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PMID: 11285293 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. Review

The de-adhesive activity of matricellular proteins: is intermediate cell adhesion an adaptive state?

The Journal of clinical investigation ·Vol. 107 ·No. 7 ·2001-04-00 ·Pages 785-90

Murphy-Ullrich JE

Abstract

The process of cellular de-adhesion is potentially important for the ability of a cell to participate in morphogenesis and to respond to injurious stimuli. Cellular de-adhesion is induced by the highly regulated matricellular proteins TSP1 and 2, tenascin-C, and SPARC. These proteins induce a rapid transition to an intermediate state of adhesiveness characterized by loss of actin-containing stress fibers and restructuring of the focal adhesion plaque that includes loss of vinculin and alpha-actinin, but not of talin or integrin. This process involves intracellular signaling mediators, which are engaged in response to matrix protein-receptor interactions. Each of these proteins employs different receptors and signaling pathways to achieve this common morphologic endpoint. What is the function of this intermediate adhesive state and what is the physiologic significance of this action of the matricellular proteins? Given that matricellular proteins are expressed in response to injury and during development, one can speculate that the intermediate adhesive state is an adaptive condition that facilitates expression of specific genes that are involved in repair and adaptation. Since cell shape is maintained in weakly adherent cells, this state might induce survival signals to prevent apoptosis due to loss of strong cell adhesion, but yet allow for cell locomotion. The three matricellular proteins considered here might each preferentially facilitate one or more aspects of this adaptive response rather than all of these equally. Currently, we have only preliminary data to support the specific ideas proposed in this article. It will be interesting in the next several years to continue to elucidate the biological roles of the intermediate adhesive state induced by these matricellular proteins. and focal adhesions in a cell that nevertheless maintains a spread, extended morphology and integrin clustering. TSP1, tenascin-C, and SPARC induce the intermediate adhesive state, as shown by the red arrows. The significance of each adhesive state for cell behavior is indicated beneath the cells. The weak adhesive state would be consistent with cells undergoing apoptosis during remodeling or those undergoing cytokinesis. The strong adhesive state is characteristic of a differentiated, quiescent cell, whereas cells in the intermediate adhesive state would include those involved in responding to injury during wound healing or in tissue remodeling during morphogenesis.

MeSH Terms
Adaptation, Physiological Animals Annexin A2/metabolism Binding Sites Calcium-Binding Proteins/metabolism Calreticulin Cell Adhesion/physiology Extracellular Matrix Proteins/metabolism Glycoproteins/metabolism Humans Osteonectin/metabolism Ribonucleoproteins/metabolism Signal Transduction/physiology Tenascin/metabolism Thrombospondin 1/metabolism Thrombospondins/metabolism
Chemicals
Annexin A2 Calcium-Binding Proteins Calreticulin Extracellular Matrix Proteins Glycoproteins Osteonectin Ribonucleoproteins Tenascin Thrombospondin 1 Thrombospondins thrombospondin 2
Authors & Affiliations
1 authors, click to expand affiliations / ORCID
Murphy-Ullrich J E
Department of Pathology, University of Alabama at Birmingham, G038 Volker Hall, 1670 University Boulevard, Birmingham, Alabama 35294-0019, USA. murphy@path.uab.edu
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Article Info
Journal
The Journal of clinical investigation
Abbr.
J Clin Invest
ISSN
0021-9738
Published
2001-04-00
Pages
785-90
Language
English
Region
United States
NLM ID
7802877
PMCID
PMC199582
Subset
IM
Grants
NHLBI NIH HHS · HL-44575 · United States
Corrections
CommentIn
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