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Effects of inflammatory cytokines IL‐1β, IL‐6, and TNFα on the intracellular localization of retinoid receptors in Schwann cells
Author(s) -
Mey Jörg,
Schrage Kirsten,
Wessels Inga,
VollprachtCrijns Ilona
Publication year - 2006
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.20444
Subject(s) - proinflammatory cytokine , retinoid , retinoid x receptor , biology , retinoic acid , receptor , schwann cell , microbiology and biotechnology , intracellular , tumor necrosis factor alpha , endocrinology , nuclear receptor , medicine , immunology , inflammation , biochemistry , transcription factor , gene
It was investigated whether retinoic acid (RA) and the proinflammatory cytokines IL‐1β, IL‐6, and TNFα influence the intracellular distribution of retinoic acid receptors (RAR) and retinoid X receptors (RXR) in Schwann cells. This question arose because nuclear translocation of RARα, RXRα, and RXRβ was observed after nerve injury, and because mutual interactions exist between the signal transduction pathways of RA and proinflammatory cytokines. Schwann cell primary cultures from the rat sciatic nerve were incubated with IL‐1β, IL‐6, and TNFα, with all‐ trans RA and with a combination of IL‐1β and RA. After incubation periods ranging from 5 min to 5 h, the intracellular distributions of RARα, RARβ, RXRα, and RXRβ were analyzed. All three cytokines caused a shift of RARα from the cytosolic compartments into the cell nuclei. This was also observed with RA, and combining RA with IL‐1β produced an additive effect. IL‐1β and IL‐6 also affected the distribution of RARβ, although immunoreactivity of this receptor always remained stronger in the cytosol. No effect of the cytokines on RXRα or RXRβ was observed, whereas RA treatment caused a stronger nuclear signal of both receptors. Effects on the subcellular localization of retinoid receptors may provide a link in a feedback loop between RA/RAR and cytokines. © 2006 Wiley‐Liss, Inc.