Abstract:
:Previous studies have shown that PC12 cells overexpressing beta/A4 amyloid peptide display altered morphology characterized by pronounced membrane ruffling and extensive intercellular appositions. Having observed other cell types in which these features accompany increased connexin43 (Cx43) production and gap junctional communication, we examined Cx43 in normal and beta/A4-transfected PC12 cells. Studies of two beta/A4-transfected PC12 clones revealed an induction of Cx43 expression by Western blotting, intracellular and plasma membrane-associated Cx43 in some cells of cultures processed by immunofluorescence, dye-transfer between some cells microinjected with Lucifer Yellow, and gap junctions between cells examined by EM. Normal and vector-transfected PC12 cells exhibited none of these properties. Increased immunofluorescence in some clusters of beta/A4-transfected cells was also observed with a monoclonal antibody against connexin32. The results suggest that beta/A4 amyloid peptide may cause aberrant intercellular communication and gap junction formation through induction or increased expression of connexins in cells that are not normally coupled or only poorly coupled by gap junctions.
journal_name
J Neurosci Resjournal_title
Journal of neuroscience researchauthors
Nagy JI,Hossain MZ,Hertzberg EL,Marotta CAdoi
10.1002/(SICI)1097-4547(19960415)44:2<124::AID-JNRsubject
Has Abstractpub_date
1996-04-15 00:00:00pages
124-32issue
2eissn
0360-4012issn
1097-4547pii
10.1002/(SICI)1097-4547(19960415)44:2<124::AID-JNRjournal_volume
44pub_type
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