scholarly journals Is interleukin-1α a luteotrophic or luteolytic agent in cattle?

Reproduction ◽  
2010 ◽  
Vol 139 (3) ◽  
pp. 665-672 ◽  
Author(s):  
Magdalena Majewska ◽  
Izabela Woclawek-Potocka ◽  
Mamadou M Bah ◽  
Joanna Hapunik ◽  
Katarzyna K Piotrowska ◽  
...  
Keyword(s):  
Estrous Cycle ◽  
Early Pregnancy ◽  
Luteal Phase ◽  
Late Luteal Phase ◽  
Interleukin 1Α ◽  
And Function ◽  
Different Doses

Cytokines are thought to regulate prostaglandin (PG) secretion in the bovine endometrium. However, there is no consensus about the role of interleukin-1α (IL1A) on PG secretion. The objective of this study was to examine the influence of IL1A on basal and interferon-τ (IFNT)-regulated PGin vitrosecretion, as well its effects on PG secretion, progesterone (P4) output, and corpus luteum (CL)in vivolifespan. Explants of bovine endometrium (days 16–17 of the estrous cycle or early pregnancy) were stimulated with IL1A (10 ng/ml), IFNT (30 ng/ml), or IL1A combined with IFN. IL1A alone strongly stimulated luteotrophic PGE2secretion by endometrial tissues of both pregnant and nonpregnant cows. IL1A also stimulated luteolytic PGF2αoutput in the late luteal phase. IFNT augmented the stimulatory effect of IL1A on PGE2secretion. In anin vivoexperiment, saline or IL1A at different doses (0.001–10 μg/per animal) was applied to the uterine lumen on day 16 of the cycle. Only the highest dose of IL1A caused a temporal increase in PGF2αsecretion, while it had no effect on P4secretion or CL lifespan. Application of 0.1 and 1 μg IL1A stimulated P4and PGE2output and prolonged the CL lifespan. Although IL1A may stimulatein vitroluteolytic PGF2αsecretion during the estrous cycle, it only acts as a luteotrophic factorin vivo. IL1A increased luteotrophic PGE2and P4output, inhibiting spontaneous luteolysis. These luteotrophic effects may result in appropriate luteal development and function in cows during the estrous cycle and early pregnancy.

scholarly journals Leukotrienes modulate secretion of progesterone and prostaglandins during the estrous cycle and early pregnancy in cattle: an in vivo study

Reproduction ◽  
2010 ◽  
Vol 140 (5) ◽  
pp. 767-776 ◽  
Author(s):  
Anna J Korzekwa ◽  
Mamadou M Bah ◽  
Andrzej Kurzynowski ◽  
Karolina Lukasik ◽  
Agnieszka Groblewska ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Estrous Cycle ◽  
Early Pregnancy ◽  
Luteal Phase ◽  
Reproductive Tract ◽  
Cell Function ◽  
Ovarian Cell

Recently, we showed that leukotrienes (LTs) regulate ovarian cell functionin vitro. The aim of this study was to examine the role of LTs in corpus luteum (CL) function during both the estrous cycle and early pregnancyin vivo. mRNA expression of LT receptors (BLTfor LTB4andCYSLTfor LTC4), and 5-lipoxygenase (5-LO) in CL tissue and their localization in the ovary were studied during the estrous cycle and early pregnancy. Moreover, concentrations of LTs (LTB4and C4) in the CL tissue and blood were measured.5-LOandBLTmRNA expression increased on days 16–18 of the cycle, whereasCYSLTmRNA expression increased on days 16–18 of the pregnancy. The level of LTB4was evaluated during pregnancy compared with the level of LTC4, which increased during CL regression. LT antagonists influenced the duration of the estrous cycle: the LTC4antagonist (azelastine) prolonged the luteal phase, whereas the LTB4antagonist (dapsone) caused earlier luteolysisin vivo. Dapsone decreased progesterone (P4) secretion and azelastine increased P4secretion during the estrous cycle. In summary, LT action in the bovine reproductive tract is dependent on LT type: LTB4is luteotropic during the estrous cycle and supports early pregnancy, whereas LTC4is luteolytic, regarded as undesirable in early pregnancy. LTs are produced/secreted in the CL tissue, influence prostaglandin function, and serve as important factors during the estrous cycle and early pregnancy in cattle.

