; D011493:Protein Kinase C / Q000037:antagonists & inhibitors*; D011506:Proteins / Q000235:genetics; D012333:RNA, Messenger / Q000032:analysis; D011982:Receptors, Prostaglandin / Q000235:genetics; D012756:Sheep / Q000378:metabolism*; D014446:Tyrosine 3-Monooxygenase
D048948:14-3-3 Proteins; D004791:Enzyme Inhibitors; D009419:Nerve Tissue Proteins; D011506:Proteins; D012333:RNA, Messenger; D011982:Receptors, Prostaglandin; C034671:prostaglandin F2alpha receptor; D011374:Progesterone; D004958:Estradiol; D015237:Dinoprost; D014446:Tyrosine 3-Monooxygenase; D011493:Protein Kinase C