Relaxin-like factor (RLF) mRNA expression in the fallow deer

Hombach‐Klonisch, Sabine; Kauffold, Johannes; Rautenberg, Tanja; Steger, Klaus; Tetens, Frank; Fischer, Bernd; Klonisch, Thomas

doi:10.1016/s0303-7207(99)00190-2

Cited by 26 publications

(15 citation statements)

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“…Studies in humans show that, unlike testicular steroids, which are acutely governed by the components of the HPG axis, INSL3 appears to be constitutively expressed, and thus representative of the quality (functionality and number) of the Leydig cells present in the testes [16,18,19]. Nevertheless, as Leydig cells alter their differentiation state (e.g., in aging [44], seasonal breeders [43,46,47], mouse mutants [2], Leydig cell tumors [48], androgen-treated men [16], or in those subject to a male hormonal contraceptive regimen [8 and Anand-Ivell and Ivell, unpublished results]), INSL3 expression is also correspondingly altered. It can be argued that INSL3 offers a more accurate parameter to determine true hypogonadism than those that are influenced by factors perturbing the HPG axis.…”

Section: Discussionmentioning

confidence: 99%

Dynamics of INSL3 Peptide Expression in the Rodent Testis1

Anand‐Ivell

Heng

Hafen

et al. 2009

Biology of Reproduction

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The Leydig cell-specific factor insulin-like peptide 3 (INSL3) is involved in testicular descent during embryo development, and has been suggested to regulate spermatogenesis and bone metabolism in the adult. Using a new, sensitive assay specific for rodent INSL3, we have mapped the secretion of INSL3 into peripheral blood in mice and during postnatal male rat development (in female rats, circulating INSL3 is at the level of detection). Maximum INSL3 is measured at Postnatal Day (PD) 40 in the rat and decreases to a significantly lower, stable value by PD60, indicating an "overshoot" effect in the establishment of Leydig cell functionality during the first wave of spermatogenesis. Aging rats ( approximately 24 mo) have markedly reduced circulating INSL3 levels, as do humans. Treatment of young adult rats with ethane dimethylsulfonate (EDS) leads to loss of mature Leydig cells and no detectable INSL3 in peripheral blood. INSL3 can be detected first at Day 27 after EDS treatment, returning to near normal levels by Day 37. Both primary rat Leydig cells and the mouse MA-10 tumor cell line secrete substantial amounts of INSL3 into the culture media in a constitutive manner, unregulated by common effectors, including hCG. Analysis of different testicular fluid compartments shows highest INSL3 concentration in the interstitial fluid (391.4 +/- 47.8 ng/ml). However, INSL3 evidently traverses the blood-testis barrier to enter the seminiferous compartment, rete testis, and epididymis in sufficient concentration to be able to address the specific INSL3 receptors (RXFP2) on post-meiotic germ cells and in the epididymis.

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Section: Discussionmentioning

confidence: 99%

Dynamics of INSL3 Peptide Expression in the Rodent Testis1

Anand‐Ivell

Heng

Hafen

et al. 2009

Biology of Reproduction

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“…Multi-species protein alignment using Pile-up (Genetics Computer Group, Madison, USA) included the following sequences (Genbank accession numbers in parentheses) (15): pig INSL3 (X73636), cow relaxinlike factor (RLF) (AF094580), marmoset RLF (AJ011961), goat RLF (AF233686), mouse INSL3 (X95603), RAT (AF139919), sheep Leydig insulinlike factor (16) and deer RLF (17). The INSL3 DNA and protein sequence are numbered in accordance with Burkhardt and colleagues (18).…”

Section: Dna Sequencing and Protein Alignmentsmentioning

confidence: 99%

Genetic analysis of the INSL3 gene in patients with maldescent of the testis

et al. 2001

European Journal of Endocrinology

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Objective: Testicular maldescent is important because it is a common congenital disorder that is associated with an increased risk of infertility and testicular cancer. Murine studies indicate that testicular maldescent can result from disruption of insulin-like factor 3 (INSL3) activity and that it may be more severe when there is concurrent undermasculinisation. Therefore, the INSL3 gene was screened for mutations and polymorphisms that may contribute to testicular maldescent in patients with undermasculinisation as well as those with isolated testicular maldescent. Methods and Results: The patient groups consisted of individuals with isolated testicular maldescent n 28 and patients with undermasculinised genitalia and intra-abdominal n 24 or inguinal gonads n 33X The three control groups were: normal males n 15Y males with undermasculinised genitalia and scrotal gonads n 29 and females n 82X SSCP/HA mutation screening detected eight variants, five of which were predicted to alter the protein sequence (A-1G, V19L, P25S, A36T, R78H). Three of the amino acid changes (A-1G, V19L, R78H) each occurred in a single control sample and one was identified in a male with undermasculinised genitalia and intraabdominal testes (P25S). The A36T amino acid polymorphism was found in both patient and control groups at a similar frequency. Conclusions: The evidence suggests that INSL3 mutations and polymorphisms are not a major cause of testicular maldescent with or without associated undermasculinisation.

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“…Originally discovered as a differentially expressed testicular product, 1,2 RLF has been identified as a marker for differentiated postpubertal Leydig cells in various species, including human. [3][4][5] In rodents, testicular RLF gene expression is controlled developmentally and up-regulated during puberty. 6,7 Targeted disruption of the murine RLF gene results in failure of gubernaculum development during embryogenesis causing bilateral cryptorchidism.…”

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confidence: 99%