scholarly journals Luteotrophic effects of relaxin, chorionic gonadotrophin and FSH in common marmoset monkeys (Callithrix jacchus)

Reproduction ◽  
2010 ◽  
Vol 139 (5) ◽  
pp. 923-930 ◽  
Author(s):  
Nicola Beindorff ◽  
Almuth Einspanier
Keyword(s):  
Early Pregnancy ◽  
Luteal Phase ◽  
Common Marmoset ◽  
Chorionic Gonadotrophin ◽  
Traditional Role ◽  
Local Effects ◽  
Ringer’S Solution ◽  
Late Luteal Phase ◽  
Marmoset Monkeys

In early pregnant primates, relaxin (RLX) is highly upregulated within the corpus luteum (CL), suggesting that RLX may have an important role in the implantation of the blastocyst. Therefore, the aim of the present study was to investigate the local effects of RLX and gonadotrophins on the maintenance of the CL using anin vitromicrodialysis system. CLs of common marmoset monkeys were collected by luteectomy during different stages of the luteal phase and early pregnancy. Each CL was perfused with either Ringer's solution alone or Ringer's solution supplemented with either porcine RLX (250, 500 and 1000 ng/ml) or gonadotrophins (50 IU/ml). Application of RLX provoked a significant luteal response of progesterone (P4) and oestradiol (E2) secretions during the mid-luteal phase (500 ng/ml: P454±42%, E224±11%; 1000 ng/ml: E216±13%), and especially during the late luteal phase (250 ng/ml: P453±10%; 500 ng/ml: P444±15%; 1000 ng/ml: P462±15%, E218±7%). The effects of RLX on steroid secretion were irrespective of the RLX dosages. While treatment with human chorionic gonadotrophin did not affect luteal steroid or RLX secretion, the application of FSH resulted in a significant increase in the secretion of both P4(20±8%) and E2(37±28%), and a prominent rise in RLX during early pregnancy. In conclusion, our results demonstrate that RLX and FSH have a luteotrophic function in the marmoset monkeys; moreover, FSH has a function beyond its traditional role just as a follicle-stimulating hormone.

scholarly journals Evidence for a PGF2α auto-amplification system in the endometrium in mares

Reproduction ◽  
2016 ◽  
Vol 151 (5) ◽  
pp. 517-526 ◽  
Author(s):  
Keisuke Kozai ◽  
Shota Tokuyama ◽  
Anna Z Szóstek ◽  
Yuko Toishi ◽  
Nobuo Tsunoda ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Stromal Cells ◽  
Luteal Phase ◽  
Endometrial Cell ◽  
Late Luteal Phase ◽  
Prostaglandin F ◽  
Amplification System ◽  
Prostaglandin Endoperoxide Synthase

AbstractIn mares, prostaglandin F2α(PGF2α) secreted from the endometrium is a major luteolysin. Some domestic animals have an auto-amplification system in which PGF2αcan stimulate its own production. Here, we investigated whether this is also the case in mares. In anin vivostudy, mares at the mid-luteal phase (days 6–8 of estrous cycle) were injected i.m. with cloprostenol (250 µg) and blood samples were collected at fixed intervals until 72 h after treatment. Progesterone (P4) concentrations started decreasing 45 min after the injection and continued to decrease up to 24 h (P < 0.05). In turn, 13,14-dihydro-15-keto-PGF2α(PGFM) metabolite started to increase 4h after an injection and continued to increase up to 72 h (P < 0.05). PGF receptor (PTGFR) mRNA expression in the endometrium was significantly higher in the late luteal phase than in the early and regressed luteal phases (P < 0.05).In vitro, PGF2αsignificantly stimulated (P < 0.05) PGF2αproduction by endometrial tissues and endometrial epithelial and stromal cells and significantly increased (P < 0.05) the mRNA expression of prostaglandin-endoperoxide synthase-2 (PTGS2), an enzyme involved in PGF2αsynthesis in endometrial cell. These findings strongly suggest the existence of an endometrial PGF2αauto-amplification system in mares.

