Role of Prostaglandins in Fish Reproduction

1982 ◽  
Vol 39 (1) ◽  
pp. 92-98 ◽  
Author(s):  
N. E. Stacey ◽  
F. W. Goetz
Keyword(s):  
Sexual Behavior ◽  
Brook Trout ◽  
Yellow Perch ◽  
Salmo Gairdneri ◽  
Fish Reproduction ◽  
Synthesis Inhibitor ◽  
Female Sexual Behavior ◽  
Goldfish Carassius Auratus

Prostaglandins (PGs) have been identified in gonads, semen, ovarian fluid, blood, and in vitro ovarian incubates from a variety of teleosts. In teleosts, PGs appear to be involved in ovulation (follicular rupture) and female sexual behavior, and possibly in gonadotropin (GtH) secretion. An increase in prostaglandin F (PGF) levels associated with GtH-induced ovulation occurs in vivo in the pond loach (Misgurnus anguillicaudatus) and goldfish (Carassius auratus). Indomethacin (PG synthesis inhibitor) blocks ovulation in these species and, in goldfish, PG injection reverses this blockade. PGF2α stimulates in vitro ovulation in rainbow trout (Salmo gairdneri), brook trout (Salvelinus fontinalis), and yellow perch (Perca flavescens); however, in perch, PGE2 is the most potent prostaglandin. Addition of melatonin to incubation medium both inhibits ovulation and decreases PGE and PGF synthesis in yellow perch, while addition of epinephrine and theophylline both enhances ovulation and increases PGE and PGF synthesis. Several studies indicate that PG, released from the ovaries or oviduct in response to the presence of ovulated oocytes, acts on the brain to stimulate female spawning behavior in the goldfish. Other externally fertilizing teleosts may use similar mechanisms to synchronize female sexual behavior with ovulation.Key words: prostaglandins, fish reproduction, ovulation, sexual behavior

scholarly journals In Vitro Oocyte Maturation and Ovulation in Rainbow Trout (Salmo gairdneri), Northern Pike (Esox lucius), and Goldfish (Carassius auratus)

1976 ◽  
Vol 33 (4) ◽  
pp. 974-988 ◽  
Author(s):  
Bernard Jalabert
Keyword(s):  
Oocyte Maturation ◽  
Sensu Stricto ◽  
Salmo Gairdneri ◽  
Follicular Maturation ◽  
Goldfish Carassius Auratus ◽  
Control Oocyte ◽  
Follicle Maturation ◽  
Ovulatory Process ◽  
Matured Oocyte

The endocrine processes which control oocyte maturation (resumption of meiosis) and ovulation have been studied in vitro in the trout Salmo gairdneri. Follicular maturation is ultimately under the control of a pituitary gonadotropin which induces the follicle to synthesize specific steroids; these steroids act in turn directly on the oocyte to promote maturation. The systematic study of the in vitro efficiency of various steroids have shown that 17α-hydroxy-20β-dihydroprogesterone plays a preferential role in initiating maturation; this steroid has a high affinity for a plasma protein system. The efficiency of this steroid, similarly to the efficiency of the gonadotropin, can be modulated by other circulating steroids. The precise chronology of some events of follicle maturation have been defined using inhibitors of protein and RNA synthesis.The ovulatory process (sensu stricto: expulsion of matured oocyte from the follicular envelopes) has been experimentally dissociated from oocyte maturation, and some mediators likely to act on ovulation have been identified.These data permit the consideration of novel means of intervention at the ovarian level to synchronize maturation and ovulation in fish, in order to give new tools for progress in aquaculture.

Comparaison des échanges branchiaux de Cl− en eau douce chez Salmo gairdneri in vivo et in vitro sur la tête isolée perfusée

1978 ◽  
Vol 35 (4) ◽  
pp. 477-479 ◽  
Author(s):  
P. Payan ◽  
P. Pic ◽  
G. De Renzis
Keyword(s):  
Salmo Gairdneri ◽  
Net Uptake

The Cl− influxes are identical in vivo and in vitro providing that the gills are externally irrigated during the preparation of the isolated head. A net uptake of Cl− is observed. When no irrigation is used the Cl− influx is reduced by 66% and Cl− is lost by the preparation.

scholarly journals Infection of porcine small intestinal enteroids with human and pig rotavirus A strains reveals contrasting roles for histo-blood group antigens and terminal sialic acids

