The effects of the broadband UVA radiation on myeloid leukemia cells

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

Darius Leszczynski, Susanna Fagerholm, Kirsti Leszczynski

    Research output: Contribution to journalArticle

    9 Citations (Scopus)

    Abstract

    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.

    Original languageEnglish
    Pages (from-to)936-942
    Number of pages7
    JournalPhotochemistry and Photobiology
    Volume64
    Issue number6
    DOIs
    Publication statusPublished - Dec 1996

    Cite this

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    title = "The effects of the broadband UVA radiation on myeloid leukemia cells: the possible role of protein kinase C in mediation of UVA-induced effects",
    abstract = "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.",
    author = "Darius Leszczynski and Susanna Fagerholm and Kirsti Leszczynski",
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    The effects of the broadband UVA radiation on myeloid leukemia cells : the possible role of protein kinase C in mediation of UVA-induced effects. / Leszczynski, Darius; Fagerholm, Susanna; Leszczynski, Kirsti.

    In: Photochemistry and Photobiology, Vol. 64, No. 6, 12.1996, p. 936-942.

    Research output: Contribution to journalArticle

    TY - JOUR

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    AU - Fagerholm, Susanna

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    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.

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    M3 - Article

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