BCL-2, Ca, and Apoptosis in Breast Cancer
Abstract
Apoptosis of non-transformed mammary cells 31 EG4 was associated with an apparent 50% reduction of the ER Ca store, and Ca entry through Ca channels was also reduced (imaging microscopy). Deconvolution microscopy showed that degenerating nuclei in apoptosing cells contained regions of very high Ca, likely due to the accumulation of endoplasmic reticulum within lobed nuclei. Confluent monolayers also absorbed Na through apical ENaC (Na channels) and secreted C1 through apical CFTR (C1 channels); fluid was absorbed or secreted depending on the relative activities of these channels and the properties of tight junctions. Fluid transport could contribute to fluid accumulation in breast cysts. It was expected that dissolution of tight junctions would need to occur in a very coordinated way during apoptosis. Control cells had a predicted array of F-actin, ZO-l and occludin. Mechanical disruption of the monolayer caused cells adjacent to the wounds to lose the organized actin/ZO 1 /occludin-containing junctions in an organized sequence, while junctions were retained between adjacent cells. Following migration of cells to fill the wound, tight junctions rapidly reformed in a stereotypical sequence at points of initial contact between cells from opposite sides of the wound using cytosolic pools of proteins.
Document Details
- Document Type
- Technical Report
- Publication Date
- Aug 01, 2000
- Accession Number
- ADA391146
Entities
People
- Terry Machen
Organizations
- University of California, Berkeley