2021 ◽  
Vol 17 (1) ◽  
pp. e1009237
Author(s):  
Yusheng Guo ◽  
Rosario Adriana Candelero-Rueda ◽  
Linda Jean Saif ◽  
Anastasia Nickolaevna Vlasova
Keyword(s):  
Blood Group ◽  
Functional Model ◽  
Surface Protein ◽  
Sialic Acids ◽  
Viral Gastroenteritis ◽  
Blood Group Antigens ◽  
Synthesis Inhibitor ◽  
Rotavirus A

Rotaviruses (RVs) are a leading cause of acute viral gastroenteritis in young children and livestock worldwide. Growing evidence suggests that host cellular glycans, such as histo-blood group antigens (HBGAs) and sialic acids (SA), are recognized by the RV surface protein VP4. However, a mechanistic understanding of these interactions and their effects on RV infection and pathogenesis is lacking. Here, we established a porcine crypt-derived 3D intestinal enteroids (PIEs) culture system which contains all intestinal epithelial cells identified in vivo and represents a unique physiologically functional model to study RV-glycan interactions in vitro. PIEs expressing different HBGAs (A+, H+, and A+/H+) were established and isolation, propagation, differentiation and RV infection conditions were optimized. Differentiated PIEs were infected with human RV (HRV) G1P[8] Wa, porcine RV (PRV) G9P[13], PRV Gottfried G4P[6] or PRV OSU G5P[7] virulent and attenuated strains and virus replication was measured by qRT-PCR. Our results indicated that virulent HRV G1P[8] Wa replicated to the highest titers in A+ PIEs, while a distinct trend was observed for PRV G9P[13] or G5P[7] with highest titers in H+ PIEs. Attenuated Wa and Gottfried strains replicated poorly in PIEs while the replication of attenuated G9P[13] and OSU strains in PIEs was relatively efficient. However, the replication of all 4 attenuate strains was less affected by the PIE HBGA phenotypes. HBGA synthesis inhibitor 2-F-Peracetyl-Fucose (2F) treatment demonstrated that HBGAs are essential for G1P[8] Wa replication; however, they may only serve as a cofactor for PRVs G9P[13] and OSU G5P[7]. Interestingly, contrasting outcomes were observed following sialidase treatment which significantly enhanced G9P[13] replication, but inhibited the growth of G5P[7]. These observations suggest that some additional receptors recognized by G9P[13] become unmasked after removal of terminal SA. Overall, our results confirm that differential HBGAs-RV and SA-RV interactions determine replication efficacy of virulent group A RVs in PIEs. Consequently, targeting individual glycans for development of therapeutics may not yield uniform results for various RV strains.

scholarly journals Role of Hyaluronan in Human Adipogenesis: Evidence from in-Vitro and in-Vivo Studies

2019 ◽  
Vol 20 (11) ◽  
pp. 2675 ◽  
Author(s):  
Nicholas Wilson ◽  
Robert Steadman ◽  
Ilaria Muller ◽  
Mohd Draman ◽  
D. Aled Rees ◽  
...  
Keyword(s):  
Stem Cell Differentiation ◽  
In Vivo Studies ◽  
Peroxisome Proliferator ◽  
Synthesis Inhibitor ◽  
Peroxisome Proliferator Activated Receptor ◽  
Inhibitory Role ◽  
The Impact

Hyaluronan (HA), an extra-cellular matrix glycosaminoglycan, may play a role in mesenchymal stem cell differentiation to fat but results using murine models and cell lines are conflicting. Our previous data, illustrating decreased HA production during human adipogenesis, suggested an inhibitory role. We have investigated the role of HA in adipogenesis and fat accumulation using human primary subcutaneous preadipocyte/fibroblasts (PFs, n = 12) and subjects of varying body mass index (BMI). The impact of HA on peroxisome proliferator-activated receptor gamma (PPARγ) expression was analysed following siRNA knockdown or HA synthase (HAS)1 and HAS2 overexpression. PFs were cultured in complete or adipogenic medium (ADM) with/without 4-methylumbelliferone (4-MU = HA synthesis inhibitor). Adipogenesis was evaluated using oil red O (ORO), counting adipogenic foci, and measurement of a terminal differentiation marker. Modulating HA production by HAS2 knockdown or overexpression increased (16%, p < 0.04) or decreased (30%, p = 0.01) PPARγ transcripts respectively. The inhibition of HA by 4-MU significantly enhanced ADM-induced adipogenesis with 1.52 ± 0.18- (ORO), 4.09 ± 0.63- (foci) and 2.6 ± 0.21-(marker)-fold increases compared with the controls, also increased PPARγ protein expression (40%, (p < 0.04)). In human subjects, circulating HA correlated negatively with BMI and triglycerides (r = −0.396 (p = 0.002), r = −0.269 (p = 0.038), respectively), confirming an inhibitory role of HA in human adipogenesis. Thus, enhancing HA action may provide a therapeutic target in obesity.