The extracellular matrix of the developing cornea: diversity, deposition and function*

Development ◽  
1988 ◽  
Vol 103 (Supplement) ◽  
pp. 195-205
Author(s):  
J. B. L. Bard ◽  
M. K. Bansal ◽  
A. S. A. Ross
Keyword(s):  
Extracellular Matrix ◽  
Chondroitin Sulphate ◽  
Corneal Stroma ◽  
Experimental System ◽  
Collagen I ◽  
And Function ◽  
20 Nm

This paper examines the role of the extracellular matrix (ECM) in the development of the cornea. After a brief summary of the corneal structure and ECM, we describe evidence suggesting that the differentiation of neural crest (NC) cells into endothelium and fibroblasts is under the control of ocular ECM. We then examine the role of collagen I in stromal morphogenesis by comparing normal corneas with those of homozygous Movl3 mice which do not make collagen I. We report that, in spite of this absence, the cellular morphology of the Movl3 eye is indistinguishable from that of the wild type. In the 16-day mutant stroma, however, the remaining collagens form small amounts of disorganized, thin fibrils rather than orthogonally organized 20 nm-diameter fibrils; a result implying that collagen I plays only a structural role and that its absence is not compensated for. It also suggests that, because these remaining collagens will not form the normal fibrils that they will in vitro, fibrillogenesis in the corneal stroma differs from that elsewhere. The latter part of the paper describes our current work on chick stromal deposition using corneal epithelia isolated with an intact basal lamina that lay down in vitro ∼3μm-thick stromas of organized fibrils similar to that seen in vivo. This experimental system has yielded two unexpected results. First, the amount of collagen and proteoglycans produced by such epithelia is not dependent on whether its substratum is collagenous and we therefore conclude that stromal production by the intact epithelium is more autonomous than hitherto thought. Second, chondroitin sulphate (CS), the predominant proteoglycan, appears to play no role in stromal morphogenesis: epithelia cultured in testicular hyaluronidase, which degrades CS, lay down stromas whose organization and fibrildiameter distribution are indistinguishable from controls. One possible role for CS, however, is as a lubricant which facilitates corneal growth: it could allow fibrils to move over one another without deforming their orthogonal organization. Finally, we have examined the processes of fibrillogenesis in the corneal stroma and conclude that they are different from those elsewhere in the embryo and in vitro, perhaps because there is in the primary stroma an unidentified, highly hydrated ECM macromolecule that embeds the fibrils and that may mediate their morphogenesis.

scholarly journals Characterization and function of Ca2+-activated K+ channels in arteriolar muscle cells

1998 ◽  
Vol 274 (1) ◽  
pp. H27-H34 ◽  
Author(s):  
William F. Jackson ◽  
Kevin L. Blair
Keyword(s):  
Single Channel ◽  
Muscle Cells ◽  
Hill Coefficient ◽  
Apparent Lack ◽  
Maximal Activation ◽  
And Function ◽  
Resting Tone

