Am J Physiol Cell Physiol AJP: Gastrointestinal and Liver Physiology
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Am J Physiol Cell Physiol (July 24, 2002). doi:10.1152/ajpcell.00429.2001
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Articles in PresS, published online ahead of print July 24, 2002
Am J Physiol Cell Physiol, 10.1152/ajpcell.00429.2001
Submitted on September 6, 2001
Accepted on July 16, 2002

ESSENTIAL ROLE OF Ca2+-DEPENDENT PHOSPHOLIPASE A2 IN ESTRADIOL-INDUCED LYSOSOME ACTIVATION

Bruno Burlando1*, Barbara Marchi2, Isabella Panfoli3, and Aldo Viarengo1

1 Dipartimento di Scienze e Tecnologie Avanzate, Universita' del Piemonte Orientale, Alessandria, Alessandria, Italy
2 Dipartimento di Biologia Sperimentale Ambientale ed Applicata, Universita' di Genova, Genova, Genova, Italy
3 Dipartimento di Oncologia, Biologia e Genetica, Universita' di Genova, Genova, Genova, Italy

* To whom correspondence should be addressed. E-mail: burlando{at}unipmn.it.

The mechanism of lysosome activation by 17ß-estradiol has been studied in mussel blood cells. Cell treatment with estradiol induced a sustained increase of cytosolic free Ca2+ that was completely prevented by pre-incubating the cells with the Ca2+ chelator, BAPTA-AM. Estradiol treatment was also followed by destabilization of the lysosomal membranes, as detected in terms of the lysosomes' increased permeability to neutral red. The effect of estradiol on lysosomes was almost completely prevented by pre-incubation with the inhibitor of cytosolic Ca2+-dependent PLA2 (cPLA2), AACOCF3, and was significantly reduced by pre-incubation with BAPTA-AM. In contrast, it was virtually unaffected by pre-incubation with the inhibitor of Ca2+-independent PLA2, BEL. The Ca2+ ionophore A23187 yielded similar effects on [Ca2+]i and lysosomes. Exposure to estradiol also resulted in cPLA2 translocation from cytosol to membranes, lysosome enlargement, and increased protein degradation. These results suggest that the destabilization of lysosomal membranes following cell exposure to estradiol occurs mainly through a Ca2+-dependent mechanism involving activation of Ca2+-dependent PLA2. This mechanism promotes lysosome fusion and catabolic activities, and may mediate short-term estradiol effects.




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