Protein kinase C δ and η differently regulate the expression of loricrin and Jun family proteins in human keratinocytes
Barrier function of the epidermis is maintained by precise expression of keratinocyte-specific structural proteins to form the cornified cell envelope (CE). Loricrin, a major component of the CE, is expressed at the late stage of keratinocyte differentiation. In this study, we reveal the isoform-spe...
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| Published in | Biochemical and biophysical research communications Vol. 394; no. 1; pp. 106 - 111 |
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| Main Authors | , , , , , , |
| Format | Journal Article |
| Language | English |
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Elsevier Inc
26.03.2010
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| Abstract | Barrier function of the epidermis is maintained by precise expression of keratinocyte-specific structural proteins to form the cornified cell envelope (CE). Loricrin, a major component of the CE, is expressed at the late stage of keratinocyte differentiation. In this study, we reveal the isoform-specific function of protein kinase C (PKC) in the regulation of loricrin expression. Both PKCδ and PKCη have been recognized as differentiation-promoting isoforms. However, loricrin expression was inversely controlled by PKCδ and PKCη in cultured keratinocytes and 3D skin culture; i.e. loricrin expression was decreased by PKCδ and increased by PKCη. To clarify the mechanisms that PKCδ and PKCη oppositely regulate the loricrin expression, we examined the expression of activator protein-1 (AP-1) family proteins, which modulate the transcription of loricrin and are downstream molecules of PKC. PKCδ decreased c-Jun expression, whereas PKCη increased JunD, which are positive regulators of loricrin transcription. These findings suggest that inverse effects of PKCδ and PKCη on loricrin expression attributes to the expression of c-Jun and JunD. |
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| AbstractList | Barrier function of the epidermis is maintained by precise expression of keratinocyte-specific structural proteins to form the cornified cell envelope (CE). Loricrin, a major component of the CE, is expressed at the late stage of keratinocyte differentiation. In this study, we reveal the isoform-specific function of protein kinase C (PKC) in the regulation of loricrin expression. Both PKCδ and PKCη have been recognized as differentiation-promoting isoforms. However, loricrin expression was inversely controlled by PKCδ and PKCη in cultured keratinocytes and 3D skin culture; i.e. loricrin expression was decreased by PKCδ and increased by PKCη. To clarify the mechanisms that PKCδ and PKCη oppositely regulate the loricrin expression, we examined the expression of activator protein-1 (AP-1) family proteins, which modulate the transcription of loricrin and are downstream molecules of PKC. PKCδ decreased c-Jun expression, whereas PKCη increased JunD, which are positive regulators of loricrin transcription. These findings suggest that inverse effects of PKCδ and PKCη on loricrin expression attributes to the expression of c-Jun and JunD. Barrier function of the epidermis is maintained by precise expression of keratinocyte-specific structural proteins to form the cornified cell envelope (CE). Loricrin, a major component of the CE, is expressed at the late stage of keratinocyte differentiation. In this study, we reveal the isoform-specific function of protein kinase C (PKC) in the regulation of loricrin expression. Both PKCdelta and PKCeta have been recognized as differentiation-promoting isoforms. However, loricrin expression was inversely controlled by PKCdelta and PKCeta in cultured keratinocytes and 3D skin culture; i.e. loricrin expression was decreased by PKCdelta and increased by PKCeta. To clarify the mechanisms that PKCdelta and PKCeta oppositely regulate the loricrin expression, we examined the expression of activator protein-1 (AP-1) family proteins, which modulate the transcription of loricrin and are downstream molecules of PKC. PKCdelta decreased c-Jun expression, whereas PKCeta increased JunD, which are positive regulators of loricrin transcription. These findings suggest that inverse effects of PKCdelta and PKCeta on loricrin expression attributes to the expression of c-Jun and JunD. |
| Author | Honma, Ikuo Kamioka, Nagisa Kuroki, Toshio Iijima, Masafumi Ohba, Motoi Akahane, Tomoko Kohno, Yoko |
| Author_xml | – sequence: 1 givenname: Nagisa surname: Kamioka fullname: Kamioka, Nagisa organization: Institute of Molecular Oncology, Showa University, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan – sequence: 2 givenname: Tomoko surname: Akahane fullname: Akahane, Tomoko organization: Department of Obstetrics and Gynecology, Keio University, 35 Shinanomachi, Shinjuku-ku, Tokyo, Japan – sequence: 3 givenname: Yoko surname: Kohno fullname: Kohno, Yoko organization: Department of Oral Pathology, Showa University School of Dentistry, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan – sequence: 4 givenname: Toshio surname: Kuroki fullname: Kuroki, Toshio organization: Research Center Science Systems, Japan Society for the Promotion of Science, 6 Ichibancho, Chiyoda-ku, Tokyo, Japan – sequence: 5 givenname: Masafumi surname: Iijima fullname: Iijima, Masafumi organization: Department of Dermatology, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan – sequence: 6 givenname: Ikuo surname: Honma fullname: Honma, Ikuo organization: Department of Physiology, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan – sequence: 7 givenname: Motoi surname: Ohba fullname: Ohba, Motoi email: moba@pharm.showa-u.ac.jp organization: Institute of Molecular Oncology, Showa University, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan |
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| CitedBy_id | crossref_primary_10_1038_cddis_2015_21 crossref_primary_10_1074_jbc_M113_543165 crossref_primary_10_1371_journal_pone_0038599 crossref_primary_10_1074_jbc_M110_205245 crossref_primary_10_1016_j_jbc_2024_105692 crossref_primary_10_1371_journal_ppat_1006247 crossref_primary_10_1016_j_virol_2017_12_012 crossref_primary_10_1371_journal_pone_0036941 crossref_primary_10_1128_JVI_00443_13 crossref_primary_10_3390_cancers11020214 |
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| Keywords | Keratinocytes Differentiation Protein kinase C |
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| SubjectTerms | Cells, Cultured Differentiation Gene Expression Regulation Humans Keratinocytes Keratinocytes - metabolism Membrane Proteins - genetics Protein kinase C Protein Kinase C - genetics Protein Kinase C - metabolism Protein Kinase C-delta - genetics Protein Kinase C-delta - metabolism Proto-Oncogene Proteins c-jun - genetics Proto-Oncogene Proteins c-jun - metabolism RNA Interference Transcription Factor AP-1 - genetics Transcription Factor AP-1 - metabolism |
| Title | Protein kinase C δ and η differently regulate the expression of loricrin and Jun family proteins in human keratinocytes |
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