Defect of growth/differentiation regulation caused psoriasis-like skin inflammation.

2016 Fiscal Year Final Research Report

• Project/Area Number: 26293071
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: Pathological medical chemistry
• Research Institution: Tokyo University of Pharmacy and Life Science
• Principal Investigator: FUKAMI KIYOKO 東京薬科大学, 生命科学部, 教授 (40181242)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: リン脂質代謝 / 炎症性皮膚疾患 / 皮膚バリア

Outline of Final Research Achievements

We showed here that downregulation of phospholipase C (PLC) δ1 impairs the barrier functions of the stratum corneum. PLCδ1 downregulation also impairs localization of tight junction proteins. Loss of PLCδ1 leads to a decrease in intracellular Ca2+ concentrations and nuclear factor of activated T cells (NFAT) activity, along with hyperactivation of p38 mitogen-activated protein kinase (MAPK) and inactivation of RhoA. These findings demonstrate that PLCδ1 is essential for epidermal barrier integrity. This study also suggests a possible link between PLCδ1 downregulation, p38 MAPK hyperactivation, and barrier defects in psoriasis-like skin inflammation.

Free Research Field

皮膚科学