Evidence for Cl−-dependent K+ secretion by the blood–testis barrier of brook trout

1988 ◽  
Vol 66 (7) ◽  
pp. 1603-1609 ◽  
Author(s):  
William S. Marshall ◽  
Sharon E. Bryson
Keyword(s):  
Brook Trout ◽  
Transepithelial Transport ◽  
High Concentration ◽  
Sperm Duct ◽  
K Secretion ◽  
Net Flux ◽  
Mucosal Side ◽  
Blood Testis Barrier

The transepithelial transport of 86Rb+, a tracer for K+, was examined in the isolated sperm duct of brook trout (Salvelinus fontinalis). Fluxes of 86Rb+ at 1.0 mM Rb+ in voltage-clamped ducts bathed with Ringer's solution on both sides revealed net secretion of Rb+ averaging 31–58 nequiv.∙cm−2∙h−1 after stimulation by 1.0 mM dibutyryl-cAMP. Unstimulated tissues had no net Rb+ transport. The stimulated Rb+ transport was reduced 70% by bilateral replacement of Cl− with gluconate, indicating that Rb+ secretion is dependent on Cl−. Ba2+ (2.0 mM) added to the luminal (mucosal) side had no effect on Rb+ secretion rate, suggesting that apical Ba2+-sensitive K+ channels are not involved. When added on the blood side (serosal), Ba2+ stimulated Rb+ net flux by 68%, possibly as a result of blockade of basal K+ channels and increased intracellular [K+]. Injection of the antiandrogen cyproterone acetate (3 × 0.4 mg∙kg−1 over 7 days in vivo) significantly reduced stimulated Rb+ secretion (in vitro), suggesting that androgens may maintain the active transport characteristics of the blood – testis barrier. The active K+ secretion by the sperm duct accounts for the high concentration of K+ in seminal plasma which in turn is important in maintaining quiescence of developing spermatozoa.

scholarly journals Endogenous thyroid hormones modulate pituitary somatotroph differentiation during chicken embryonic development

2004 ◽  
Vol 180 (1) ◽  
pp. 45-53 ◽  
Author(s):  
L Liu ◽  
TE Porter
Keyword(s):  
Thyroid Hormone ◽  
Embryonic Development ◽  
Thyroid Hormones ◽  
Synthesis Inhibitor ◽  
Hormone Synthesis ◽  
Thyroid Hormone Synthesis ◽  
Growth Hormone Cell ◽  
Thyroid Hormone Levels

Growth hormone cell differentiation normally occurs between day 14 and day 16 of chicken embryonic development. We reported previously that corticosterone (CORT) could induce somatotroph differentiation in vitro and in vivo and that thyroid hormones could act in combination with CORT to further augment the abundance of somatotrophs in vitro. The objective of the present study was to test our hypothesis that endogenous thyroid hormones regulate the abundance of somatotrophs during chicken embryonic development. Plasma samples were collected on embryonic day (e) 9-14. We found that plasma CORT and thyroid hormone levels increased progressively in mid-embryogenesis to e 13 or e 14, immediately before normal somatotroph differentiation. Administration of thyroxine (T4) and triiodothyronine (T3) into the albumen of fertile eggs on e 11 increased somatotroph proportions prematurely on e 13 in the developing chick embryos in vivo. Furthermore, administration of methimazole, the thyroid hormone synthesis inhibitor, on e 9 inhibited somatotroph differentiation in vivo, as assessed on e 14; this suppression was completely reversed by T3 replacement on e 11. Since we reported that T3 alone was ineffective in vitro, we interpret these findings to indicate that the effects of treatments in vivo were due to interactions with endogenous glucocorticoids. These results indicate that treatment with exogenous thyroid hormones can modulate somatotroph abundance and that endogenous thyroid hormone synthesis likely contributes to normal somatotroph differentiation.

