The concept of cellular “fight-or-flight” reaction to stress

As animals respond to environmental stress with a set of default reactions described as the “fight-or-flight” response, so do epithelial and endothelial cells when they are confronting stressors in their microenvironment. This review will summarize a growing body of data suggesting the existence of a set of stereotypical cellular reactions to stress, provide some examples of diseases that are characterized by excessive flight reactions, describe the cellular mechanisms whereby the fight-or-flight reaction is accomplished, as well as cellular mechanisms triggering either fight or flight. It is proposed that cell-matrix adhesion is a sensitive indicator of the severity of stress. This indicator is interfaced with several default programs for cellular survival or death, thus dictating the fate of the cell. Some diagnostic and therapeutic applications of the concept, presently used and potentially useful, are outlined. The essential feature of this concept is its ability to categorize cellular events in terms of either type of default reaction, predict the details of each, and potentially exploit them clinically.

Download Full-text

Mechanisms regulating endothelial cell barrier function

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.2000.279.3.l419 ◽

2000 ◽

Vol 279 (3) ◽

pp. L419-L422 ◽

Cited By ~ 166

Author(s):

Troy Stevens ◽

Joe G. N. Garcia ◽

D. Michael Shasby ◽

Jahar Bhattacharya ◽

Asrar B. Malik

Keyword(s):

Endothelial Cell ◽

Barrier Function ◽

Significant Progress ◽

Physical Barrier ◽

Cellular Mechanisms ◽

Macromolecular Transport ◽

Cell Matrix ◽

Cell Matrix Adhesion ◽

Transport Of Macromolecules ◽

Made In

Endothelium forms a physical barrier that separates blood from tissue. Communication between blood and tissue occurs through the delivery of molecules and circulating substances across the endothelial barrier by directed transport either through or between cells. Inflammation promotes macromolecular transport by decreasing cell-cell and cell-matrix adhesion and increasing centripetally directed tension, resulting in the formation of intercellular gaps. Inflammation may also increase the selected transport of macromolecules through cells. Significant progress has been made in understanding the molecular and cellular mechanisms that account for constitutive endothelial cell barrier function and also the mechanisms activated during inflammation that reduce barrier function. Current concepts of mechanisms regulating endothelial cell barrier function were presented in a symposium at the 2000 Experimental Biology Conference and are reviewed here.

Download Full-text

Faculty Opinions recommendation of Cell-matrix adhesion controls Golgi organization and function through Arf1 activation in anchorage-dependent cells.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.733708071.793549021 ◽

2018 ◽

Author(s):

Martin A Schwartz

Keyword(s):

Matrix Adhesion ◽

Cell Matrix ◽

And Function ◽

Golgi Organization ◽

Cell Matrix Adhesion

Download Full-text

Interaction between Galectin-3 and Integrins Mediates Cell-Matrix Adhesion in Endothelial Cells and Mesenchymal Stem Cells

International Journal of Molecular Sciences ◽

10.3390/ijms22105144 ◽

2021 ◽

Vol 22 (10) ◽

pp. 5144

Author(s):

Antonín Sedlář ◽

Martina Trávníčková ◽

Pavla Bojarová ◽

Miluše Vlachová ◽

Kristýna Slámová ◽

...

Keyword(s):

Stem Cells ◽

Endothelial Cells ◽

Cell Adhesion ◽

Vascular Tissue ◽

Cell Functions ◽

Matrix Adhesion ◽

Cell Matrix ◽

Selective Ligand ◽

Galectin 3 ◽

Cell Matrix Adhesion

Galectin-3 (Gal-3) is a β-galactoside-binding protein that influences various cell functions, including cell adhesion. We focused on the role of Gal-3 as an extracellular ligand mediating cell-matrix adhesion. We used human adipose tissue-derived stem cells and human umbilical vein endothelial cells that are promising for vascular tissue engineering. We found that these cells naturally contained Gal-3 on their surface and inside the cells. Moreover, they were able to associate with exogenous Gal-3 added to the culture medium. This association was reduced with a β-galactoside LacdiNAc (GalNAcβ1,4GlcNAc), a selective ligand of Gal-3, which binds to the carbohydrate recognition domain (CRD) in the Gal-3 molecule. This ligand was also able to detach Gal-3 newly associated with cells but not Gal-3 naturally present on cells. In addition, Gal-3 preadsorbed on plastic surfaces acted as an adhesion ligand for both cell types, and the cell adhesion was resistant to blocking with LacdiNAc. This result suggests that the adhesion was mediated by a binding site different from the CRD. The blocking of integrin adhesion receptors on cells with specific antibodies revealed that the cell adhesion to the preadsorbed Gal-3 was mediated, at least partially, by β1 and αV integrins—namely α5β1, αVβ3, and αVβ1 integrins.

Download Full-text

Cell–matrix adhesion

Journal of Cellular Physiology ◽

10.1002/jcp.21237 ◽

2007 ◽

Vol 213 (3) ◽

pp. 565-573 ◽

Cited By ~ 576

Author(s):

Allison L. Berrier ◽

Kenneth M. Yamada

Keyword(s):

Matrix Adhesion ◽

Cell Matrix ◽

Cell Matrix Adhesion

Download Full-text

Adhesive multiplicity in the interaction of embryonic fibroblasts and myoblasts with extracellular matrices.

The Journal of Cell Biology ◽

10.1083/jcb.99.4.1398 ◽

1984 ◽

Vol 99 (4) ◽

pp. 1398-1404 ◽

Cited By ~ 44

Author(s):

C Decker ◽

R Greggs ◽

K Duggan ◽

J Stubbs ◽

A Horwitz

Keyword(s):

Skeletal Muscle ◽

Cardiac Muscle ◽

Cardiac Fibroblasts ◽

Cell Types ◽

Extracellular Matrices ◽

Common Denominator ◽

Cell Matrix ◽

Skeletal Myoblasts ◽

A Cell ◽

Cell Matrix Adhesion

Neff et al. (1982, J. Cell Biol., 95:654-666) have described a monoclonal antibody, CSAT, directed against a cell surface antigen that participates in the adhesion of skeletal muscle to extracellular matrices. We used the same antibody to compare and parse the determinants of adhesion and morphology on myogenic and fibrogenic cells. We report here that the antigen is present on skeletal and cardiac muscle and on tendon, skeletal, dermal, and cardiac fibroblasts; however, its contribution to their morphology and adhesion is different. The antibody produces large alterations in the morphology and adhesion of skeletal myoblasts and tendon fibroblasts; in contrast, its effects on the cardiac fibroblasts are not readily detected. The effects of CSAT on the other cell types, i.e., dermal and skeletal fibroblasts, cardiac muscle, 5-bromodeoxyuridine-treated skeletal muscle, lie between these extremes. The effects of CSAT on the skeletal myoblasts depends on the calcium concentration in the growth medium and on the culture age. We interpret these differential responses to CSAT as revealing differences in the adhesion of the various cells to extracellular matrices. This interpretation is supported by parallel studies using quantitative assays of cell-matrix adhesion. The likely origin of these adhesive differences is the progressive display of different kinds of adhesion-related molecules and their organizational complexes on increasingly adhesive cells. The antigen to which CSAT is directed is present on all of the above cells and thus appears to be a lowest common denominator of their adhesion to extracellular matrices.

Download Full-text