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Targeted silencing of DEFB4 in a bioengineered skin-humanized mouse model for psoriasis: development of siRNA SECosome-based novel therapies

STEFANIE BRACKE (UGent) , Marta Carretero, Sara Guerrero-Aspizua, Eline Desmet (UGent) , Nuria Illera, Manuel Navarro, Jo Lambert (UGent) and Marcela Del Rio
(2014) EXPERIMENTAL DERMATOLOGY. 23(3). p.199-201
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Organization
Abstract
Psoriasis is a complex inflammatory skin disease that presents a wide variety of clinical manifestations. Human β defensin-2 (hBD-2) is highly up-regulated in psoriatic lesions and has been defined as a biomarker for disease activity. We explored the potential benefits of targeting hBD-2 by topical application of DEFB4-siRNA-containing SECosomes in a bioengineered skin-humanized mouse model for psoriasis. A significant improvement in the psoriatic phenotype was observed by histological examination, with a normalization of the skin architecture and a reduction in the number and size of blood vessels in the dermal compartment. Treatment leads to the recovery of transglutaminase activity, filaggrin expression and stratum corneum appearance to the levels similar to those found in normal regenerated human skin. The availability of a reliable skin-humanized mouse model for psoriasis in conjunction with the use of the SECosome technology may provide a valuable preclinical tool for identifying potential therapeutic targets for this disease.
Keywords
NF-KAPPA-B, LYMPHOMA U937 CELLS, IN-VIVO, GENE-EXPRESSION, HUMAN KERATINOCYTES, ASTAXANTHIN, APOPTOSIS, INFLAMMATION, MICE, siRNA, SECosomes, skin-humanized mouse model, INDUCED OXIDATIVE STRESS, hBD-2, psoriasis

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MLA
BRACKE, STEFANIE, et al. “Targeted Silencing of DEFB4 in a Bioengineered Skin-Humanized Mouse Model for Psoriasis: Development of SiRNA SECosome-Based Novel Therapies.” EXPERIMENTAL DERMATOLOGY, vol. 23, no. 3, 2014, pp. 199–201, doi:10.1111/exd.12321.
APA
BRACKE, S., Carretero, M., Guerrero-Aspizua, S., Desmet, E., Illera, N., Navarro, M., … Del Rio, M. (2014). Targeted silencing of DEFB4 in a bioengineered skin-humanized mouse model for psoriasis: development of siRNA SECosome-based novel therapies. EXPERIMENTAL DERMATOLOGY, 23(3), 199–201. https://doi.org/10.1111/exd.12321
Chicago author-date
BRACKE, STEFANIE, Marta Carretero, Sara Guerrero-Aspizua, Eline Desmet, Nuria Illera, Manuel Navarro, Jo Lambert, and Marcela Del Rio. 2014. “Targeted Silencing of DEFB4 in a Bioengineered Skin-Humanized Mouse Model for Psoriasis: Development of SiRNA SECosome-Based Novel Therapies.” EXPERIMENTAL DERMATOLOGY 23 (3): 199–201. https://doi.org/10.1111/exd.12321.
Chicago author-date (all authors)
BRACKE, STEFANIE, Marta Carretero, Sara Guerrero-Aspizua, Eline Desmet, Nuria Illera, Manuel Navarro, Jo Lambert, and Marcela Del Rio. 2014. “Targeted Silencing of DEFB4 in a Bioengineered Skin-Humanized Mouse Model for Psoriasis: Development of SiRNA SECosome-Based Novel Therapies.” EXPERIMENTAL DERMATOLOGY 23 (3): 199–201. doi:10.1111/exd.12321.
Vancouver
1.
BRACKE S, Carretero M, Guerrero-Aspizua S, Desmet E, Illera N, Navarro M, et al. Targeted silencing of DEFB4 in a bioengineered skin-humanized mouse model for psoriasis: development of siRNA SECosome-based novel therapies. EXPERIMENTAL DERMATOLOGY. 2014;23(3):199–201.
IEEE
[1]
S. BRACKE et al., “Targeted silencing of DEFB4 in a bioengineered skin-humanized mouse model for psoriasis: development of siRNA SECosome-based novel therapies,” EXPERIMENTAL DERMATOLOGY, vol. 23, no. 3, pp. 199–201, 2014.
@article{5847216,
  abstract     = {{Psoriasis is a complex inflammatory skin disease that presents a wide variety of clinical manifestations. Human β defensin-2 (hBD-2) is highly up-regulated in psoriatic lesions and has been defined as a biomarker for disease activity. We explored the potential benefits of targeting hBD-2 by topical application of DEFB4-siRNA-containing SECosomes in a bioengineered skin-humanized mouse model for psoriasis. A significant improvement in the psoriatic phenotype was observed by histological examination, with a normalization of the skin architecture and a reduction in the number and size of blood vessels in the dermal compartment. Treatment leads to the recovery of transglutaminase activity, filaggrin expression and stratum corneum appearance to the levels similar to those found in normal regenerated human skin. The availability of a reliable skin-humanized mouse model for psoriasis in conjunction with the use of the SECosome technology may provide a valuable preclinical tool for identifying potential therapeutic targets for this disease.}},
  author       = {{BRACKE, STEFANIE and Carretero, Marta and Guerrero-Aspizua, Sara and Desmet, Eline and Illera, Nuria and Navarro, Manuel and Lambert, Jo and Del Rio, Marcela}},
  issn         = {{0906-6705}},
  journal      = {{EXPERIMENTAL DERMATOLOGY}},
  keywords     = {{NF-KAPPA-B,LYMPHOMA U937 CELLS,IN-VIVO,GENE-EXPRESSION,HUMAN KERATINOCYTES,ASTAXANTHIN,APOPTOSIS,INFLAMMATION,MICE,siRNA,SECosomes,skin-humanized mouse model,INDUCED OXIDATIVE STRESS,hBD-2,psoriasis}},
  language     = {{eng}},
  number       = {{3}},
  pages        = {{199--201}},
  title        = {{Targeted silencing of DEFB4 in a bioengineered skin-humanized mouse model for psoriasis: development of siRNA SECosome-based novel therapies}},
  url          = {{http://dx.doi.org/10.1111/exd.12321}},
  volume       = {{23}},
  year         = {{2014}},
}
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