scholarly journals Corrigendum: Effects of LPXRFamide peptides on chub mackerel gonadotropin secretion

Author(s):  
Hirofumi Ohga ◽  
Michiya Matsuyama
Author(s):  
Hirofumi Ohga ◽  
Michiya Matsuyama

Abstract Gonadotropin-inhibitory hormone (GnIH), a neuropeptide, suppresses gonadotropin (GTH) secretion in birds and mammals. In fish, the GnIH homolog LPXRFamide (LPXRFa) produces mature peptides with species-dependent effects on sexual reproduction. Here, we investigated the effects of LPXRFa on GTH secretion in the chub mackerel (cm; Scomber japonicus). We cloned cmlpxrfa (603 bp) and cmlpxrfa-r (1,416 bp). Additionally, we isolated lpxrfa from the bluefin tuna (Thunnus orientalis) to confirm the conservation of the LPXRFa mature sequence. Phylogenetic analysis showed that the LPXRFa precursor protein produces three mature peptides, LPXRFa-1, −2, and − 3, in both species. Reverse transcription-quantitative PCR revealed that cmlpxrfa is expressed in the hypothalamus and thalamus and midbrain (T.MB), and sexual differences were observed. Receptor expression was observed in the pre-optic area, hypothalamus, T.MB, and pituitary. Female hypothalamic lpxrfa expression did not change during puberty. Reporter gene assay showed that LPXRFa induced receptor activation via the CRE and SRE signaling pathways. However, in the presence of forskolin, an intracellular cyclic AMP enhancer, none of the LPXRFa could suppress receptor activity. The in vitro bioassay results showed that gonadotropin-releasing hormone-1 (GnRH1) had no effect on follicle-stimulating hormone (FSH) secretion, whereas the three LPXRFa significantly increased FSH secretion in pituitary cells from male chub mackerel. Contrarily, GnRH1 and three LPXRFa significantly increased luteinizing hormone (LH) secretion. The in vivo administration of LPXRFa had no effect on fshb and lhb expression in pre-pubertal and mature male chub mackerel. Overall, cmLPXRFa lacks the ability to suppress GTH secretion but can promote GTH secretion.


1998 ◽  
Vol 5 (1) ◽  
pp. 93A-93A
Author(s):  
E CHEN ◽  
M LUTHER ◽  
A MORENO ◽  
T KING ◽  
R SCHENKEN

1987 ◽  
Vol 116 (3_Suppl) ◽  
pp. S187-S188 ◽  
Author(s):  
O. ORTMANN ◽  
G. EMONS ◽  
R. KNUPPEN ◽  
K.J. CATT

1988 ◽  
Vol 117 (4_Suppl) ◽  
pp. S93-S94
Author(s):  
M. BETTENDORF ◽  
F. DE ZEGHER ◽  
N. ALBERS ◽  
S. L. KAPLAN ◽  
M. M. GRUMBACH

BMC Genomics ◽  
2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Vengala Rao Yenuganti ◽  
Dirk Koczan ◽  
Jens Vanselow

Abstract Background Metabolic stress, as negative energy balance on one hand or obesity on the other hand can lead to increased levels of free fatty acids in the plasma and follicular fluid of animals and humans. In an earlier study, we showed that increased oleic acid (OA) concentrations affected the function of cultured bovine granulosa cells (GCs). Here, we focus on genome wide effects of increased OA concentrations. Results Our data showed that 413 genes were affected, of which 197 were down- and 216 up-regulated. Specifically, the expression of FSH-regulated functional key genes, CCND2, LHCGR, INHA and CYP19A1 and 17-β-estradiol (E2) production were reduced by OA treatment, whereas the expression of the fatty acid transporter CD36 was increased and the morphology of the cells was changed due to lipid droplet accumulation. Bioinformatic analysis revealed that associated pathways of the putative upstream regulators “FSH” and “Cg (choriogonadotropin)” were inhibited and activated, respectively. Down-regulated genes are over-represented in GO terms “reproductive structure/system development”, “ovulation cycle process”, and “(positive) regulation of gonadotropin secretion”, whereas up-regulated genes are involved in “circulatory system development”, “vasculature development”, “angiogenesis” or “extracellular matrix/structure organization”. Conclusions From these data we conclude that besides inhibiting GC functionality, increased OA levels seemingly promote angiogenesis and tissue remodelling, thus suggestively initiating a premature fulliculo-luteal transition. In vivo this may lead to impeded folliculogenesis and ovulation, and cause sub-fertility.


1989 ◽  
Vol 264 (19) ◽  
pp. 10939-10942
Author(s):  
S S Stojilković ◽  
E Rojas ◽  
A Stutzin ◽  
S Izumi ◽  
K J Catt

1985 ◽  
Vol 40 (4) ◽  
pp. 297-302 ◽  
Author(s):  
David R. Mann ◽  
Diane Evans ◽  
Festus Edoimioya ◽  
Freja Kamel ◽  
George M. Butterstein

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