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Human Spermatogenesis (human + spermatogenesis)
Selected AbstractsORIGINAL ARTICLE: The Role of IL-6, IL-10, TNF-, and its Receptors TNFR1 and TNFR2 in the Local Regulatory System of Normal and Impaired Human SpermatogenesisAMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 1 2009gorzata Bia Problem, To investigate the expression of genes coding for selected cytokines with antagonistic functions (IL-6, IL-10, TNF-,) as well as TNF-, receptors (TNFR1 and TNFR2) in correct spermatogenesis (normal proliferation), maturation arrest (proliferation inhibited) and testicular tumors (overgrowth). Method of study, Transcription levels of genes coding for IL-6, IL-10, TNF-,, TNFR1 and TNFR2 were quantitatively examined using a real-time RT-PCR. Results, Significantly higher amounts of IL-6 mRNA were observed in testicular tumor samples than in normal spermatogenesis or in some syndromes with maturation arrest (MA at spermatid level or SCOS), while IL-10 gene levels were fairly stable. In homogenates with maturation arrest, the expression of TNFR1 gene was markedly higher than in testicular tumors, while the opposite phenomenon was found in respect to TNFR2 gene. Conclusion, The results obtained indicate that changes in activities of intra-testicular cytokines may promote different distinct pathologies such as testicular cancer or infertility. [source] Androgen insensitivity and male infertility,INTERNATIONAL JOURNAL OF ANDROLOGY, Issue 1 2003O. Hiort Summary Abnormal human spermatogenesis can be caused by defects in androgen action because of androgen insensitivity. A variety of mutations have been described in the human androgen receptor gene associated with male infertility. These can be attributed to two molecular mechanisms. First, point mutations in the androgen receptor gene cause alterations in the amino acid sequence and, hence, lead to apparently slight changes in the androgen receptor effector mechanisms and mild androgen insensitivity. Secondly, variations in the polymorphic poly glutamine segment within the N-terminal end of the androgen receptor have been ascribed to correlate with fertility aspects possibly because of modifications of transcriptional regulatory mechanisms. It has been postulated that longer poly glutamine segments are associated with decreased sperm counts. However, the molecular mechanisms that lead to inhibition of spermatogenesis because of a mutated androgen receptor are poorly understood and will need more focus in the future. [source] Reproductive stem cell research and its application to urologyINTERNATIONAL JOURNAL OF UROLOGY, Issue 2 2008Takehiko Ogawa Abstract: Germ cells are defined by their innate potential to transmit genetic information to the next generation through fertilization. Males produce numerous sperm for long periods to maximize chances of fertilization. Key to the continuous production of large numbers of sperm are germline stem cells and their immediate daughter cells, functioning as transit amplifying cells. Recently, it has become possible to expand germline stem cells of rodents in vitro. In addition, multipotent stem cells, which are functionally the same as embryonic stem cells, have been established from neonatal mouse testes. These stem cells derived from the testis should contribute to biological research and technologies. On the other hand, the nature of human spermatogenesis is largely unknown due to the lack of an appropriate experimental system. However, the prevailing testicular sperm extraction procedure unraveled hitherto unknown facets of human spermatogenesis. The establishment of a culturing method for human spermatogonial stem cells in hopefully the near future would be a great benefit for achieving further insight into human spermatogenesis and should lead to more sophisticated diagnostic and therapeutic clinical measures for male infertility. [source] TEM, FISH and molecular studies in infertile men with pericentric inversion of chromosome 9ANDROLOGIA, Issue 4 2006G. Collodel Summary Pericentric inversions involving the secondary constriction (qh) region of chromosome 9 are considered to be normal variants of human karyotype. A number of investigators have suggested that chromosomal anomalies can contribute to human infertility causing spermatogenetic derangement. The present study was aimed at verifying the influence of chromosome 9 inversion on human spermatogenesis. Semen samples of 18 male carriers of chromosome 9 inversion, analysed by light microscopy, revealed that five patients were azoospermic. PCR analysis demonstrated that two of them also had Y microdeletions. The other 13 showed generally normal sperm concentrations and reduced motility. The morphological characteristics of sperm were studied by TEM and the data were elaborated by a mathematical formula. Sperm pathologies resulted more frequently in the studied group compared to controls, particularly apoptosis. Partial sequences of the A-kinase anchoring protein (Akap) 4 and 3 genes were performed in all patients, as a previous study by our group highlighted Dysplasia of Fibrous Sheath (DFS) defect in two men with inv 9 investigations. The possible effect of chromosome 9 inversion on meiotic chromosome segregation was investigated by FISH, which showed an increased incidence of diploidy. We hypothesized that this inversion could have variable effects on spermatogenesis, from azoospermia to severely altered sperm morphology, motility and meiotic segregation. [source] Angiotensin I-converting enzyme and potential substrates in human testis and testicular tumoursAPMIS, Issue 1 2003Review article The angiotensin I-converting enzyme (ACE, kininase II, CD143) shows a broad specificity for various oligopeptides. Besides the well-known conversion of angiotensin I to II, ACE degrades efficiently kinins and the tetrapeptide AcSDKP (goralatide) and thus equally participates in the renin-angiotensin system, the kallikrein-kinin system, and the regulation of stem cell proliferation. In the mammalian testis, ACE occurs in two isoforms. The testicular isoform (tACE) is exclusively expressed during spermatogenesis and is generally thought to represent the germ cell-specific isozyme. However, we have previously demonstrated that, in addition to tACE, the somatic isoform (sACE) is also present in human germ cells. Similar to other oncofoetal markers, sACE exhibits a transient expression during foetal germ cell development and appears to be a constant feature of intratubular germ cell neoplasm, the so-called carcinoma-in-situ (CIS) and, in particular, of classic seminoma. This demands the existence of specific paracrine functions during male germ cell differentiation and development of male germ cell tumours, which are mediated by either of the two ACE isoforms. Considering the complexity of current data about ACE, a logical connection is required between () the precise localisation of ACE isoforms, (I) the local access to potential substrates and (II) functional data obtained by knockout mice models. The present article summarises the current knowledge about ACE and its potential substrates with special emphasis on the differentiation-restricted ACE expression during human spermatogenesis and prespermatogenesis, the latter being closely linked to the pathogenesis of human germ cell tumours. 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