Decreased expression of suprabasin induces aberrant differentiation and apoptosis of epidermal keratinocytes: Possible role for atopic dermatitis

Aoshima, Masahiro; Phadungsaksawasdi, Pawit; Nakazawa, Shinsuke; Iwasaki, Manami; Sakabe, Jun‐ichi; Umayahara, Takatsune; Yatagai, Tsuyoshi; Ikeya, Shigeki; Shimauchi, Takatoshi; Tokura, Y.

doi:10.1016/j.jdermsci.2019.07.009

Cited by 23 publications

(38 citation statements)

References 23 publications

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“…In our Sbsn -/mice, SBSN deficiency led to the ultrastructural difference in the stratum corneum and keratohyalin granules, and CEs fragility. These ultrastructural features were also observed in our study using Sbsn knockdown human epidermal keratinocytes 17 .…”

Section: Discussionsupporting

confidence: 85%

“…We have demonstrated that the amount of SBSN is decreased in the stratum corneum and the sera of AD patients compared to normal subjects 16,17 . Another group of investigators also reported that SBSN deficiency is one of the factors related to AD pathogenesis 4 .…”

Section: Discussionmentioning

confidence: 84%

“…We also revealed that the expression of SBSN, unlike FLG, is unaffected by IL-4 and IL-13 in the epidermis. In SBSN-deficient 3-dimensional-reconstructed epidermis, there was abnormal epidermal differentiation, including compact stratum corneum and immature keratohyalin granules, independent of other differentiation markers, such as involucrin (IVL), claudin-1, and calpain-1 17 .…”

mentioning

confidence: 99%

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Suprabasin-null mice retain skin barrier function and show high contact hypersensitivity to nickel upon oral nickel loading

Nakazawa

Shimauchi

Funakoshi

et al. 2020

Sci Rep

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Suprabasin (SBSn) is expressed not only in epidermis but also in epithelial cells of the upper digestive tract where metals such as nickel are absorbed. We have recently shown that SBSn level is decreased in the stratum corneum and serum of atopic dermatitis (AD) patients, especially in intrinsic AD, which is characterized by metal allergy. By using SBSn-null (Sbsn-/-) mice, this study was conducted to investigate the outcome of SBSN deficiency in relation to AD. Sbsn-/mice exhibited skin barrier dysfunction on embryonic day 16.5, but after birth, their barrier function was not perturbed despite the presence of ultrastructural changes in stratum corneum and keratohyalin granules. Sbsn-/mice showed a comparable ovalbumin-specific skin immune response to wild type (WT) mice and rather lower contact hypersensitivity (cHS) responses to haptens than did Wt mice. the blood nickel level after oral feeding of nickel was significantly higher in Sbsn-/mice than in Wt mice, and cHS to nickel was elevated in Sbsn-/mice under nickel-loading condition. our study suggests that the completely SBSN deficient mice retain normal barrier function, but harbor abnormal upper digestive tract epithelium that promotes nickel absorption and high cHS to nickel, sharing the features of intrinsic AD.

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Section: Discussionsupporting

confidence: 85%

Section: Discussionmentioning

confidence: 84%

mentioning

confidence: 99%

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Suprabasin-null mice retain skin barrier function and show high contact hypersensitivity to nickel upon oral nickel loading

Nakazawa

Shimauchi

Funakoshi

et al. 2020

Sci Rep

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“…SPBN is expressed in the suprabasal layers of tongue, stomach, and epidermis (92). It is required for keratinocyte differentiation in an in vitro skin model (93) and skin development in murine embryos (94). The speci c activity of CDHR4 is not described in the literature, but family member CDHR2 is expressed in gastrointestinal epithelial cells and is associated with microvillus development (95), while family member CHDR3 is expressed in ciliated respiratory epithelial cells and is associated with ciliary development and intercellular interactions (96).…”

Section: Discussionmentioning

confidence: 99%

RNA sequencing identifies transcriptional changes in the rabbit larynx in response to low humidity challenge

