The reduced susceptibility of mouse keratinocytes to retinoic acid may be involved in the keratinization of oral and esophageal mucosal epithelium
Shoji Miyazono, Takahito Otani, Kayoko Ogata, Norio Kitagawa, Hiroshi Iida, Yuko Inai, Takashi Matsuura, Tetsuichiro Inai
農業生物科学
Keratinocytes take up serum-derived retinol (vitamin A) and metabolize it to all-trans-retinoic acid (atRA), which binds to the nuclear retinoic acid receptor (RAR). We previously reported that serum-affected keratinocyte differentiation and function; namely, it inhibited keratinization, decreased loricrin (LOR) and claudin (CLDN) 1 expression, increased keratin (K) 4 and CLDN4 levels, and reduced paracellular permeability in three-dimensional (3D) cultures of mouse keratinocytes (COCA). Contrarily, RAR inhibition reversed these changes. Here, we aimed to examine whether atRA exerted the same effects as serum, and whether it was involved in the differential oral mucosa keratinization among animal species. Porcine oral mucosal keratinocytes, which form non-keratinized epithelium in vivo, established keratinized epithelium in 3D cultures. Both mouse and porcine sera induced non-keratinized epithelium at 0.1% in COCA 3D cultures. Although atRA caused the same changes as serum, its effective concentration differed. atRA inhibited keratinization at 0.1 nM and 1 nM in porcine or human keratinocytes and COCA, respectively. Furthermore, atRA upregulated CLDN7 in the cytoplasm but not in cell–cell contacts. These atRA-induced changes were reverted by RAR inhibition. The results indicate that serum-induced changes are probably due to the effect of serum-derived atRA, and that mouse keratinocytes require higher atRA concentrations to suppress keratinization than porcine and human keratinocytes. We propose that the lower susceptibility of mouse keratinocytes to atRA, rather than a lower retinol concentration, is a possible reason for the keratinization of mouse oral mucosal epithelium.
Histochemistry and Cell Biology
医療検査技術
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Tretinoin Medicine & Life Sciences 100%
Keratinocytes Medicine & Life Sciences 94%
Epithelium Medicine & Life Sciences 74%
Retinoic Acid Receptors Medicine & Life Sciences 42%
Serum Medicine & Life Sciences 34%
Vitamin A Medicine & Life Sciences 34%
loricrin Medicine & Life Sciences 17%
Miyazono, S., Otani, T., Ogata, K., Kitagawa, N., Iida, H., Inai, Y., Matsuura, T., & Inai, T. (2020). The reduced susceptibility of mouse keratinocytes to retinoic acid may be involved in the keratinization of oral and esophageal mucosal epithelium. Histochemistry and Cell Biology, 153(4), 225-237. https://doi.org/10.1007/s00418-020-01845-1
The reduced susceptibility of mouse keratinocytes to retinoic acid may be involved in the keratinization of oral and esophageal mucosal epithelium. / Miyazono, Shoji; Otani, Takahito; Ogata, Kayoko; Kitagawa, Norio; Iida, Hiroshi; Inai, Yuko; Matsuura, Takashi; Inai, Tetsuichiro.
In: Histochemistry and Cell Biology, Vol. 153, No. 4, 01.04.2020, p. 225-237.
Miyazono, S, Otani, T, Ogata, K, Kitagawa, N, Iida, H, Inai, Y, Matsuura, T & Inai, T 2020, 'The reduced susceptibility of mouse keratinocytes to retinoic acid may be involved in the keratinization of oral and esophageal mucosal epithelium', Histochemistry and Cell Biology, vol. 153, no. 4, pp. 225-237. https://doi.org/10.1007/s00418-020-01845-1
Miyazono S, Otani T, Ogata K, Kitagawa N, Iida H, Inai Y et al. The reduced susceptibility of mouse keratinocytes to retinoic acid may be involved in the keratinization of oral and esophageal mucosal epithelium. Histochemistry and Cell Biology. 2020 4 1;153(4):225-237. https://doi.org/10.1007/s00418-020-01845-1
Miyazono, Shoji ; Otani, Takahito ; Ogata, Kayoko ; Kitagawa, Norio ; Iida, Hiroshi ; Inai, Yuko ; Matsuura, Takashi ; Inai, Tetsuichiro. / The reduced susceptibility of mouse keratinocytes to retinoic acid may be involved in the keratinization of oral and esophageal mucosal epithelium. In: Histochemistry and Cell Biology. 2020 ; Vol. 153, No. 4. pp. 225-237.
