Reduced numbers of Sertoli, germ, and spermatogonial stem cells in impaired spermatogenesis.
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Reduced numbers of Sertoli, germ, and spermatogonial stem cells in impaired spermatogenesis. / Hentrich, Anna; Wolter, Martin; Szardening-Kirchner, Carolin; Lüers, Georg; Bergmann, Martin; Kliesch, Sabine; Konrad, Lutz.
in: MODERN PATHOL, Jahrgang 24, Nr. 10, 10, 2011, S. 1380-1389.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - Reduced numbers of Sertoli, germ, and spermatogonial stem cells in impaired spermatogenesis.
AU - Hentrich, Anna
AU - Wolter, Martin
AU - Szardening-Kirchner, Carolin
AU - Lüers, Georg
AU - Bergmann, Martin
AU - Kliesch, Sabine
AU - Konrad, Lutz
PY - 2011
Y1 - 2011
N2 - A key step in the investigation of male infertility is the appropriate classification of impaired spermatogenesis. In this study, we precisely identified Sertoli and distinct germ-cell types in the rat, the mouse, and in the human testis. As a proof of principle, we studied testis biopsy samples from azoospermic patients with defined spermatogenic defects. Remarkably, we found that already the numbers of Sertoli cells, spermatogonia and a subset of spermatogonia including stem cells are significantly reduced in patients with maturation arrest at the level of primary spermatocytes (n=33) compared with patients with histologically normal spermatogenesis (n=33). In patients with hypospermatogenesis (n=44) a significant reduction of spermatogonial cell numbers was observed. The numbers of primary and diplotene spermatocytes were reduced by 84%. However, the strongest reduction (96%) was revealed in the numbers of spermatids in patients with maturation arrest. In contrast, patients with hypospermatogenesis showed only modestly reduced numbers of spermatocytes and spermatids compared with normal spermatogenesis. No correlation was found with age or obstruction. For a detailed analysis of the patients, we distinguished between 'pool of founder cells'-related deficiencies (reduced numbers of Sertoli cells, spermatogonia, and spermatogonial stem cells) and 'meiotic' deficiencies (reduced numbers of spermatocytes, meiotic divisions, and spermatids). Interestingly, patients with maturation arrest showed meiotic deficiencies (36%), while the majority additionally demonstrated deficiencies in the founder pool (58%). In contrast, patients with normal spermatogenesis most often had no deficiencies at all (45%) or founder pool-related deficiencies (33%) but an apparently normal meiosis. This is the first report showing that many infertile patients face besides meiotic defects the problem of reduced numbers of Sertoli cells, spermatogonia, and spermatogonial stem cells.
AB - A key step in the investigation of male infertility is the appropriate classification of impaired spermatogenesis. In this study, we precisely identified Sertoli and distinct germ-cell types in the rat, the mouse, and in the human testis. As a proof of principle, we studied testis biopsy samples from azoospermic patients with defined spermatogenic defects. Remarkably, we found that already the numbers of Sertoli cells, spermatogonia and a subset of spermatogonia including stem cells are significantly reduced in patients with maturation arrest at the level of primary spermatocytes (n=33) compared with patients with histologically normal spermatogenesis (n=33). In patients with hypospermatogenesis (n=44) a significant reduction of spermatogonial cell numbers was observed. The numbers of primary and diplotene spermatocytes were reduced by 84%. However, the strongest reduction (96%) was revealed in the numbers of spermatids in patients with maturation arrest. In contrast, patients with hypospermatogenesis showed only modestly reduced numbers of spermatocytes and spermatids compared with normal spermatogenesis. No correlation was found with age or obstruction. For a detailed analysis of the patients, we distinguished between 'pool of founder cells'-related deficiencies (reduced numbers of Sertoli cells, spermatogonia, and spermatogonial stem cells) and 'meiotic' deficiencies (reduced numbers of spermatocytes, meiotic divisions, and spermatids). Interestingly, patients with maturation arrest showed meiotic deficiencies (36%), while the majority additionally demonstrated deficiencies in the founder pool (58%). In contrast, patients with normal spermatogenesis most often had no deficiencies at all (45%) or founder pool-related deficiencies (33%) but an apparently normal meiosis. This is the first report showing that many infertile patients face besides meiotic defects the problem of reduced numbers of Sertoli cells, spermatogonia, and spermatogonial stem cells.
KW - Adult
KW - Animals
KW - Biopsy
KW - Humans
KW - Male
KW - Middle Aged
KW - Young Adult
KW - Immunohistochemistry
KW - Mice
KW - Mice, Inbred C57BL
KW - Rats
KW - Rats, Sprague-Dawley
KW - Microscopy, Fluorescence
KW - Linear Models
KW - Biological Markers/analysis
KW - Azoospermia/metabolism/pathology
KW - Meiosis
KW - Sertoli Cells/chemistry/pathology
KW - Sperm Count
KW - Spermatogenesis
KW - Spermatogonia/chemistry/pathology
KW - Spermatozoa/chemistry/pathology
KW - Stem Cells/chemistry/pathology
KW - Adult
KW - Animals
KW - Biopsy
KW - Humans
KW - Male
KW - Middle Aged
KW - Young Adult
KW - Immunohistochemistry
KW - Mice
KW - Mice, Inbred C57BL
KW - Rats
KW - Rats, Sprague-Dawley
KW - Microscopy, Fluorescence
KW - Linear Models
KW - Biological Markers/analysis
KW - Azoospermia/metabolism/pathology
KW - Meiosis
KW - Sertoli Cells/chemistry/pathology
KW - Sperm Count
KW - Spermatogenesis
KW - Spermatogonia/chemistry/pathology
KW - Spermatozoa/chemistry/pathology
KW - Stem Cells/chemistry/pathology
M3 - SCORING: Journal article
VL - 24
SP - 1380
EP - 1389
JO - MODERN PATHOL
JF - MODERN PATHOL
SN - 0893-3952
IS - 10
M1 - 10
ER -
