scholarly journals Fertility in luteinizing hormone receptor-knockout mice after wild-type ovary transplantation demonstrates redundancy of extragonadal luteinizing hormone action

2005 ◽  
Vol 115 (7) ◽  
pp. 1862-1868 ◽  
Author(s):  
T. Pakarainen
Keyword(s):  
Luteinizing Hormone ◽  
Knockout Mice ◽  
Hormone Receptor ◽  
Luteinizing Hormone Receptor ◽  
Hormone Action ◽  
Wild Type ◽  
Ovary Transplantation

Identification of Gubernacular Androgen Responsive Genes in Luteinizing Hormone Receptor Knockout Mice.

2011 ◽  
Vol 85 (Suppl_1) ◽  
pp. 564-564
Author(s):  
Yong Siow ◽  
Shengqiang Li ◽  
Jing Lin ◽  
Xian Li ◽  
Zi-Jian Lan ◽  
...  
Keyword(s):  
Luteinizing Hormone ◽  
Knockout Mice ◽  
Hormone Receptor ◽  
Luteinizing Hormone Receptor

scholarly journals Transcriptome analysis reveals an unexpected role of a collagen tyrosine kinase receptor gene, Ddr2, as a regulator of ovarian function

2009 ◽  
Vol 39 (2) ◽  
pp. 120-129 ◽  
Author(s):  
Hirokazu Matsumura ◽  
Kiyoshi Kano ◽  
Caralina Marín de Evsikova ◽  
James A. Young ◽  
Patsy M. Nishina ◽  
...  
Keyword(s):  
Luteinizing Hormone ◽  
Transcriptome Analysis ◽  
Hormone Receptor ◽  
Ovarian Function ◽  
Luteinizing Hormone Receptor ◽  
Unknown Etiology ◽  
Intrinsic Defect ◽  
Tyrosine Kinase Receptor ◽  
Fertilization In Vitro ◽  
Wild Type

Mice homozygous for the smallie ( slie) mutation lack a collagen receptor, discoidin domain receptor 2 (DDR2), and are dwarfed and infertile due to peripheral dysregulation of the endocrine system of unknown etiology. We used a systems biology approach to identify biological networks affected by Ddr2slie/slie mutation in ovaries using microarray analysis and validate findings using molecular, cellular, and functional biological assays. Transcriptome analysis indicated several altered gene categories in Ddr2slie/slie mutants, including gonadal development, ovulation, antiapoptosis, and steroid hormones. Subsequent biological experiments confirmed the transcriptome analysis predictions. For instance, a significant increase of TUNEL-positive follicles was found in Ddr2slie/slie mutants vs. wild type, which confirm the transcriptome prediction for decreased chromatin maintenance and antiapoptosis. Decreases in gene expression were confirmed by RT-PCR and/or qPCR; luteinizing hormone receptor and prostaglandin type E and F receptors in Ddr2slie/slie mutants, compared with wild type, confirm hormonal signaling pathways involved in ovulation. Furthermore, deficiencies in immunohistochemistry for DDR2 and luteinizing hormone receptor in the somatic cells, but not the oocytes, of Ddr2slie/slie mutant ovaries suggest against an intrinsic defect in germ cells. Indeed, Ddr2slie/slie mutants ovulated significantly fewer oocytes; their oocytes were competent to complete meiosis and fertilization in vitro. Taken together, our convergent data signify DDR2 as a novel critical player in ovarian function, which acts upon classical endocrine pathways in somatic, rather than germline, cells.

scholarly journals Constitutive Activating and Inactivating Mutants of Eel Luteinizing Hormone Receptor

2020 ◽  
Author(s):  
Munkhzaya Byambaragchaa ◽  
Dong-An Kim ◽  
Dae-Jung Kim ◽  
Sun-Mee Hong ◽  
Myung-Hwa Kang ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Luteinizing Hormone ◽  
Cell Surface ◽  
Hormone Receptor ◽  
Luteinizing Hormone Receptor ◽  
Cell Surface Receptors ◽  
Wild Type ◽  
Surface Receptors ◽  
Agonist Stimulation ◽  
In Cells

We analyzed signal transduction of three constitutively activating mutants (M410T, L469R, and D590Y) and two inactivating mutants (D417N and Y558F) of the eel luteinizing hormone receptor (eel LHR), known to occur in human LHR. The objective of this study was to assess the functional effects of these mutations in signal transduction and cell surface loss of receptor. Mutant receptors were transiently expressed in Chinese hamster ovary (CHO-K1) cells. Eel LH-stimulated accumulation of cyclic adenosine monophosphate (cAMP) was measured by homogeneous time-resolved fluorescence (HTRF) assays. The loss of receptors from the cells surface was measured using an enzyme-linked immunosorbent assay (ELISA) in human embryonic kidney (HEK) 293 cells. The cAMP response in cells expressing the wild type eel LHR was increased in a dose-dependent manner using eel LH ligand stimulation. Compared with the wild type, cells expressing the activating mutants (M410T, L469R, and D590Y), exhibited a 4.0-, 19.1-, and 7.8-fold increase in basal cAMP response without agonist stimulation, respectively. Their maximal responses to agonist stimulation were approximately 65%, 52%, and 98%, respectively, of those of the wild type. The inactivating mutants (D417N and Y558F) did not completely impair signal transduction, and their maximal responses were only 33% and25 % of those of wild type. These data clearly showed that the eel LHR-L469R and D590Y, activating mutants enhanced the rate of the loss of cell surface receptors following treatment with eel LH. Thus, the loss of cell surface receptors in cells expressing mutant eel LHRs was consistent with the eel LH agonist-induced production of cAMP. Our results suggested that the activation of the eel LHR requires appropriate loss of LHR-ligand complexes from the cell surface.

scholarly journals De NovoTestosterone Production in Luteinizing Hormone Receptor Knockout Mice after Transplantation of Leydig Stem Cells

Endocrinology ◽  
2004 ◽  
Vol 145 (9) ◽  
pp. 4011-4015 ◽  
Author(s):  
Kirk C. Lo ◽  
Zhenmin Lei ◽  
Ch. Venkateswara Rao ◽  
Josie Beck ◽  
Dolores J. Lamb
Keyword(s):  
Stem Cells ◽  
Luteinizing Hormone ◽  
Knockout Mice ◽  
Hormone Receptor ◽  
Luteinizing Hormone Receptor

Luteinizing hormone receptor

2007 ◽  
Author(s):  
Thomas Buech ◽  
Pascal Nurwakagari ◽  
David Ben-Menahem ◽  
Thomas Gudermann
Keyword(s):  
Luteinizing Hormone ◽  
Hormone Receptor ◽  
Luteinizing Hormone Receptor
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