Oxytocin stimulates LH production by the anterior pituitary gland of the rat

1992 ◽  
Vol 132 (2) ◽  
pp. 277-283 ◽  
Author(s):  
G. Robinson ◽  
J. J. Evans ◽  
K. J. Catt
Keyword(s):  
Female Rats ◽  
Release Mechanism ◽  
Protein Synthesis Inhibitor ◽  
Pituitary Cells ◽  
Synthesis Inhibitor ◽  
Mechanical Dispersion ◽  
Lh Release

ABSTRACT Gonadotrophin-releasing activity of oxytocin has previously been demonstrated in vitro and in vivo. This study investigated whether oxytocin is also able to induce LH accumulation in pituitary cells. Following trypsin digestion and mechanical dispersion, pituitary cells from female rats were incubated with oxytocin (100 nmol/l) for 24 h. LH release stimulated by oxytocin increased (P < 0·001) progressively during the incubation indicating a different secretory pattern from the more rapid but less sustained secretion stimulated by gonadotrophin-releasing hormone. Oxytocin also enhanced (P < 0·01) total LH accumulation in the incubation system (released plus cell contents) which was apparent after 7–11 h of stimulation. The release of LH stimulated by oxytocin was reduced by the protein synthesis inhibitor cycloheximide (10 μmol/l). However, cycloheximide did not completely block oxytocin-stimulated LH release; there remained some LH release above that seen in non-stimulated controls (P < 0·01) revealing the presence of a cycloheximide-resistant component in the release mechanism. Furthermore, accumulation of total LH in 24 h incubations was suppressed (P < 0·01) by cycloheximide. The advancement in LH release which oxytocin has been shown to induce in vivo in pro-oestrous rats was accompanied by an early reduction of pituitary LH stores. However, the fall normally observed in LH content during the surge was markedly attenuated by the oxytocin treatment. Thus, loss of pituitary LH stores was less in oxytocin-treated rats than in saline-treated controls, even though net LH release into plasma was increased. Therefore, oxytocin stimulated the replenishment of LH stores. Although the mechanism(s) remains to be defined and the relationships between in-vitro and in-vivo results are as yet uncharacterized, the present study demonstrates that oxytocin treatment stimulates LH production in both dispersed cells and intact pituitaries in situ. Journal of Endocrinology (1992) 132, 277–283

scholarly journals Long Noncoding RNA EGFR-AS1 Promotes Cell Proliferation by Increasing EGFR mRNA Stability in Gastric Cancer

2018 ◽  
Vol 49 (1) ◽  
pp. 322-334 ◽  
Author(s):  
Jiaojiao Hu ◽  
Yingying Qian ◽  
Lipan Peng ◽  
Ling Ma ◽  
Tianzhu Qiu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cancer Progression ◽  
Mrna Stability ◽  
Noncoding Rna ◽  
Synthesis Inhibitor ◽  
Egfr Expression ◽  
Gastric Cancer Progression

Background/Aims: LncRNA EGFR-AS1 is an antisense transcript of EGFR, which plays a key role in gastric cancer progression. This study was aimed to explore the effects of lncRNA EGFR-AS1 on GC and the underling mechanisms. Methods: The silencing of EGFR-AS1 expression was performed by using EGFR-AS1 shRNA lentivirus in MGC803 and SGC-7901 GC cell. The levels of lncRNA EGFR-AS1 and EGFR were detected by qPCR and western blot. Cell proliferation was assessed by CCK-8, EdU, and colony formation assays. The EGFR mRNA stability was explored by using RNA synthesis inhibitor α-amanitin. Results: In our study, EGFR-AS1 significantly up-regulated in GC tissues and correlated with tumor size. And the expression of EGFR-AS1 positively correlated with EGFR in tissues. Moreover, knock-down of EGFR-AS1 inhibited the proliferation of GC cells via suppressing EGFR-dependent PI3K/AKT pathway in vitro and in vivo. Mechanismly, depletion of EGFR-AS1 was found to decrease EGFR expression by reduction of EGFR mRNA stability. Conclusion: Our findings suggested that EGFR-AS1 might have an oncogenic effect on GC and serve as a potential target of GC.

