Interactions between apoptotic signal transduction and capacitation in human spermatozoa  

Oleh:

Grunewald, S. ; Kriegel, C. ; Baumann, T. ; Glander, H.-J. ; Paasch, U.

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Human Reproduction vol. 24 no. 09 (Sep. 2009), page 2071-2078.
Topik: sperm; capacitation; apoptotic signalling; calpain; calmodulin

Ketersediaan

Perpustakaan FK Nomor Panggil: H07.K.2009.03 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

BACKGROUND: Capacitation of sperm is a prerequisite for successful fertilization, determined by hyperactivated motility, increased tyrosine phosphorylation (TyrP) and membrane changes. However, the exact molecular mechanism is not fully clarified. The calpain–calmodulin-system is essential for membrane fusion during capacitation. Recently, interactions with caspase (CP) activation, a main feature of apoptotic cells, were postulated. The objective of our study was to examine interactions between apoptosis signalling and the calpain–calmodulin-system during capacitation. METHODS: Semen samples from 20 healthy donors were incubated in human tubal fluid at 37°C, 5% CO2 for 3 h without additives (control), with 3% BSA (capacitation), 10 µM calpain-inhibitor III, 20 µM CP-1 inhibitor or 20 µM calmodulin-antagonist. Capacitation was monitored by computer assisted sperm motion analyzer, chlortetracycline (CTC)-assay and western blot (TyrP). Activation of caspases and integrity of transmembrane mitochondrial potential (TMP) were evaluated by flow cytometry. RESULTS: Capacitation, as measured by CTC assay, increased TyrP levels and hyperactivation, resulted in inactivation of CP-9, CP-3 and improved integrity of the TMP. Inhibition of calpain and CP-1 during capacitation reduced the capacitation-related parameters, but did not lead to apoptosis. Inhibition of calmodulin resulted in blocking of capacitation and stimulation of apoptosis. CONCLUSION: Interaction of the capacitation and apoptosis signalling systems seems to enable the capacitation process by prevention of apoptosis.

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