Titre du document / Document title
Adenine nucleotide and protein kinase C regulation of renal tubular epithelial cell wound healing
Auteur(s) / Author(s)
SPONSEL H. T. ;
BRECKON R. ;
ANDERSON R. J. ;
Affiliation(s) du ou des auteurs / Author(s) Affiliation(s)
Denver veterans affairs medical cent., dep. medicine, Denver CO 80220, ETATS-UNIS
Résumé / Abstract
Adenine nucleotide and protein kinase C regulation of renal tubular epithelial cell wound healing. The present studies were done to determine the effect of selected adenine nucleotides on healing of wounds made by mechanically denuding areas in confluent monolayers of renal tubular epithelial cells. We found that hydrolyzable and nonhydrolyzable forms of ATP but not UTP stimulated healing of LLC-PK
1 cell wounds, while both ATP and UTP promoted healing of MDCK cell wounds, suggesting that different subtypes of purinoceptors regulated wound healing in these cells. Stimulation of wound healing by ATP was equivalent in control cells and in cells in which irradiation suppressed proliferation, suggesting a prominent role for cell migration in the healing process. Since ATP receptors are often linked to activation of protein kinase C, the effect of a protein kinase C activator (4β-phorbol 12-myristate 13-acetate, PMA) on wound healing was studied. Long-term (24 hr) exposure to PMA inhibited while short-term (30-120 min) exposure to PMA enhanced cell wound healing. Two chemically and mechanistically dissimilar protein kinase C inhibitors (calphostin C and chelerythrine) inhibited LLC-PK
1 and MDCK cell wound healing, and calphostin C prevented ATP enhancement of LLC-PK, healing. These observations suggest a role for protein kinase C in regulation of basal and adenine nucleotide-stimulated wound healing. Adenosine triphosphate did not affect cell-cell adhesion of either LLC-PK
1 or MDCK cells. Adenine nucleotides and PMA enhanced and calphostin C inhibited short-term adhesion of LLC-PK
1 and MDCK cells to plastic and to other substrates such as fibronectin, laminin and collagen type IV. These results demonstrate that ATP and protein kinase C can stimulate healing of two types of renal tubular epithelial cell wounds. The effects of ATP to promote wound healing appear to occur by purinoceptors which stimulate cell migration, and a protein kinase C mechanism may be involved in this migration.
Revue / Journal Title
Kidney international
ISSN
0085-2538
CODEN KDYIA5
Source / Source
1995, vol. 48, n
o1, pp. 85-92 (42 ref.)
Langue / Language
Anglais
Editeur / Publisher
Nature Publishing Group, Basingstoke, ROYAUME-UNI
(1972)
(Revue)
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Localisation / Location
INIST-CNRS, Cote INIST : 15906, 35400005173969.0110
Nº notice refdoc (ud4) : 3593623