@article{28f8d20dae6047419df5c08e03d834d5,
title = "The reduced susceptibility of mouse keratinocytes to retinoic acid may be involved in the keratinization of oral and esophageal mucosal epithelium",
abstract = "Keratinocytes take up serum-derived retinol (vitamin A) and metabolize it to all-trans-retinoic acid (atRA), which binds to the nuclear retinoic acid receptor (RAR). We previously reported that serum-affected keratinocyte differentiation and function; namely, it inhibited keratinization, decreased loricrin (LOR) and claudin (CLDN) 1 expression, increased keratin (K) 4 and CLDN4 levels, and reduced paracellular permeability in three-dimensional (3D) cultures of mouse keratinocytes (COCA). Contrarily, RAR inhibition reversed these changes. Here, we aimed to examine whether atRA exerted the same effects as serum, and whether it was involved in the differential oral mucosa keratinization among animal species. Porcine oral mucosal keratinocytes, which form non-keratinized epithelium in vivo, established keratinized epithelium in 3D cultures. Both mouse and porcine sera induced non-keratinized epithelium at 0.1% in COCA 3D cultures. Although atRA caused the same changes as serum, its effective concentration differed. atRA inhibited keratinization at 0.1 nM and 1 nM in porcine or human keratinocytes and COCA, respectively. Furthermore, atRA upregulated CLDN7 in the cytoplasm but not in cell–cell contacts. These atRA-induced changes were reverted by RAR inhibition. The results indicate that serum-induced changes are probably due to the effect of serum-derived atRA, and that mouse keratinocytes require higher atRA concentrations to suppress keratinization than porcine and human keratinocytes. We propose that the lower susceptibility of mouse keratinocytes to atRA, rather than a lower retinol concentration, is a possible reason for the keratinization of mouse oral mucosal epithelium.",
author = "Shoji Miyazono and Takahito Otani and Kayoko Ogata and Norio Kitagawa and Hiroshi Iida and Yuko Inai and Takashi Matsuura and Tetsuichiro Inai",
note = "Funding Information: This study was supported in part by a Grant-in-Aid for Scientific Research (C) (No. 26460285) from the Ministry of Education, Culture, Sports, Science, and Technology in Japan. Publisher Copyright: {\textcopyright} 2020, Springer-Verlag GmbH Germany, part of Springer Nature.",
doi = "10.1007/s00418-020-01845-1",
journal = "Histochemistry and Cell Biology",
T1 - The reduced susceptibility of mouse keratinocytes to retinoic acid may be involved in the keratinization of oral and esophageal mucosal epithelium
AU - Miyazono, Shoji
AU - Otani, Takahito
AU - Ogata, Kayoko
AU - Kitagawa, Norio
AU - Iida, Hiroshi
AU - Inai, Yuko
AU - Matsuura, Takashi
AU - Inai, Tetsuichiro
N1 - Funding Information: This study was supported in part by a Grant-in-Aid for Scientific Research (C) (No. 26460285) from the Ministry of Education, Culture, Sports, Science, and Technology in Japan. Publisher Copyright: © 2020, Springer-Verlag GmbH Germany, part of Springer Nature.
N2 - Keratinocytes take up serum-derived retinol (vitamin A) and metabolize it to all-trans-retinoic acid (atRA), which binds to the nuclear retinoic acid receptor (RAR). We previously reported that serum-affected keratinocyte differentiation and function; namely, it inhibited keratinization, decreased loricrin (LOR) and claudin (CLDN) 1 expression, increased keratin (K) 4 and CLDN4 levels, and reduced paracellular permeability in three-dimensional (3D) cultures of mouse keratinocytes (COCA). Contrarily, RAR inhibition reversed these changes. Here, we aimed to examine whether atRA exerted the same effects as serum, and whether it was involved in the differential oral mucosa keratinization among animal species. Porcine oral mucosal keratinocytes, which form non-keratinized epithelium in vivo, established keratinized epithelium in 3D cultures. Both mouse and porcine sera induced non-keratinized epithelium at 0.1% in COCA 3D cultures. Although atRA caused the same changes as serum, its effective concentration differed. atRA inhibited keratinization at 0.1 nM and 1 nM in porcine or human keratinocytes and COCA, respectively. Furthermore, atRA upregulated CLDN7 in the cytoplasm but not in cell–cell contacts. These atRA-induced changes were reverted by RAR inhibition. The results indicate that serum-induced changes are probably due to the effect of serum-derived atRA, and that mouse keratinocytes require higher atRA concentrations to suppress keratinization than porcine and human keratinocytes. We propose that the lower susceptibility of mouse keratinocytes to atRA, rather than a lower retinol concentration, is a possible reason for the keratinization of mouse oral mucosal epithelium.
AB - Keratinocytes take up serum-derived retinol (vitamin A) and metabolize it to all-trans-retinoic acid (atRA), which binds to the nuclear retinoic acid receptor (RAR). We previously reported that serum-affected keratinocyte differentiation and function; namely, it inhibited keratinization, decreased loricrin (LOR) and claudin (CLDN) 1 expression, increased keratin (K) 4 and CLDN4 levels, and reduced paracellular permeability in three-dimensional (3D) cultures of mouse keratinocytes (COCA). Contrarily, RAR inhibition reversed these changes. Here, we aimed to examine whether atRA exerted the same effects as serum, and whether it was involved in the differential oral mucosa keratinization among animal species. Porcine oral mucosal keratinocytes, which form non-keratinized epithelium in vivo, established keratinized epithelium in 3D cultures. Both mouse and porcine sera induced non-keratinized epithelium at 0.1% in COCA 3D cultures. Although atRA caused the same changes as serum, its effective concentration differed. atRA inhibited keratinization at 0.1 nM and 1 nM in porcine or human keratinocytes and COCA, respectively. Furthermore, atRA upregulated CLDN7 in the cytoplasm but not in cell–cell contacts. These atRA-induced changes were reverted by RAR inhibition. The results indicate that serum-induced changes are probably due to the effect of serum-derived atRA, and that mouse keratinocytes require higher atRA concentrations to suppress keratinization than porcine and human keratinocytes. We propose that the lower susceptibility of mouse keratinocytes to atRA, rather than a lower retinol concentration, is a possible reason for the keratinization of mouse oral mucosal epithelium.
U2 - 10.1007/s00418-020-01845-1
DO - 10.1007/s00418-020-01845-1
JO - Histochemistry and Cell Biology
JF - Histochemistry and Cell Biology