Bailey

Santos

Nascimento

et al. 2020

Preprint

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Background Voice disorders are a worldwide problem impacting human health, particularly for occupational voice users. Avoidance of surface dehydration is commonly prescribed as a protective factor against the development of dysphonia. The available literature inconclusively supports this practice and a biological mechanism for how surface dehydration of the laryngeal tissue affects voice has not been described. In this study, we used an in vivo male New Zealand white rabbit model to elucidate biological changes based on gene expression within the vocal folds from surface dehydration. Surface dehydration was induced by exposure to low humidity air (18.6% ± 4.3%) for 8 hours. Exposure to moderate humidity (43.0% ± 4.3%) served as the control condition. Ilumina-based RNA sequencing was performed and used for transcriptome analysis with validation by RT-qPCR. Results There were 103 genes identified through Cuffdiff with 64 genes meeting significance by both false discovery rate and fold change. Functional annotation enrichment and predicted protein interaction mapping showed enrichment of various loci, including cellular stress and inflammatory response, ciliary function, and keratinocyte development. Eight genes were selected for RT-qPCR validation. Matrix metalloproteinase 12 (MMP12) and macrophage cationic peptide 1 (MCP1) were significantly upregulated and an epithelial chloride channel protein (ECCP) was significantly downregulated after surface dehydration by RNA-Seq and RT-qPCR. Suprabasin (SPBN) and zinc activated cationic channel (ZACN) were marginally, but non-significantly down- and upregulated by RT-qPCR, respectively. Conclusions The data together support the notion that surface dehydration induces physiological changes in the vocal folds and justifies targeted analysis to further explore the underlying biology of compensatory fluid/ion flux and inflammatory mediators in response to airway surface dehydration.

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“…SPBN is expressed in the suprabasal layers of tongue, stomach, and epidermis (86). It is required for keratinocyte differentiation in an in vitro skin model (87) and skin development in murine embryos (88). The speci c activity of CDHR4 is not described in the literature, but family member CDHR2 is expressed in gastrointestinal epithelial cells and is associated with microvillus development (89), while family member CHDR3 is expressed in ciliated respiratory epithelial cells and is associated with ciliary development and intercellular interactions (90).…”

Section: Discussionmentioning

confidence: 99%

RNA sequencing identifies transcriptional changes in the rabbit larynx in response to low humidity challenge

Bailey

Santos

Nascimento

et al. 2020

Preprint

View full text Add to dashboard Cite

Background: Voice disorders are a worldwide problem impacting human health, particularly for occupational voice users. Avoidance of surface dehydration is commonly prescribed as a protective factor against the development of dysphonia. The available literature inconclusively supports this practice and a biological mechanism for how surface dehydration of the laryngeal tissue affects voice has not been described. In this study, we used an in vivo male New Zealand white rabbit model to elucidate biological changes based on gene expression within the vocal folds from surface dehydration. Surface dehydration was induced by exposure to low humidity air (18.6% + 4.3%) for 8 hours. Exposure to moderate humidity (43.0% + 4.3%) served as the control condition. Ilumina-based RNA sequencing was performed and used for transcriptome analysis with validation by RT-qPCR. Results: There were 103 statistically significant differentially expressed genes identified through Cuffdiff with 61 genes meeting significance by both false discovery rate and fold change. Functional annotation enrichment and predicted protein interaction mapping showed enrichment of various loci, including cellular stress and inflammatory response, ciliary function, and keratinocyte development. Eight genes were selected for RT-qPCR validation. Matrix metalloproteinase 12 (MMP12) and macrophage cationic peptide 1 (MCP1) were significantly upregulated and an epithelial chloride channel protein (ECCP) was significantly downregulated after surface dehydration by RNA-Seq and RT-qPCR. Suprabasin (SPBN) and zinc activated cationic channel (ZACN) were marginally, but non-significantly down- and upregulated as evidenced by RT-qPCR, respectively. Conclusions: The data together support the notion that surface dehydration induces physiological changes in the vocal folds and justifies targeted analysis to further explore the underlying biology of compensatory fluid/ion flux and inflammatory mediators in response to airway surface dehydration.

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Decreased expression of suprabasin induces aberrant differentiation and apoptosis of epidermal keratinocytes: Possible role for atopic dermatitis

Cited by 23 publications

References 23 publications

Suprabasin-null mice retain skin barrier function and show high contact hypersensitivity to nickel upon oral nickel loading

Suprabasin-null mice retain skin barrier function and show high contact hypersensitivity to nickel upon oral nickel loading

RNA sequencing identifies transcriptional changes in the rabbit larynx in response to low humidity challenge

RNA sequencing identifies transcriptional changes in the rabbit larynx in response to low humidity challenge

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