Role of Cocaine- and Amphetamine-Regulated Transcript (CART) in Regulation of Antral Follicle Development in Cattle: Demonstration of Inhibitory Effects of the CART Peptide on Follicular Estradiol Production and Granulosa Cell Aromatase mRNA In Vivo and Potential FSH Regulation of CART Receptor Binding.

2009 ◽  
Vol 81 (Suppl_1) ◽  
pp. 156-156
Author(s):  
Joseph K. Folger ◽  
Fermin Jimenez-Krassel ◽  
James J. Ireland ◽  
George W. Smith
Keyword(s):  
Granulosa Cell ◽  
Receptor Binding ◽  
Antral Follicle ◽  
Follicle Development ◽  
Inhibitory Effects ◽  
Cart Peptide ◽  
Aromatase Mrna

scholarly journals The role of IGFs in the regulation of ovarian follicular growth in the brushtail possum (Trichosurus vulpecula)

Reproduction ◽  
2010 ◽  
Vol 140 (2) ◽  
pp. 295-303 ◽  
Author(s):  
Jennifer L Juengel ◽  
Lisa J Haydon ◽  
Brigitta Mester ◽  
Brian P Thomson ◽  
Michael Beaumont ◽  
...  
Keyword(s):  
Granulosa Cell ◽  
Granulosa Cells ◽  
Cell Function ◽  
Antral Follicle ◽  
Brushtail Possum ◽  
Follicular Growth ◽  
Theca Cells ◽  
Ovarian Follicular Growth

IGFs are known to be key regulators of ovarian follicular growth in eutherian mammals, but little is known regarding their role in marsupials. To better understand the potential role of IGFs in the regulation of follicular growth in marsupials, expression of mRNAs encoding IGF1, IGF2, IGF1R, IGF-binding protein 2 (IGFBP2), IGFBP4 and IGFBP5 was localized by in situ hybridization in developing ovarian follicles of the brushtail possum. In addition, the effects of IGF1 and IGF2 on granulosa cell function were tested in vitro. Both granulosa and theca cells synthesize IGF mRNAs, with the theca expressing IGF1 mRNA and granulosa cell expressing IGF2 mRNA. Oocytes and granulosa cells express IGF1R. Granulosa and theca cells expressed IGFBP mRNAs, although the pattern of expression differed between the BPs. IGFBP5 mRNA was differentially expressed as the follicles developed with granulosa cells of antral follicles no longer expressing IGFBP5 mRNA, suggesting an increased IGF bioavailability in the antral follicle. The IGFBP protease, PAPPA mRNA, was also expressed in granulosa cells of growing follicles. Both IGF1 and IGF2 stimulated thymidine incorporation but had no effect on progesterone production. Thus, IGF may be an important regulator of ovarian follicular development in marsupials as has been shown in eutherian mammals.

Role of Receptor Binding and Gene Transcription for Both of Stimulatory and Inhibitory Effects of Interleukin-1 In Pancreatic β-Cells

Autoimmunity ◽  
1992 ◽  
Vol 12 (2) ◽  
pp. 127-133 ◽  
Author(s):  
Décio L. Eizirik ◽  
Daniel E. Tracey ◽  
Klaus Bendtzen ◽  
Stellan Sandler
Keyword(s):  
Gene Transcription ◽  
Receptor Binding ◽  
Interleukin 1 ◽  
Inhibitory Effects ◽  
Β Cells ◽  
Pancreatic Β Cells

Abstract 13598: The G-protein BetaGamma Subunits Regulate Platelet Function

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Ahmed Alarabi ◽  
Zubair Karim ◽  
Victoria Hinojos ◽  
Patricia A Lozano ◽  
Keziah Hernandez ◽  
...  
Keyword(s):  
G Protein ◽  
Platelet Function ◽  
Thrombus Formation ◽  
Human Platelets ◽  
Inhibitory Effects ◽  
Clot Retraction ◽  
Betagamma Subunits