We examined the functional role of large-conductance Ca2+-activated K+(KCa) channels in the hamster cremasteric microcirculation by intravital videomicroscopy and characterized the single-channel properties of these channels in inside-out patches of membrane from enzymatically isolated cremasteric arteriolar muscle cells. In second-order (39 ± 1 μm, n = 8) and third-order (19 ± 2 μm, n = 8) cremasteric arterioles with substantial resting tone, superfusion with the KCa channel antagonists tetraethylammonium (TEA, 1 mM) or iberiotoxin (IBTX, 100 nM) had no significant effect on resting diameters ( P > 0.05). However, TEA potentiated O2-induced arteriolar constriction in vivo, and IBTX enhanced norepinephrine-induced contraction of cremasteric arteriolar muscle cells in vitro. Patch-clamp studies revealed unitary K+-selective and IBTX-sensitive currents with a single-channel conductance of 240 ± 2 pS between −60 and 60 mV ( n = 7 patches) in a symmetrical 140 mM K+ gradient. The free Ca2+ concentration ([Ca2+]) for half-maximal channel activation was 44 ± 3, 20 ± 1, 6 ± 0.4, and 3 ± 0.5 μM at membrane potentials of −60, −30, +30, and +60 mV, respectively ( n = 5), with a Hill coefficient of 1.9 ± 0.2. Channel activity increased e-fold for a 16 ± 1 mV ( n = 6) depolarization. The plot of log[Ca2+] vs. voltage for half-maximal activation ( V ½) was linear ( r 2 = 0.9843, n = 6); the change in V ½ for a 10-fold change in [Ca2+] was 84 ± 5 mV, and the [Ca2+] for half-maximal activation at 0 mV (Ca0; the Ca2+ set point) was 9 μM. Thus, in vivo, KCa channels are silent in cremasteric arterioles at rest but can be recruited during vasoconstriction. We propose that the high Ca0 is responsible for the apparent lack of activity of these channels in resting cremasteric arterioles, and we suggest that this may result from expression of unique KCa channels in the microcirculation.

PSGL-1 regulates platelet P-selectin-mediated endothelial activation and shedding of P-selectin from activated platelets

2007 ◽  
Vol 98 (10) ◽  
pp. 806-812 ◽  
Author(s):  
Vandana Dole ◽  
Wolfgang Bergmeier ◽  
Ian Patten ◽  
Junichi Hirahashi ◽  
Tanya Mayadas ◽  
...  
Keyword(s):  
Endothelial Activation ◽  
Leukocyte Rolling ◽  
Wild Type ◽  
Platelet Surface ◽  
Activated Platelets ◽  
And Function ◽  
Body Secretion

SummaryWe have previously shown that activated platelets in circulation stimulate release of endothelial Weibel-Palade bodies thus increasing leukocyte rolling in venules. P-selectin on the activated platelets mediates adhesion to leukocytes via PSGL-1 and is rapidly shed into plasma. We were interested in studying the role of PSGL-1 in regulating expression and function of platelet P-selectin. We show here that PSGL-1 is critical for the activation of endothelial cells in venules of mice infused with activated platelets. The interaction of platelet P-selectin with PSGL-1 is also required for P-selectin shedding, as P-selectin was retained significantly longer on the surface of activated platelets infused into PSGL-1-/- compared to wild-type mice. The leukocyte integrin αMβ2 (Mac-1) was not required for P-selectin shedding. In addition to shedding, P-selectin can be downregulated from the platelet surface through internalization and this is the predominant mechanism in the absence of PSGL-1. We demonstrate that leukocyte- neutrophil elastase,known to cleave P-selectin in vitro, is not the major sheddase for P-selectin in vivo. In conclusion, interaction of platelet P-selectin with PSGL-1 is crucial for activation of the endothelium andWeibel-Palade body secretion. The interaction with PSGL-1 also results in rapid shedding of P-selectin thus downregulating the inflammatory potential of the platelet.

scholarly journals Talin is required for integrin-mediated platelet function in hemostasis and thrombosis

2007 ◽  
Vol 204 (13) ◽  
pp. 3103-3111 ◽  
Author(s):  
Brian G. Petrich ◽  
Patrizia Marchese ◽  
Zaverio M. Ruggeri ◽  
Saskia Spiess ◽  
Rachel A.M. Weichert ◽  
...  
Keyword(s):  
Platelet Adhesion ◽  
Ex Vivo ◽  
Focal Adhesions ◽  
Β1 Integrin ◽  
Normal Morphology ◽  
And Function ◽  
Specific Deletion

