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Two degradation pathways of endoplasmic reticulum in fish hepatocytes
Author(s) -
Veranič Peter,
Pipan Nada
Publication year - 1995
Publication title -
biology of the cell
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.543
H-Index - 85
eISSN - 1768-322X
pISSN - 0248-4900
DOI - 10.1016/0248-4900(96)89933-3
Subject(s) - endoplasmic reticulum , endomembrane system , biology , autophagy , vacuole , stimulation , microbiology and biotechnology , cytosol , golgi apparatus , cytoplasm , biochemistry , endocrinology , enzyme , apoptosis
Summary— Zebrafish hepatocytes respond to stimulation with estradiol 17β (E2) with an extreme enlargement of the endomembrane system, especially the endoplasmic reticulum (ER), and when stimulation is stopped with a rapid degradation of enlarged endomembranes. Two pathways for degradation of ER were studied: a) the autophagy which was evaluated by stereological measurement; and b) the activity of cytosolic phospholipase B (PL‐B) measured by a titration method. After a 30‐day treatment with E2 a six‐fold increase of the surface density of ER was accompanied by an increase of both autophagy and PL‐B activity. 2 days after stopping the stimulation with E2 the ER vesiculated and its surface density decreased to the half value. Interestingly, at the same time autophagic vacuoles (AV) almost disappeared from hepatocytes, while the activity of PL‐B reached its maximum at which it persisted for a further 4 days. After 4–6 days without E2 the cistern of ER became flattened again and new AVs reappeared. The data suggest that the regulation mechanisms of endomembrane degradation by PL‐B and autophagy do not depend on each other and also that the appearance of AV is strongly related to the shape of ER.