Mika Murai
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Mika Murai has a total of 7 co-authors. Here are the top co-authors by number of shared publications:
- Akiko Hashimoto-Hachiya
Department of Dermatology, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan
3 shared publications - Gaku Tsuji
Department of Dermatology, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan
3 shared publications - Masutaka Furue
Department of Dermatology, Graduate School of Medical Sciences Kyushu University Fukuoka Japan
3 shared publications - Chikage Mitoma
Department of Dermatology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan
2 shared publications - Kazuhiko Yamamura
Department of Dermatology Graduate School of Medical Sciences, Kyushu University Fukuoka Japan
1 shared publication - Xianghong Yan
Research and Development, Kobe Innovation Center, Procter and Gamble Innovation GK, Kobe 651-0088, Japan
1 shared publication
Latest Publications
- 1 July 2018
- Published by Elsevier in Journal of Dermatological Science
- Vol. 91 (1) , 97-103
Tryptophan photo-product FICZ upregulates AHR/MEK/ERK-mediated MMP1 expression: Implications in anti-fibrotic phototherapy
- 1 July 2018
- Published by Elsevier in Journal of Dermatological Science
- Vol. 91 (1) , 97-103
Tryptophan photo-product FICZ upregulates AHR/MEK/ERK-mediated MMP1 expression: Implications in anti-fibrotic phototherapy
- Open Access
- 4 June 2018
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 19 (6) , 1654
Upregulation of FLG, LOR, and IVL Expression by Rhodiola crenulata Root Extract via Aryl Hydrocarbon Receptor: Differential Involvement of OVOL1
Rhodiola species are antioxidative, salubrious plants that are known to inhibit oxidative stress induced by ultraviolet and γ-radiation in epidermal keratinocytes. As certain phytochemicals activate aryl hydrocarbon receptors (AHR) or OVO-like 1 (OVOL1) to upregulate the expression of epidermal barrier proteins such as filaggrin (FLG), loricrin (LOR), and involucrin (IVL), we investigated such regulation by Rhodiola crenulata root extract (RCE). We demonstrated that RCE induced FLG and LOR upregulation in an AHR-OVOL1-dependent fashion. However, RCE-mediated IVL upregulation was AHR-dependent but OVOL1-independent. Coordinated upregulation of skin barrier proteins by RCE via AHR may be beneficial in the management of barrier-disrupted inflammatory skin diseases such as atopic dermatitis.
- 4 June 2018
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 19 (6) , 1654
Open AccessUpregulation of FLG, LOR, and IVL Expression by Rhodiola crenulata Root Extract via Aryl Hydrocarbon Receptor: Differential Involvement of OVOL1
Rhodiola species are antioxidative, salubrious plants that are known to inhibit oxidative stress induced by ultraviolet and γ-radiation in epidermal keratinocytes. As certain phytochemicals activate aryl hydrocarbon receptors (AHR) or OVO-like 1 (OVOL1) to upregulate the expression of epidermal barrier proteins such as filaggrin (FLG), loricrin (LOR), and involucrin (IVL), we investigated such regulation by Rhodiola crenulata root extract (RCE). We demonstrated that RCE induced FLG and LOR upregulation in an AHR-OVOL1-dependent fashion. However, RCE-mediated IVL upregulation was AHR-dependent but OVOL1-independent. Coordinated upregulation of skin barrier proteins by RCE via AHR may be beneficial in the management of barrier-disrupted inflammatory skin diseases such as atopic dermatitis.
- 1 January 2018
- Published by Elsevier in Journal of Dermatological Science
- Vol. 89 (1) , 19-26
An endogenous tryptophan photo-product, FICZ, is potentially involved in photo-aging by reducing TGF-β-regulated collagen homeostasis
- 1 January 2018
- Published by Elsevier in Journal of Dermatological Science
- Vol. 89 (1) , 19-26
An endogenous tryptophan photo-product, FICZ, is potentially involved in photo-aging by reducing TGF-β-regulated collagen homeostasis