The effects of the broadband UVA radiation on myeloid leukemia cells: the possible role of protein kinase C in mediation of UVA-induced effects

TY - JOUR

T1 - The effects of the broadband UVA radiation on myeloid leukemia cells

T2 - the possible role of protein kinase C in mediation of UVA-induced effects

AU - Leszczynski, Darius

AU - Fagerholm, Susanna

AU - Leszczynski, Kirsti

PY - 1996/12

Y1 - 1996/12

N2 - We examined the effects of broadband UVA radiation (320-400 nm) on a rat myeloid leukemia cell line-chloroma (ChL), A Phillips face tanner model HE 171/A was used as a light source, Chloroma were irradiated through a 5 mm thick glass filter that cut off all of the UVB contamination, The irradiances were measured, from 250 to 400 nm, with a well-characterized and calibrated double-grating spectroradiometer Optronic 742, The overall uncertainty of dose evaluation was estimated to he +/- 15% (2 sigma), The cells were irradiated with UVA doses of 4 and 8 J/cm2 and cultured thereafter for 24 h, After this period of time, a marked decline up to 50% was observed in cell proliferation in UVA-irradiated ChL cultures, The cell proliferation decline was found to be caused by simultaneously occurring G2/M phase cell cycle arrest and apoptosis in part of the UVA-irradiated ChL population, Concomitantly, with the decline in cell proliferation, an increase was observed in the expression of the major histocompatibility (MHC) class I and II antigens, Because protein kinase C (PKC) is known to regulate cell proliferation, apoptosis and expression of MHC antigens, and because UVA was shown to regulate PKC activity/expression, we therefore examined whether UVA irradiation has any effect on the expression of isozymes of PKC. Western blots revealed that ChL express alpha, beta I, delta, epsilon, eta, and zeta/l isozymes of PKC and that expression of all isozymes declined 24 h after UVA irradiation (8 J/cm2), Finally, PKC activation in ChL by exposure to phorbol ester caused cell cycle arrest in G1 phase but did not induce apoptosis, This suggests that the previously shown WA-induced PKC activation in ChL might be responsible for the induction of MHC antigens but the simultaneously observed ChL apoptosis is likely to be mediated by PKC down-regulation, All together, our results suggest that UVA, at irradiance levels that resemble the outdoor exposure, may have profound effects on the immune-related properties of leukocytes, Thus, we speculate that in vivo the immune functions of leukocytes passing through dermal capillaries might be altered by exposure to solar UVA radiation.

AB - We examined the effects of broadband UVA radiation (320-400 nm) on a rat myeloid leukemia cell line-chloroma (ChL), A Phillips face tanner model HE 171/A was used as a light source, Chloroma were irradiated through a 5 mm thick glass filter that cut off all of the UVB contamination, The irradiances were measured, from 250 to 400 nm, with a well-characterized and calibrated double-grating spectroradiometer Optronic 742, The overall uncertainty of dose evaluation was estimated to he +/- 15% (2 sigma), The cells were irradiated with UVA doses of 4 and 8 J/cm2 and cultured thereafter for 24 h, After this period of time, a marked decline up to 50% was observed in cell proliferation in UVA-irradiated ChL cultures, The cell proliferation decline was found to be caused by simultaneously occurring G2/M phase cell cycle arrest and apoptosis in part of the UVA-irradiated ChL population, Concomitantly, with the decline in cell proliferation, an increase was observed in the expression of the major histocompatibility (MHC) class I and II antigens, Because protein kinase C (PKC) is known to regulate cell proliferation, apoptosis and expression of MHC antigens, and because UVA was shown to regulate PKC activity/expression, we therefore examined whether UVA irradiation has any effect on the expression of isozymes of PKC. Western blots revealed that ChL express alpha, beta I, delta, epsilon, eta, and zeta/l isozymes of PKC and that expression of all isozymes declined 24 h after UVA irradiation (8 J/cm2), Finally, PKC activation in ChL by exposure to phorbol ester caused cell cycle arrest in G1 phase but did not induce apoptosis, This suggests that the previously shown WA-induced PKC activation in ChL might be responsible for the induction of MHC antigens but the simultaneously observed ChL apoptosis is likely to be mediated by PKC down-regulation, All together, our results suggest that UVA, at irradiance levels that resemble the outdoor exposure, may have profound effects on the immune-related properties of leukocytes, Thus, we speculate that in vivo the immune functions of leukocytes passing through dermal capillaries might be altered by exposure to solar UVA radiation.

U2 - 10.1111/j.1751-1097.1996.tb01858.x

DO - 10.1111/j.1751-1097.1996.tb01858.x

M3 - Article

SN - 0031-8655

VL - 64

SP - 936

EP - 942

JO - Photochemistry and Photobiology

JF - Photochemistry and Photobiology

IS - 6

ER -