Prostaglandin F2α Receptor Concentrations in Corpora Lutea of Cycling, Pregnant, and Pseudopregnant Pigs1

Gadsby, John E.; Lovdal, J. A.; Britt, J.H.; Fitz, T. A.

doi:10.1095/biolreprod49.3.604

Cited by 44 publications

(22 citation statements)

References 17 publications

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“…We also tested 11␤-PGF 2␣ because it has an affinity for the FP receptor equal to PGF 2␣ (20) and is a PGF synthase product of PGD 2 (40 was the only eicosanoid besides PGF 2␣ to produce an increase in protein content at 10 Ϫ8 M, and the increase produced by the two FP receptor-specific agonists at 10 Ϫ8 M was equal to that produced by 100-fold higher concentrations of PGD 2 , PGE 2 , and PGF 1␣ . These results support the assumption that the growth-stimulatory effects of PGD 2 , PGE 2 , and PGF 1␣ at 10 (41). The potency of PGF 2␣ as a stimulus for myocyte growth in comparison with other eicosanoids (Fig.…”

Section: Protein Synthesis Is Increased In Ventricular Myocytessupporting

confidence: 84%

“…We found that PGF 2␣ stimulated the incorporation of [ 3 H]phenylalanine by cardiomyocytes at concentrations as low as 0.1 nM and obtained 50% of maximal stimulation at 11 nM. Our EC 50 value compares favorably with dissociation constants of 9 -47 nM for high affinity PGF 2␣ binding sites determined on luteal cells taken from cycling, pregnant, and pseudopregnant pigs (41) and the dissociation constant of 1.3 nM for COS cells transiently transfected with a murine FP receptor expression vector (20). In addition, our EC 50 (15) and agrees well with that calculated for phosphatidylinositol hydrolysis in transfected COS-1 cells (10 nM) (20).…”

Section: Discussionsupporting

confidence: 57%

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Prostaglandin F2α Stimulates Hypertrophic Growth of Cultured Neonatal Rat Ventricular Myocytes

Adams

Migita²,

Yu³

et al. 1996

Journal of Biological Chemistry

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During embryonic development the myocardium enlarges by the proliferation of cardiac myocytes. Shortly after birth, cardiac myocytes lose their capacity for mitogenesis, and further growth of the myocardium to meet the increasing hemodynamic demand of an elevated blood pressure and blood volume occurs by enlargement of existing muscle cells (hypertrophy). Similarly, the restoration of myocardial contractile performance lost to ischemia or viral infection is dependent on the recovery of injured myocytes and on the compensatory enlargement of agonist myocytes. Thus, an understanding of the controlling factors of myocardial protein synthesis and growth has implications for cardiac ontogeny, adaptation to chronic physiologic and pathophysiologic stimuli, and recovery from injury.Cardiac hypertrophy is produced by a variety of stimuli in culture and in vivo (1), including, but not limited to, mechanical stretch (2, 3), neurotransmitters (4, 5), and hormones (6, 7). As the biochemistry of myocardial growth is experimentally revealed, some common intracellular signaling pathways appear among primary stimuli. For example, stretch-induced cardiomyocyte hypertrophy is mediated, in part, by the local production of angiotensin II (8), and several hypertrophic stimuli, angiotensin II, norepinephrine, and endothelin-1, act through G q protein-coupled receptors (9 -11) and activate mitogen-activated protein kinases (12, 13). Direct evidence of G q involvement in cardiac growth was provided by microinjection of G q neutralizing antibodies to block the hypertrophic response of neonatal rat ventricular myocytes to the ␣ 1 -adrenergic agonist phenylephrine (9). Thus cardiac hypertrophy appears to be mediated, at least for several stimuli, by agonists of G q proteincoupled receptors.In addition to promoting myocardial growth, angiotensin II, norepinephrine, and endothelin-1 are vasoactive substances. Interestingly, Katz (14) speculated that angiotensin II evolved from a primitive growth factor and assumed additional regulatory roles in the cardiovascular system, such as stimulation of aldosterone production and smooth muscle contraction. It is conceivable that other vasoactive substances went through a similar evolutionary process, especially in consideration of the finding that Ca 2ϩ signaling is important for angiotensin II activation of mitogen-activated protein kinase in cardiac myocytes (13).Prostaglandin F 2␣ (PGF 2␣ ) 1 is a vasoactive substance that stimulates protein synthesis in skeletal and smooth muscle cells in culture (15,16). Moreover, PGF 2␣ regulates, in part, stretch-induced skeletal myoblast growth (16), and the effects of exogenous PGF 2␣ on vascular smooth muscle hypertrophy are most likely mediated by a PGF-specific receptor (15). As to the heart, PGF 2␣ was increased in the left ventricles of rabbits by acute pressure overload (17), and PG synthase inhibitors blocked cardiac growth induced by hypertension (18) and clenbuterol (19). These observations and others suggested that PGF 2␣ may play a role in the con...

