PMID- 30703869 OWN - NLM STAT- MEDLINE DCOM- 20190422 LR - 20240204 IS - 0219-1032 (Electronic) IS - 1016-8478 (Print) IS - 1016-8478 (Linking) VI - 42 IP - 2 DP - 2019 Feb 28 TI - Alleviation of Ultraviolet-B Radiation-Induced Photoaging by a TNFR Antagonistic Peptide, TNFR2-SKE. PG - 151-160 LID - 10.14348/molcells.2018.0423 [doi] AB - Ultraviolet (UV) radiation of the sunlight, especially UVA and UVB, is the primary environmental cause of skin damage, including topical inflammation, premature skin aging, and skin cancer. Previous reports show that activation of nuclear factor-kappaB (NF-kappaB) in human skin fibroblasts and keratinocytes after UV exposure induces the expression and release of proinflammatory cytokines, such as interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-alpha), and subsequently leads to the production of matrix metalloproteases (MMPs) and growth factor basic fibroblast growth factor (bFGF). Here, we demonstrated that TNFR2-SKEE and TNFR2-SKE, oligopeptides from TNF receptor-associated factor 2 (TRAF2)-binding site of TNF receptor 2 (TNFR2), strongly inhibited the interaction of TNFR1 as well as TNFR2 with TRAF2. In particular, TNFR2-SKE suppressed UVB- or TNF-alpha-induced nuclear translocalization of activated NF-kappaB in mouse fibroblasts. It decreased the expression of bFGF, MMPs, and COX2, which were upregulated by TNF-alpha, and increased procollagen production, which was reduced by TNF-alpha. Furthermore, TNFR2-SKE inhibited the UVB-induced proliferation of keratinocytes and melanocytes in the mouse skin and the infiltration of immune cells into inflamed tissues. These results suggest that TNFR2-SKE may possess the clinical potency to alleviate UV-induced photoaging in human skin. FAU - Lee, Kyoung-Jin AU - Lee KJ AD - Department of Anatomy and Cell Biology, School of Medicine, Kangwon National University, Chuncheon 24341, Korea. FAU - Park, Kyeong Han AU - Park KH AD - Department of Anatomy and Cell Biology, School of Medicine, Kangwon National University, Chuncheon 24341, Korea. FAU - Hahn, Jang-Hee AU - Hahn JH AD - Department of Anatomy and Cell Biology, School of Medicine, Kangwon National University, Chuncheon 24341, Korea. LA - eng PT - Journal Article DEP - 20190124 PL - United States TA - Mol Cells JT - Molecules and cells JID - 9610936 RN - 0 (NF-kappa B) RN - 0 (Peptides) RN - 0 (Receptors, Tumor Necrosis Factor, Type I) RN - 0 (Receptors, Tumor Necrosis Factor, Type II) RN - 0 (TNF Receptor-Associated Factor 2) RN - 0 (Tumor Necrosis Factor-alpha) SB - IM MH - Animals MH - Cell Proliferation/drug effects MH - Fibroblasts/drug effects/metabolism MH - Gene Expression Regulation/drug effects MH - Humans MH - Hyperplasia MH - Inflammation/pathology MH - Lymphocytes/drug effects/metabolism MH - Melanocytes/drug effects/metabolism/pathology MH - Mice MH - NF-kappa B/metabolism MH - NIH 3T3 Cells MH - Peptides/*pharmacology MH - Protein Binding/drug effects MH - Receptors, Tumor Necrosis Factor, Type I/antagonists & inhibitors/metabolism MH - Receptors, Tumor Necrosis Factor, Type II/*antagonists & inhibitors/metabolism MH - Skin/drug effects/pathology/radiation effects MH - Skin Aging/*drug effects/*radiation effects MH - TNF Receptor-Associated Factor 2/metabolism MH - Tumor Necrosis Factor-alpha/pharmacology MH - *Ultraviolet Rays PMC - PMC6399009 OTO - NOTNLM OT - NF-kappaB OT - TNFR antagonist OT - TNFR2-SKE OT - inflammation OT - photoaging EDAT- 2019/02/02 06:00 MHDA- 2019/04/23 06:00 PMCR- 2019/02/28 CRDT- 2019/02/02 06:00 PHST- 2018/11/08 00:00 [received] PHST- 2018/12/13 00:00 [revised] PHST- 2019/01/01 00:00 [accepted] PHST- 2019/02/02 06:00 [pubmed] PHST- 2019/04/23 06:00 [medline] PHST- 2019/02/02 06:00 [entrez] PHST- 2019/02/28 00:00 [pmc-release] AID - S1016-8478(23)00383-7 [pii] AID - molce-42-2-151 [pii] AID - 10.14348/molcells.2018.0423 [doi] PST - ppublish SO - Mol Cells. 2019 Feb 28;42(2):151-160. doi: 10.14348/molcells.2018.0423. Epub 2019 Jan 24.