Platelet activation involves tightly regulated processes to ensure a proper hemostasis response, but when unbalanced, can lead to pathological consequences such as thrombus formation. G-protein coupled receptors (GPCRs) regulate platelet function by interacting with and mediating the response to various physiological agonists. To this end, an essential mediator of GPCR signaling is the G protein Gαβγ heterotrimers, in which the βγ subunits are central players in downstream signaling pathways. While much is known regarding the role of the Gα subunit in platelet function, that of the βγ remains poorly understood. Therefore, we investigated the role of Gβγ subunits in platelet function using a Gβγ (small molecule) inhibitor, namely gallein. We observed that gallein inhibits platelet aggregation and secretion in response to agonist stimulation, in both mouse and human platelets. Furthermore, gallein also exerted inhibitory effects on integrin αIIbβ3 activation and clot retraction. Finally, gallein’s inhibitory effects manifested in vivo , as documented by its ability to modulate physiological hemostasis and delay thrombus formation. Taken together, our findings demonstrate, for the first time, that Gβγ directly regulates GPCR-dependent platelet function, in vitro and in vivo . Moreover, these data highlight Gβγ as a novel therapeutic target for managing thrombotic disorders.

Role of adenosine in noradrenergic neurotransmission in spontaneously hypertensive rats

1987 ◽  
Vol 253 (4) ◽  
pp. H909-H918 ◽  
Author(s):  
E. K. Jackson
Keyword(s):  
Plasma Levels ◽  
Spontaneously Hypertensive Rat ◽  
Base Line ◽  
Inhibitory Effects ◽  
Spontaneously Hypertensive ◽  
Vascular Responses ◽  
Rat Mesentery ◽  
Wistar Kyoto

The purpose of this study was to compare the in vivo role of adenosine as a modulator of noradrenergic neurotransmission in the spontaneously hypertensive rat (SHR) and Wistar-Kyoto control rat (WKY). In the in situ blood-perfused rat mesentery, vascular responses to periarterial (sympathetic) nerve stimulation (PNS) and to exogenous norepinephrine (NE) were enhanced in SHR compared with WKY. In both SHR and WKY, vascular responses to PNS were more sensitive to inhibition by adenosine than were responses to NE. At matched base-line vascular responses, compared with WKY, SHR were less sensitive to the inhibitory effects of adenosine on vascular responses to PNS, but SHR and WKY were equally sensitive with respect to adenosine-induced inhibition of responses to NE. Antagonism of adenosine receptors with 1,3-dipropyl-8-p-sulfophenylxanthine shifted the dose-response curve to exogenous adenosine sixfold to the right yet did not influence vascular responses to PNS or NE in either SHR or WKY. Furthermore, PNS did not alter either arterial or mesenteric venous plasma levels of adenosine in SHR or WKY, and plasma levels of adenosine in both strains were always lower than the calculated threshold level required to attenuate neurotransmission. It is concluded that in vivo 1) exogenous adenosine interferes with noradrenergic neurotransmission in both SHR and WKY; 2) SHR are less sensitive to the inhibitory effects of exogenous adenosine on noradrenergic neurotransmission than are WKY; 3) endogenous adenosine does not play a role in modulating neurotransmission in either strain under the conditions of this study; and 4) enhanced noradrenergic neurotransmission in the SHR is not due to defective modulation of neurotransmission by adenosine.

scholarly journals Salt-inducible Kinases Are Critical Determinants of Female Fertility

Endocrinology ◽  
2020 ◽  
Vol 161 (7) ◽  
Author(s):  
Marah Armouti ◽  
Nicola Winston ◽  
Osamu Hatano ◽  
Elie Hobeika ◽  
Jennifer Hirshfeld-Cytron ◽  
...  
Keyword(s):  
Ovarian Function ◽  
Follicle Stimulating Hormone ◽  
Female Fertility ◽  
Camp Signaling ◽  
Follicle Development ◽  
Pharmacological Modulation ◽  
Ovarian Granulosa Cells ◽  
Different Levels

