In 2001 we reported on the "Blockade of regulatory volume decrease (RVD) of HeLa cells by extra-cellularly applied BH4 domain peptides of anti-apoptotic Bcl-XL."

Meanwhile a correlation of cell volume regulation and apoptosis was demonstrated.

To focus on plasmalemma-standing VDAC may help to promote future research in the exciting field of sepsis discussed here by Iwata et al.

For more details see my homepage: http//www.futhin.de

2001 Abstract:
F.P. Thinnes*, K.P. Hellmann and N. Hilschmann (2001), Blockade of regulatory volume decrease (RVD) of HeLa cells by extra-cellularly applied BH4 domain peptides of anti-apoptotic Bcl-XL.
- Joint Congress of the Scandinavian and the German Physiology Societies 10 - 13 March 2001, Berlin;
- Pflügers Arch - European Journal of Physiology, Supplement to Volume 441, No. 6 (2001), Abstracts, R 137.

Applying highly specific anti-human type-1 porin/VDAC antibodies, we recently showed that cell membrane integrated human VDAC functions as a channel that is relevant for cell volume regulation (Thinnes et al., Mol Gen Metab 69, 31-337, 2000). Others have documented that BH4 domain peptides of the anti-apoptotic Bcl-XL protein close VDAC in vitro after incorporation in liposomes. Applied in vivo at outer mitochondrial membranes the peptides inhibit apoptotic mitochondrial changes and cell death (Shimizu et al., PNAS 97, 3100-3105, 2000). Combining the rationale of both approaches we show that the peptides block the RVD of HeLa cells in a way corresponding to anti-human VDAC antibodies and DIDS. The present study thus corroborates former data on VDAC. Concerning research on cell volume regulation the results suggest that the peptides inhibit plasmalemma-integrated VDAC channels as a relevant part of the process.

Max-Planck-Institut für Experimentelle Medizin, Abteilung Immunchemie, Hermann-Rein-Strasse 3, D-37075 Göttingen, Germany