Passive solute and fluid transport in brook trout (Salvelinus fontinalis) urinary bladder epithelium

1988 ◽  
Vol 66 (4) ◽  
pp. 912-918 ◽  
Author(s):  
William S. Marshall
Keyword(s):  
Hydraulic Conductivity ◽  
Urinary Bladder ◽  
Brook Trout ◽  
Fluid Transport ◽  
Salvelinus Fontinalis ◽  
Bladder Epithelium ◽  
Solute Permeability ◽  
Tight Epithelia

The passive transport of solutes across the brook trout (Salvelinus fontinalis) urinary bladder epithelium was examined in vitro in Ussing-style membrane chambers. The low transepithelial conductance (average 0.14–0.20 mS∙cm−2) and low mannitol permeability (6.9 ± 1.4 × 10−11 cm∙s−1, mean ± SE) indicate that both the transcellular and paracellular pathways have limited solute permeability. Fluid transport measurements in in vitro bag preparations indicate low hydraulic conductivity (1.6 ± 0.4 × 10−7 cm∙s−1∙atm−1; 1 atm = 101.325 kPa) and suggest that the absorbate is hyperosmotic, 5-fold more concentrated than the bathing solutions. Voltage clamping experiments with unidirectional 22Na+ and 36Cl− fluxes indicated that Na+ passive diffusion occurs primarily via a transcellular pathway, whereas the epithelium behaves as a simple resistive barrier to Cl−; thus, a diffusional portion of the Cl− flux may be paracellular. The balance of the Cl− serosa-to-mucosa flux is nonconductive and apparently represents anion exchange. Current–voltage relations were nonlinear as is typical of some tight epithelia. Bladder urine is highly hypotonic, with sodium, potassium and chloride contents of 2.00 ± 0.36, 0.76 ± 0.19 and 1.31 ± 0.20 mM, respectively. In addition to the previously demonstrated absorptive neutral NaCl active transport, present results indicate a barrier function of the urinary bladder epithelium in which hydraulic conductivity and ion and uncharged solute permeabilities are low. These characterisitics are in turn consistent with the production in vivo of a very dilute urine.

scholarly journals Endogenous Ceramide Contributes to the Transcytosis of oxLDL across Endothelial Cells and Promotes Its Subendothelial Retention in Vascular Wall

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Wenjing Li ◽  
Xiaoyan Yang ◽  
Shasha Xing ◽  
Fang Bian ◽  
Wanjing Yao ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
De Novo ◽  
Vascular Endothelial Cells ◽  
Atherosclerotic Lesion ◽  
Vascular Wall ◽  
Acid Sphingomyelinase ◽  
Synthesis Inhibitor ◽  
Ceramide Production

Oxidized low density of lipoprotein (oxLDL) is the major lipid found in atherosclerotic lesion and elevated plasma oxLDL is recognized to be a risk factor of atherosclerosis. Whether plasma oxLDL could be transported across endothelial cells and initiate atherosclerotic changes remains unknown. In an establishedin vitrocellular transcytosis model, the present study found that oxLDL could traffic across vascular endothelial cells and further that the regulation of endogenous ceramide production by ceramide metabolizing enzyme inhibitors significantly altered the transcytosis of oxLDL across endothelial cells. It was found that acid sphingomyelinase inhibitor, desipramine (DES), andde novoceramide synthesis inhibitor, myriocin (MYR), both decreasing the endogenous ceramide production, significantly inhibited the transcytosis of oxLDL. Ceramidase inhibitor, N-oleoylethanolamine (NOE), and sphingomyelin synthase inhibitor, O-Tricyclo[5.2.1.02,6]dec-9-yl dithiocarbonate potassium salt (D609), both increasing the endogenous ceramide production, significantly upregulated the transcytosis of oxLDL.In vivo, injection of fluorescence labeled oxLDL into mice body also predisposed to the subendothelial retention of these oxidized lipids. The observations provided in the present study demonstrate that endogenous ceramide contributes to the transcytosis of oxLDL across endothelial cells and promotes the initiating step of atherosclerosis—the subendothelial retention of lipids in vascular wall.

Sign in / Sign up

Export Citation Format

Share Document