Progranulin deficiency exaggerates, whereas progranulin‐derived Atsttrin attenuates, severity of dermatitis in mice. Issue 12 (10th May 2013)

• Record Type: Journal Article
• Authors: Zhao, Yun-Peng; Tian, Qing-Yun; Liu, Chuan-Ju
• Is Part Of: FEBS letters. Volume 587:Issue 12(2013)
• Page Start: 1805
• Page End: 1810
• Publication Date: 2013-05-10
• Subjects: PGRN -- progranulin -- WT -- wild type -- TNF-α -- tumor necrosis factor α -- IL-1β -- interleukin-1β -- IL-6 -- interleukin-6 -- NF-κB -- nuclear factor-KappaB -- pIκB-α -- phosphorylated IκB-α -- COX-2 -- cyclooxygenase-2 -- iNOS -- inducible nitric oxide synthase -- OXA -- oxazolone -- VEH -- vehicle -- Progranulin -- Atsttrin -- Dermatitis -- NF-κB signaling; Biochemistry -- Periodicals; Biophysics -- Periodicals; Molecular biology -- Periodicals; Biochimie -- Périodiques; Biochemistry; Biophysics; Molecular biology; Periodicals; 572.05
• DOI: 10.1016/j.febslet.2013.04.037
• Languages: English
• ISSNs: 0014-5793

Abstract

Abstract : PGRN and its derived engineered protein, Atsttrin, were reported to antagonize TNFα and protect against inflammatory arthritis [Tang, W. et al. (2011) The growth factor progranulin binds to TNF receptors and is therapeutic against inflammatory arthritis in mice. Science 332 (6028) 478–484]. Here we found that PGRN level was also significantly elevated in skin inflammation. PGRN−/− mice exhibited more severe inflammation following induction of oxazolone (OXA). In contrast, recombinant Atsttrin protein effectively attenuated inflammation in mice dermatitis model. In addition, the protective role of PGRN and Atsttrin in dermatitis was probably due to their inhibition on NF‐κB signaling. Collectively, PGRN, especially its derived engineered protein, Atsttrin, may represent a potential molecular target for prevention and treatment of inflammatory skin diseases. Abstract : PGRN expression was upregulated in inflammatory skin. PGRN deficiency exaggerated, while Atsttrin attenuated, dermatitis in mice. PGRN/Atsttrin may protect against dermatitis through inhibition of NF‐κB signaling.