Possible roles of barrier-to-autointegration factor 1 in regulation of keratinocyte differentiation and proliferation

Hiroyuki Takama, Kazumitsu Sugiura, Yasushi Ogawa, Yoshinao Muro, Masashi Akiyama

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Background: Barrier-to-autointegration factor 1 (BANF1) is an essential component of the nuclear lamina. Recent studies have clarified that BANF1 is a causative molecule of Nestor-Guillermo progeria syndrome. Despite recent progress in studies on BANF1, the role of BANF1 in keratinocytes has not been addressed at all. Objective: This study aims to determine the localization of BANF1 in psoriatic epidermal keratinocytes as well as in normal keratinocytes and to clarify its possible function in those keratinocytes. Methods: Immunohistochemistry of BANF1 was performed on 10 cases of psoriasis and 10 healthy control individuals. Expression of molecules associated with inflammation of the skin by HSC-1, a human skin squamous cell carcinoma cell line, stimulated by TPA and treated with siRNA to BANF1 were analyzed with quantitative PCR and Western blot. Results: Strong nuclear-dominant immunostaining of BANF1 was seen in the epidermal keratinocytes of psoriatic lesions, although in the normal epidermis, all the KCs in the upper epidermis showed cytoplasmic-dominant staining of BANF1. By BANF1 knockdown in TPA-stimulated HSC-1 cells, the mRNA levels of S100A9 were significantly elevated compared with those of control HSC-1 cells treated with siRNA to CD4. The protein expression level of S100A9 and phosphorylated c-Jun was elevated by BANF1 knockdown. Conclusion: BANF1 is translocated onto the nuclear envelope in the psoriatic epidermal keratinocytes, suggesting that BANF1 is associated with upregulated proliferation of keratinocytes in psoriatic lesions. Activation of BANF1 possibly suppresses S100A9 expression and inactivates c-Jun, resulting in suppression of cutaneous inflammation.

Original languageEnglish
Pages (from-to)100-106
Number of pages7
JournalJournal of Dermatological Science
Volume71
Issue number2
DOIs
Publication statusPublished - 01-08-2013

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Keratinocytes
Epidermis
Skin
Small Interfering RNA
Progeria
Nuclear Lamina
Inflammation
Molecules
Nuclear Envelope
Psoriasis
Squamous Cell Carcinoma
Western Blotting
Chemical activation
Immunohistochemistry
Cells
Staining and Labeling
Cell Line
Polymerase Chain Reaction
Messenger RNA
Proteins

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Molecular Biology
  • Dermatology

Cite this

Takama, Hiroyuki ; Sugiura, Kazumitsu ; Ogawa, Yasushi ; Muro, Yoshinao ; Akiyama, Masashi. / Possible roles of barrier-to-autointegration factor 1 in regulation of keratinocyte differentiation and proliferation. In: Journal of Dermatological Science. 2013 ; Vol. 71, No. 2. pp. 100-106.
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abstract = "Background: Barrier-to-autointegration factor 1 (BANF1) is an essential component of the nuclear lamina. Recent studies have clarified that BANF1 is a causative molecule of Nestor-Guillermo progeria syndrome. Despite recent progress in studies on BANF1, the role of BANF1 in keratinocytes has not been addressed at all. Objective: This study aims to determine the localization of BANF1 in psoriatic epidermal keratinocytes as well as in normal keratinocytes and to clarify its possible function in those keratinocytes. Methods: Immunohistochemistry of BANF1 was performed on 10 cases of psoriasis and 10 healthy control individuals. Expression of molecules associated with inflammation of the skin by HSC-1, a human skin squamous cell carcinoma cell line, stimulated by TPA and treated with siRNA to BANF1 were analyzed with quantitative PCR and Western blot. Results: Strong nuclear-dominant immunostaining of BANF1 was seen in the epidermal keratinocytes of psoriatic lesions, although in the normal epidermis, all the KCs in the upper epidermis showed cytoplasmic-dominant staining of BANF1. By BANF1 knockdown in TPA-stimulated HSC-1 cells, the mRNA levels of S100A9 were significantly elevated compared with those of control HSC-1 cells treated with siRNA to CD4. The protein expression level of S100A9 and phosphorylated c-Jun was elevated by BANF1 knockdown. Conclusion: BANF1 is translocated onto the nuclear envelope in the psoriatic epidermal keratinocytes, suggesting that BANF1 is associated with upregulated proliferation of keratinocytes in psoriatic lesions. Activation of BANF1 possibly suppresses S100A9 expression and inactivates c-Jun, resulting in suppression of cutaneous inflammation.",
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Possible roles of barrier-to-autointegration factor 1 in regulation of keratinocyte differentiation and proliferation. / Takama, Hiroyuki; Sugiura, Kazumitsu; Ogawa, Yasushi; Muro, Yoshinao; Akiyama, Masashi.

