Cell attachment to extracellular matrices is modulated by pulsed radiation at 820 nm and chemicals that modify the activity of enzymes in the plasma membrane.
OBJECTIVE
Adhesive interactions between cells and extracellular matrices play a regulative role in wound repair processes. The objective of this investigation is to study action mechanisms of pulsed radiation at 820 nm on cellular adhesion in vitro. Light emitting diodes (LED) at 820 nm are widely used for treatment of wounds of various etiology.


METHODS
The LED (820 +/- 10 nm, 10 Hz, 16-120 J/m(2)) is used for the irradiation of HeLa cell suspension. In parallel experiments, amiloride (5 x 10(-4) M), ouabain (7 x 10(-5) M, 7 x 10(-4) M), quinacrine (6 x 10(-4) M), arachidonic acid (1 x 10(-5) M), glucose (2 x 10(-4) M), and ATP (5 x 10(-5) M) are added to the cell suspension before or after the irradiation procedure. The cell-glass adhesion is studied using the adhesion assay technique described in Lasers Surg Med 1996; 18:171.


RESULTS
Cell-glass adhesion increases in a dose-dependent manner following the irradiation. Preirradiation eliminates the inhibition of cell attachment caused by ouabain, arachidonic acid, and ATP. The inhibitive effect of quinacrine on the cell attachment is eliminated by the irradiation performed after the treatment with the chemical. Irradiation and amiloride have a synergetic stimulative effect on the cell attachment. The threshold dose for the cell attachment stimulation by the irradiation is decreased by the treatment of the cell suspension with amiloride or ouabain.


CONCLUSIONS
The results obtained indicate that pulsed IR radiation at 820 nm increases the cell-matrix attachment. It is the modulation of the monovalent ion fluxes through the plasma membrane and not the release of arachidonic acid that is involved in the cellular signaling pathways activated by irradiation at 820 nm. Preirradiation has a protective effect against the inhibitive action of ouabain, arachidonic acid, ATP, and quinacrine on cell attachment process. It is supposed that irradiation activates those signaling pathways in cells which attenuate the inhibitive action of these chemicals.
Karu
T I
TI
Institute of Laser and Informatic Technologies, Russian Academy of Sciences, 142190 Troitsk, Moscow, Russia. karu@isan.troitsk.ru
Pyatibrat
L V
LV
Kalendo
G S
GS
D000255:Adenosine Triphosphate / Q000378:metabolism / Q000528:radiation effects; D000584:Amiloride / Q000378:metabolism / Q000528:radiation effects; D000704:Analysis of Variance; D016718:Arachidonic Acid / Q000378:metabolism / Q000528:radiation effects; D002448:Cell Adhesion / Q000502:physiology / Q000528:radiation effects; D002462:Cell Membrane / Q000201:enzymology / Q000378:metabolism* / Q000528:radiation effects*; D004121:Dimethyl Sulfoxide / Q000378:metabolism / Q000528:radiation effects; D020536:Enzyme Activators / Q000378:metabolism* / Q000528:radiation effects*; D005109:Extracellular Matrix / Q000201:enzymology / Q000378:metabolism* / Q000528:radiation effects*; D005947:Glucose / Q000378:metabolism / Q000528:radiation effects; D006367:HeLa Cells; D006801:Humans; D066298:In Vitro Techniques; D010042:Ouabain / Q000378:metabolism / Q000528:radiation effects; D011796:Quinacrine / Q000378:metabolism / Q000528:radiation effects
D020536:Enzyme Activators; D016718:Arachidonic Acid; D010042:Ouabain; D000584:Amiloride; D000255:Adenosine Triphosphate; D011796:Quinacrine; D005947:Glucose; D004121:Dimethyl Sulfoxide