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Renal Section, Department of Medicine, Evans Department of Clinical Research, Boston University School of Medicine, Boston, Massachusetts 02118
Adhesion of epithelial cells to matrix is known to
inhibit apoptosis. However, the role of cell-cell adhesion in mediating cell survival remains uncertain. Primary cultures of mouse proximal tubular (MPT) cells were used to examine the role of cell-cell adhesion
in promoting survival. When MPT cells were deprived of both cell-matrix
and cell-cell adhesion, they died by apoptosis. However, when incubated
in agarose-coated culture dishes (to prevent cell-matrix adhesion) and
at high cell density (to allow cell-cell interactions), MPT cells
adhered to one another and remained viable. Expression of E-cadherin
among suspended, aggregating cells increased with time. A His-Ala-Val
(HAV)-containing peptide that inhibits homophilic E-cadherin binding
prevented cell-cell aggregation and promoted apoptosis of MPT cells in
suspension. By contrast, inhibition of potential
1-integrin-mediated interactions between cells in
suspension did not prevent either aggregation or survival of suspended
cells. Aggregation of cells in suspension activated phosphatidylinositol 3-kinase (PI3K), an event that was markedly reduced by the presence of the HAV peptide. LY-294002, an inhibitor of
PI3K, also inhibited survival of suspended cells. In summary, we
provide novel evidence that MPT cells, when deprived of normal cell-matrix interactions, can adhere to one another in a
cadherin-dependent fashion and remain viable. Survival of aggregated
cells depends on activation of PI3K.
anoikis; survival; viability; phosphatidylinositol 3-kinase
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