In: Journal of Dermatological Science, Vol. 71, No. 2, 01.08.2013, p. 100-106.

Research output: Contribution to journalArticle

TY - JOUR

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AU - Akiyama, Masashi

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N2 - Background: Barrier-to-autointegration factor 1 (BANF1) is an essential component of the nuclear lamina. Recent studies have clarified that BANF1 is a causative molecule of Nestor-Guillermo progeria syndrome. Despite recent progress in studies on BANF1, the role of BANF1 in keratinocytes has not been addressed at all. Objective: This study aims to determine the localization of BANF1 in psoriatic epidermal keratinocytes as well as in normal keratinocytes and to clarify its possible function in those keratinocytes. Methods: Immunohistochemistry of BANF1 was performed on 10 cases of psoriasis and 10 healthy control individuals. Expression of molecules associated with inflammation of the skin by HSC-1, a human skin squamous cell carcinoma cell line, stimulated by TPA and treated with siRNA to BANF1 were analyzed with quantitative PCR and Western blot. Results: Strong nuclear-dominant immunostaining of BANF1 was seen in the epidermal keratinocytes of psoriatic lesions, although in the normal epidermis, all the KCs in the upper epidermis showed cytoplasmic-dominant staining of BANF1. By BANF1 knockdown in TPA-stimulated HSC-1 cells, the mRNA levels of S100A9 were significantly elevated compared with those of control HSC-1 cells treated with siRNA to CD4. The protein expression level of S100A9 and phosphorylated c-Jun was elevated by BANF1 knockdown. Conclusion: BANF1 is translocated onto the nuclear envelope in the psoriatic epidermal keratinocytes, suggesting that BANF1 is associated with upregulated proliferation of keratinocytes in psoriatic lesions. Activation of BANF1 possibly suppresses S100A9 expression and inactivates c-Jun, resulting in suppression of cutaneous inflammation.

AB - Background: Barrier-to-autointegration factor 1 (BANF1) is an essential component of the nuclear lamina. Recent studies have clarified that BANF1 is a causative molecule of Nestor-Guillermo progeria syndrome. Despite recent progress in studies on BANF1, the role of BANF1 in keratinocytes has not been addressed at all. Objective: This study aims to determine the localization of BANF1 in psoriatic epidermal keratinocytes as well as in normal keratinocytes and to clarify its possible function in those keratinocytes. Methods: Immunohistochemistry of BANF1 was performed on 10 cases of psoriasis and 10 healthy control individuals. Expression of molecules associated with inflammation of the skin by HSC-1, a human skin squamous cell carcinoma cell line, stimulated by TPA and treated with siRNA to BANF1 were analyzed with quantitative PCR and Western blot. Results: Strong nuclear-dominant immunostaining of BANF1 was seen in the epidermal keratinocytes of psoriatic lesions, although in the normal epidermis, all the KCs in the upper epidermis showed cytoplasmic-dominant staining of BANF1. By BANF1 knockdown in TPA-stimulated HSC-1 cells, the mRNA levels of S100A9 were significantly elevated compared with those of control HSC-1 cells treated with siRNA to CD4. The protein expression level of S100A9 and phosphorylated c-Jun was elevated by BANF1 knockdown. Conclusion: BANF1 is translocated onto the nuclear envelope in the psoriatic epidermal keratinocytes, suggesting that BANF1 is associated with upregulated proliferation of keratinocytes in psoriatic lesions. Activation of BANF1 possibly suppresses S100A9 expression and inactivates c-Jun, resulting in suppression of cutaneous inflammation.

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