Steady-state mRNA levels of interleukin-1, integrins, cJun, and cFos in hairless mouse skin during short-term chronic UV exposure and the effect of topical tretinoin
Lh. Kligman et al., Steady-state mRNA levels of interleukin-1, integrins, cJun, and cFos in hairless mouse skin during short-term chronic UV exposure and the effect of topical tretinoin, PHOTODERM P, 15(5), 1999, pp. 198-204
We have proposed that UV activation of cytokine and integrin signaling path
ways may initiate the photoaging process and that one of the effects of tre
tinoin treatment may be to alter the cytokine and integrin patterns. In pre
vious results, steady-state mRNA levels of interleukin-1 alpha, tumor necro
sis factor ct, transforming growth factor beta, collagenase, stromelysin, c
ollagen, and integrins (alpha(1) and alpha(2)) were increased in the skin o
f hairless mice that were either UV treated or concurrently treated with UV
followed by topical tretinoin for 5 weeks. The aim of this study was to fo
cus on the expression of alpha(1), alpha(2) and alpha(5), integrins, IL-1 a
lpha, IL-1 beta, cJun, and cFos at an earlier time paint (3 weeks). Animals
were UV irradiated thrice weekly For 3 weeks and were treated topically wi
th. either 0.05% tretinoin err the vehicle immediately after each exposure.
Total RNA was prepared and used in RT-PCR with radiolabeled dCTP and speci
fic primers. UV slightly increased steady-state mRNA levels for alpha(1), a
lpha(2) and alpha(5) integrins whereas UV+tretinoin increased their express
ion (3-, 2- and 7-fold respectively). Steady-state mRNA levels for IL-1 alp
ha, IL-1 beta and cJun were increased with UV (3-, 12- and 6-fold respectiv
ely) and with UV+tretinoin (6-, 7- and 9-fold respectively). In contrast, c
Fos expression was unchanged. In situ staining for IL-1 alpha. mRNA was sli
ghtly more abundant in mice treated for 3 weeks with UV and UV+tretinoin th
an in controls whereas 5 weeks of UV+tretinoin treatment gave strongly posi
tive staining. Results are consistent with cytokines and integrins mediatin
g the effects of UV on the skin, with modulation of these effects by tretin
oin.