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Section: Protein Synthesis Is Increased In Ventricular Myocytessupporting

confidence: 84%

Section: Discussionsupporting

confidence: 57%

Prostaglandin F2α Stimulates Hypertrophic Growth of Cultured Neonatal Rat Ventricular Myocytes

Adams

Migita²,

Yu³

et al. 1996

Journal of Biological Chemistry

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“…These results are not in agreement with previous studies (Gadsby et al 1990, in which a decreased amount of PGF 2a binding sites was noted in luteal cells of pregnant and pseudopregnant pigs. It is worthwhile to mention that Gadsby et al (1990Gadsby et al ( , 1993 measured the capacity of [3H]PGF 2a binding to its membrane receptors in isolated porcine luteal cells. Thus, the observed discrepancy could result from the different animal models and methods used.…”

Section: Rescue Of Luteal Function During Early Pregnancymentioning

confidence: 99%

Steroid hormones, prostanoids, and angiogenic systems during rescue of the corpus luteum in pigs

Przygrodzka¹,

Kaczmarek²,

Kaczyński³

et al. 2016

Reproduction

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In order to characterize the transition of the corpora lutea (CL) from acquisition of luteolytic sensitivity to rescue of luteal function: i) the expression of 38 factors associated with steroids, prostanoids, and angiogenic systems and ii) concentrations of the main hormones responsible for maintenance of CL function in cyclic and pregnant pigs were examined. Additionally, the effect of prostaglandin (PG) E 2 and F 2a on luteal function during the estrous cycle and pregnancy was evaluated in vitro. Significantly up-regulated gene expression was revealed in CL collected on day 14 of the estrous cycle (CYP19A1, ESR2, PTGS2, HIF1A, and EDN1) and on days 12-14 of pregnancy (SCARB1, PGRMC1, STAR, HSD3B1, NR5A1, PTGFR, PTGER4, and VEGFA). Elevated concentrations of estradiol-17b and PGE 2 occurred in CL on days 12 and 14 of pregnancy respectively, while an increased intraluteal PGF 2a content was noted on day 14 of the estrous cycle. Both PGs increased the synthesis of progesterone by cultured luteal slices obtained on day 14 of pregnancy, in contrast to the action of PGF 2a on the corresponding day of the estrous cycle. PGE 2 stimulated cAMP production via PTGER2 and PTGER4, while PGF 2a elevated the content of CREB in cultured luteal slices from CL of pregnant pigs. In silico analysis showed that infiltration of lymphocytes and apoptosis of microvascular endothelium were activated in CL on day 12 of the estrous cycle vs pregnancy. Summarizing, an abundance of E 2 and PGE 2 during pregnancy regulates specific pathways responsible for steroidogenesis, the prostanoid signaling system and angiogenesis during rescue from luteolysis in porcine CL.

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“…Although porcine CL abundantly express PGF2a receptors (PTGFR) in the early luteal phase [1,2], they remain insensitive to single treatment with exogenous PGF2a until Days 12 to 13 of the estrous cycle [3]. Interestingly, repeated injection of PGF2a on Day 5 of the estrous cycle induced luteolysis in pigs [4].…”

Section: Introductionmentioning

confidence: 99%

Expression of factors associated with apoptosis in the porcine corpus luteum throughout the luteal phase of the estrous cycle and early pregnancy: Their possible involvement in acquisition of luteolytic sensitivity

et al. 2015

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Prostaglandin F2α Receptor Concentrations in Corpora Lutea of Cycling, Pregnant, and Pseudopregnant Pigs1

Cited by 44 publications

References 17 publications

Prostaglandin F2α Stimulates Hypertrophic Growth of Cultured Neonatal Rat Ventricular Myocytes

Prostaglandin F2α Stimulates Hypertrophic Growth of Cultured Neonatal Rat Ventricular Myocytes

Steroid hormones, prostanoids, and angiogenic systems during rescue of the corpus luteum in pigs

Expression of factors associated with apoptosis in the porcine corpus luteum throughout the luteal phase of the estrous cycle and early pregnancy: Their possible involvement in acquisition of luteolytic sensitivity

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