Abstract Follicle development is the most crucial step toward female fertility and is controlled mainly by follicle-stimulating hormone (FSH). In ovarian granulosa cells (GCs), FSH activates protein kinase A by increasing 3′,5′-cyclic adenosine 5′-monophosphate (cAMP). Since cAMP signaling is impinged in part by salt-inducible kinases (SIKs), we examined the role of SIKs on the regulation of FSH actions. Here, we report that SIKs are essential for normal ovarian function and female fertility. All SIK isoforms are expressed in human and rodent GCs at different levels (SIK3>SIK2>SIK1). Pharmacological inhibition of SIK activity potentiated the stimulatory effect of FSH on markers of GC differentiation in mouse, rat, and human GCs and estradiol production in rat GCs. In humans, SIK inhibition strongly enhanced FSH actions in GCs of patients with normal or abnormal ovarian function. The knockdown of SIK2, but not SIK1 or SIK3, synergized with FSH on the induction of markers of GC differentiation. SIK inhibition boosted gonadotropin-induced GC differentiation in vivo, while the genomic knockout of SIK2 led to a significant increase in the number of ovulated oocytes. Conversely, SIK3 knockout females were infertile, FSH insensitive, and had abnormal folliculogenesis. These findings reveal novel roles for SIKs in the regulation of GC differentiation and female fertility, and contribute to our understanding of the mechanisms regulated by FSH. Furthermore, these data suggest that specific pharmacological modulation of SIK2 activity could be of benefit to treat ovulatory defects in humans and to increase the propagation of endangered species and farm mammals.

Follicular somatic cell factors and follicle development

2011 ◽  
Vol 23 (1) ◽  
pp. 32 ◽  
Author(s):  
J. Buratini ◽  
C. A. Price
Keyword(s):  
Somatic Cell ◽  
Granulosa Cell ◽  
Bone Morphogenetic Proteins ◽  
Granulosa Cells ◽  
Primordial Follicle ◽  
Antral Follicle ◽  
Follicle Development ◽  
Follicle Growth ◽  
Theca Cells ◽  
Secreted Factors

Considerable attention is currently paid to oocyte-derived secreted factors that act upon cumulus and granulosa cells. Also important for follicle development are somatic cell-derived secreted factors. This is illustrated by the ability of granulosa cell-derived Kit ligand (KITL) to promote primordial follicle activation, and the loss of follicle development that accompanies KITL gene disruption. This review summarises our current understanding of somatic cell factors during both preantral and antral follicle growth, involving not only signalling from granulosa cells to the oocyte, but also signalling between granulosa and theca cells. Principal granulosa cell-derived factors include activin, anti-Müllerian hormone (AMH), bone morphogenetic proteins (BMPs) and fibroblast growth factors (FGFs). Theca cells also secrete BMPs and FGFs. The interplay between these factors is equally important for follicle growth as the activity of oocyte-derived factors.

scholarly journals What is molt-inhibiting hormone? The role of an ecdysteroidogenesis inhibitor in the crustacean molting cycle

1989 ◽  
Vol 86 (17) ◽  
pp. 6826-6829 ◽  
Author(s):  
Yoko Naya ◽  
Mayumi Ohnishi ◽  
Midori Ikeda ◽  
Wataru Miki ◽  
Koji Nakanishi
Keyword(s):  
Procambarus Clarkii ◽  
Active Form ◽  
Xanthurenic Acid ◽  
Sinus Gland ◽  
Inhibitory Effects ◽  
Molting Cycle ◽  
Biosynthesis Inhibitors

The in vivo molt-inhibitory effects of the ecdysone biosynthesis inhibitors 3-hydroxy-L-kynurenine and xanthurenic acid were investigated. These ecdysone biosynthesis inhibitors, isolated from the eyestalks of blue crabs (Callinectes sapidus), were injected into eyestalk-ablated crayfish (Procambarus clarkii). The active factor was found to be species-nonspecific within crabs and crayfish. The seasonal profiles of the xanthurenic acid and ecdysone titers exhibited a staggered relationship. Moreover, the activity of a 3-hydroxy-L-kynurenine aminotransferase varied during the molting cycle. The data suggested that 3-hydroxy-L-kynurenine, which is secreted from the X-organ-sinus gland complex of crustaceans, is released into the hemolymph, and after accumulating at the surface of the Y-organ, is converted into the active form, xanthurenic acid. Xanthurenic acid was found to profoundly repress ecdysteroidogenesis in vitro.

