OBJECTIVE: To evaluate whether defective cyclic adenosine monophosphate responsive element modulator (CREM) expression is the causative factor of spermatid maturation arrest (SMA).DESIGN: Comparative evaluation of the testicular histology in patients with SMA or normal spermatogenesis.SETTING: University clinic of andrology.PATIENT(S): Azoospermic patients undergoing testicular biopsy.INTERVENTION(S): None.MAIN OUTCOME MEASURE(S): Expression of CREMtau in quantitative immunohistochemistry analysis of testicular biopsy samples.RESULT(S): Regular CREM expression was observed in the tubules with round, but not elongated, spermatids of patients with SMA (n = 9). Quantitative analysis showed that round spermatids of patients with SMA had a staining intensity similar to that observed in controls (n = 7).CONCLUSION(S): Lack of spermatid elongation was not due to defective CREM expression. Therefore, CREM did not play a pathogenetic role in the onset of SMA in humans

Normal expression of isoforms activating cyclic adenosine monophosphate responsive element modulator in patients with spermatid maturation arrest

BARTOLONI, Giovanni;VICARI, Enzo Saretto;CALOGERO, Aldo Eugenio
2004-01-01

Abstract

OBJECTIVE: To evaluate whether defective cyclic adenosine monophosphate responsive element modulator (CREM) expression is the causative factor of spermatid maturation arrest (SMA).DESIGN: Comparative evaluation of the testicular histology in patients with SMA or normal spermatogenesis.SETTING: University clinic of andrology.PATIENT(S): Azoospermic patients undergoing testicular biopsy.INTERVENTION(S): None.MAIN OUTCOME MEASURE(S): Expression of CREMtau in quantitative immunohistochemistry analysis of testicular biopsy samples.RESULT(S): Regular CREM expression was observed in the tubules with round, but not elongated, spermatids of patients with SMA (n = 9). Quantitative analysis showed that round spermatids of patients with SMA had a staining intensity similar to that observed in controls (n = 7).CONCLUSION(S): Lack of spermatid elongation was not due to defective CREM expression. Therefore, CREM did not play a pathogenetic role in the onset of SMA in humans
2004
CREM; SMA; AZOOSPERMIC
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.11769/3737
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