Dataset Information

Expression of Luteinizing Hormone (LH) Subunit Genes in Mouse Testis.

ABSTRACT: Gonadotropins are heterodimers consisting an alpha chain (Cg?) and a beta chain. Interestingly, presence of complicated LH-? transcripts in rat testis was accidently found; testicular LH-? transcripts were confined in seminiferous tubules to spermatids, and the translated products were localized in the elongated spermatids. We hypothesized that mouse testis has potential to produce the tissue specific LH-? with similar structure to the rat testicular forms. To verify our hypothesis, we examined the adult mouse (ICR) testis using RT-PCR and immunohistochemistry. The PCR revealed the presence of the identical products in the reactions for three LH subunit types. The expected product sizes for mouse Cg? and LH-? known as pituitary type were 224 bp and 503 bp, respectively. The testicular type LH-? products were produced by a primer set based on the rat sequences, with unexpected size of 800 bp. Sequencing revealed that the proximal and distal parts (2-82 and 661- 773 bp, respectively) were homologous to rat testicular LH-? cDNA, and middle part (83-660 bp) was a unique mouse-specific region. Both Cg? and LH-? positive signals were in the round and elongated spermatids and mature sperms, and the LH-? signals were more intense. In conclusion, our study demonstrated that the presence and localization of the LH subunits in mouse testis. Further studies will be needed to understand the precise structure and function of mouse testicular LH.

SUBMITTER: Kim HS

PROVIDER: S-EPMC5651699 | biostudies-literature | 2017 Sep

REPOSITORIES: biostudies-literature

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Expression of Luteinizing Hormone (LH) Subunit Genes in Mouse Testis.

Kim Hee Soo HS Lee Sung-Ho SH

Development & reproduction 20170930 3

Gonadotropins are heterodimers consisting an alpha chain (Cgα) and a beta chain. Interestingly, presence of complicated LH-β transcripts in rat testis was accidently found; testicular LH-β transcripts were confined in seminiferous tubules to spermatids, and the translated products were localized in the elongated spermatids. We hypothesized that mouse testis has potential to produce the tissue specific LH-β with similar structure to the rat testicular forms. To verify our hypothesis, we examined ...[more]

PMID: 29082348

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Project description:Luteinizing hormone (LH) is a pituitary heterodimeric glycoprotein essential in male and female reproduction. Its functional polymorphic variant (V-LH) is determined by two missense mutations (rs1800447, A/G, Trp8Arg; rs34349826, A/G, Ile15Thr) in the LH β-subunit encoding gene (LHB; 19q13.3; 1111 bp; 3 exons). Among women, V-LH has been associated with higher circulating LH and reduced fertility, but the knowledge of its effect on male reproductive parameters has been inconclusive. The objective of this study was to assess the effect of V-LH on hormonal, seminal and testicular parameters in the Baltic young men cohort (n = 986; age: 20.1 ± 2.1 years) and Estonian idiopathic infertility patients (n = 607; 35.1 ± 5.9 years). V-LH was detected by genotyping of the underlying DNA polymorphisms using PCR-RFLP combined with resequencing of a random subset of subjects. Genetic associations were tested using linear regression under additive model and results were combined in meta-analysis. No significant difference was detected between young men and infertility patients for the V-LH allele frequency (11.0 vs. 9.3%, respectively). V-LH was associated with higher serum LH in both, the young men cohort (p = 0.022, allelic effect = 0.26 IU/L) and the idiopathic infertility group (p = 0.008, effect = 0.59 IU/L). In meta-analysis, the statistical significance was enhanced (p = 0.0007, resistant to Bonferroni correction for multiple testing; effect = 0.33 IU/L). The detected significant association of V-LH with increased serum LH remained unchanged after additional adjustment for the SNPs previously demonstrated to affect LH levels (FSHB -211G/T, FSHR Asn680Ser, FSHR -29A/G). Additionally, a suggestive trend for association with reduced testicular volume was observed among young men, and with lower serum FSH among infertility patients. The V-LH carrier status did not affect sperm parameters and other circulating reproductive hormones. For the first time, we show a conclusive contribution of V-LH to the natural variance in male serum LH levels. Its downstream clinical consequences are still to be learned.

Project description:BackgroundLuteinizing hormone secreted by the anterior pituitary gland regulates gonadal function. Luteinizing hormone secretion is regulated both by alterations in gonadotrope responsiveness to hypothalamic gonadotropin releasing hormone and by alterations in gonadotropin releasing hormone secretion. The mechanisms that determine gonadotrope responsiveness are unknown but may involve regulators of G protein signaling (RGSs). These proteins act by antagonizing or abbreviating interaction of Galpha proteins with effectors such as phospholipase Cbeta. Previously, we reported that gonadotropin releasing hormone-stimulated second messenger inositol trisphosphate production was inhibited when RGS3 and gonadotropin releasing hormone receptor cDNAs were co-transfected into the COS cell line. Here, we present evidence for RGS3 inhibition of gonadotropin releasing hormone-induced luteinizing hormone secretion from cultured rat pituitary cells.ResultsA truncated version of RGS3 (RGS3T = RGS3 314-519) inhibited gonadotropin releasing hormone-stimulated inositol trisphosphate production more potently than did RSG3 in gonadotropin releasing hormone receptor-bearing COS cells. An RSG3/glutathione-S-transferase fusion protein bound more 35S-Gqalpha than any other member of the G protein family tested. Adenoviral-mediated RGS3 gene transfer in pituitary gonadotropes inhibited gonadotropin releasing hormone-stimulated luteinizing hormone secretion in a dose-related fashion. Adeno-RGS3 also inhibited gonadotropin releasing hormone stimulated 3H-inositol phosphate accumulation, consistent with a molecular site of action at the Gqalpha protein.ConclusionsRGS3 inhibits gonadotropin releasing hormone-stimulated second messenger production (inositol trisphosphate) as well as luteinizing hormone secretion from rat pituitary gonadotropes apparently by binding and suppressing the transduction properties of Gqalpha protein function. A version of RGS3 that is amino-terminally truncated is even more potent than intact RGS3 at inhibiting gonadotropin releasing hormone-stimulated inositol trisphosphate production.

Dataset Information

Expression of Luteinizing Hormone (LH) Subunit Genes in Mouse Testis.

Publications

Expression of Luteinizing Hormone (LH) Subunit Genes in Mouse Testis.

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