scholarly journals Contribution of progesterone, follicle stimulating hormone and glucocorticoids in survival of serum-free cultured granulosa cell explants

2001 ◽  
Vol 169 (2) ◽  
pp. 321-331 ◽  
Author(s):  
S Mussche ◽  
K D'Herde
Keyword(s):  
Granulosa Cell ◽  
Fold Increase ◽  
Substantial Evidence ◽  
Dapi Staining ◽  
Serum Free ◽  
Survival Factor ◽  
Survival Pathways

To investigate the role of progesterone (P4) as a survival factor in quail granulosa cell explants, P4 content was determined under various conditions and correlated with apoptotic indexes (AIs) evaluated by 2',6'-diamidino-2-phenylindole (DAPI)-staining. Analysis of serum-free cultures from 24 to 96 h shows decreased P4 levels in the medium paralleled by increasing AI. Inhibiting apoptosis by gonadotropic support (FSH, 100 ng/ml) stimulates a 3-fold increase of the P4 level in the medium (83.49+/-8.69 vs 26.31+/-1.61 ng/ml in serum-free controls) together with a significant decrease in AI from 8.81+/-1.06% in serum-free controls to 3.50+/-0.72%. Substantial evidence for P4 as an autocrine/paracrine survival factor can be inferred from experiments with aminoglutethimide (AG, 1 mM) and RU486 (20 microM). Blocking P4 synthesis by AG causes a 2-fold increase in apoptosis from 6.08+/-0.67% in serum-free controls to 12.53+/-1.60%. Blocking P4 receptors by RU486 causes a similar increase in AI (3.02+/-0.98% in serum-free controls to 17.07+/-3.20%) and about a 50% decrease in P4. The effect of RU486 could be attenuated by exogenous P4 but not by dexamethasone indicating selective binding of P4 to the progesterone receptor. Dexamethasone treatment promotes survival without affecting P4 levels. In further support of an autocrine/paracrine action for P4 in the granulosa cells, both the A and B form of the avian P4 receptor (PR) are identified in vivo and in vitro by Western blotting. Exogenous administration of P4 only affects survival when endogenous P4 synthesis is blocked or after 48 h of serum-free culture when endogenous P4 production is very low. Because FSH also affects survival when its stimulatory effect on P4 synthesis is blocked by AG (AI decrease from 6.08+/-0.67% in serum-free controls to 1.64+/-0.71% in FSH+AG treated) it is proposed that (1) P4 is an autocrine/paracrine survival factor in the preovulatory granulosa and (2) FSH mediates both P4-dependent and P4-independent survival pathways.

CNS Myelin: Does a Stabilizing Role in Neurodevelopment Result in Inhibition of Neuronal Repair after Adult Injury?

1998 ◽  
Vol 4 (4) ◽  
pp. 273-284 ◽  
Author(s):  
H. S. Keirstead ◽  
John D. Steeves
Keyword(s):  
Neural Development ◽  
Neurite Growth ◽  
In Vivo Studies ◽  
Inhibitory Effects ◽  
Axonal Plasticity ◽  
Collateral Sprouting ◽  
Axonal Connections

The inhibitory properties of mature oligodendrocytes and CNS myelin for neurite outgrowth were clearly documented more than a decade ago in studies involving co-cultures of dissociated glial cells and neurons. Since then, in vitro and in vivo studies have begun to characterize some of the CNS myelin-associated inhibitors of neurite growth. Furthermore, experimental techniques for neutralizing or suppressing these inhibitory effects have been developed. The results of several experiments, involving the suppression of myelination in the developing or adult CNS, suggest that the relatively late appearance of CNS myelin during neural development may serve to stabilize and restrict axonal outgrowth (e.g., collateral sprouting) after appropriate axonal connections have been established. This suggested developmental role of myelin may consolidate and limit the degree of axonal plasticity within the adult CNS; consequently, however, it might also limit axonal regeneration after injury.

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