Integrins are critical for hemostasis and thrombosis because they mediate both platelet adhesion and aggregation. Talin is an integrin-binding cytoplasmic adaptor that is a central organizer of focal adhesions, and loss of talin phenocopies integrin deletion in Drosophila. Here, we have examined the role of talin in mammalian integrin function in vivo by selectively disrupting the talin1 gene in mouse platelet precursor megakaryocytes. Talin null megakaryocytes produced circulating platelets that exhibited normal morphology yet manifested profoundly impaired hemostatic function. Specifically, platelet-specific deletion of talin1 led to spontaneous hemorrhage and pathological bleeding. Ex vivo and in vitro studies revealed that loss of talin1 resulted in dramatically impaired integrin αIIbβ3-mediated platelet aggregation and β1 integrin–mediated platelet adhesion. Furthermore, loss of talin1 strongly inhibited the activation of platelet β1 and β3 integrins in response to platelet agonists. These data establish that platelet talin plays a crucial role in hemostasis and provide the first proof that talin is required for the activation and function of mammalian α2β1 and αIIbβ3 integrins in vivo.

scholarly journals The N-Terminus ofDictyosteliumScar Interacts with Abi and HSPC300 and Is Essential for Proper Regulation and Function

2007 ◽  
Vol 18 (5) ◽  
pp. 1609-1620 ◽  
Author(s):  
Diana Caracino ◽  
Cheryl Jones ◽  
Mark Compton ◽  
Charles L. Saxe
Keyword(s):  
Actin Polymerization ◽  
Terminal Region ◽  
Wild Type ◽  
Large Molecular Weight ◽  
Weight Protein ◽  
And Function ◽  
Necessary And Sufficient

Scar/WAVE proteins, members of the conserved Wiskott-Aldrich syndrome (WAS) family, promote actin polymerization by activating the Arp2/3 complex. A number of proteins, including a complex containing Nap1, PIR121, Abi1/2, and HSPC300, interact with Scar/WAVE, though the role of this complex in regulating Scar function remains unclear. Here we identify a short N-terminal region of Dictyostelium Scar that is necessary and sufficient for interaction with HSPC300 and Abi in vitro. Cells expressing Scar lacking this N-terminal region show abnormalities in F-actin distribution, cell morphology, movement, and cytokinesis. This is true even in the presence of wild-type Scar. The data suggest that the first 96 amino acids of Scar are necessary for participation in a large-molecular-weight protein complex, and that this Scar-containing complex is responsible for the proper localization and regulation of Scar. The presence of mis-regulated or unregulated Scar has significant deleterious effects on cells and may explain the need to keep Scar activity tightly controlled in vivo either by assembly in a complex or by rapid degradation.

scholarly journals Autonomous TNF is critical for in vivo monocyte survival in steady state and inflammation

2017 ◽  
Vol 214 (4) ◽  
pp. 905-917 ◽  
Author(s):  
Yochai Wolf ◽  
Anat Shemer ◽  
Michal Polonsky ◽  
Mor Gross ◽  
Alexander Mildner ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Mononuclear Phagocytes ◽  
Autoimmune Encephalomyelitis ◽  
Wild Type Counterpart ◽  
And Function ◽  
Necrosis Factor ◽  
Experimental Autoimmune

Monocytes are circulating mononuclear phagocytes, poised to extravasate to sites of inflammation and differentiate into monocyte-derived macrophages and dendritic cells. Tumor necrosis factor (TNF) and its receptors are up-regulated during monopoiesis and expressed by circulating monocytes, as well as effector monocytes infiltrating certain sites of inflammation, such as the spinal cord, during experimental autoimmune encephalomyelitis (EAE). In this study, using competitive in vitro and in vivo assays, we show that monocytes deficient for TNF or TNF receptors are outcompeted by their wild-type counterpart. Moreover, monocyte-autonomous TNF is critical for the function of these cells, as TNF ablation in monocytes/macrophages, but not in microglia, delayed the onset of EAE in challenged animals and was associated with reduced acute spinal cord infiltration of Ly6Chi effector monocytes. Collectively, our data reveal a previously unappreciated critical cell-autonomous role of TNF on monocytes for their survival, maintenance, and function.

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