Influence of iNOS and COX on peroxiredoxin gene expression in primary macrophages |
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| Institution: | 1. Departamento de Biofisica, Universidade Federal de São Paulo, São Paulo, SP, Brazil;2. Núcleo de Pesquisa em Química Biológica, Centro de Ciências da Saúde, Universidade Federal de São João Del Rei, Divinópolis, MG, Brazil;3. Departamento de Biociências, Universidade Federal de São Paulo, Santos, SP, Brazil;4. Centro de Ciências Naturais e Humanas, Universidade Federal do ABC, Santo André, SP, Brazil;1. Department of Anatomy, Histology and Embryology, Faculty of Medicine, University of Szeged, Szeged, Hungary;2. Biotalentum Ltd., Gödöllő, Hungary;3. Department for Trauma Surgery, Medical University Vienna, Vienna, Austria;4. Molecular Animal Biotechnology Laboratory, Szent István University, Gödöllő, Hungary;1. Hebrew University Hadassah Medical School, Jerusalem, Israel;2. Department of Pharmacology and Therapeutics, McGill University, Montreal, Canada;3. Department of Obstetrics and Gynecology, University of Rochester, Rochester, USA;1. SUNY at Stony Brook, Stony Brook, NY;2. Clinical Pathology, SUNY at Stony Brook, Stony Brook, NY;3. Department of Radiology, SUNY at Stony Brook, Stony Brook, NY |
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| Abstract: | Peroxiredoxins (Prxs) are a family of multifunctional antioxidant thiol-dependent peroxidases. This study aimed to examine the regulatory mechanisms of Prx gene expression in murine bone marrow-derived macrophages (BMMs) using standardized serum-free conditions. Stimulation with LPS and IFNγ increased mRNA levels of Prx 1, 2, 4, 5, and 6 in BMMs of both C57BL/6 and BALB/c mice, with Prx 1, 2, 4, and 6 more strongly induced in C57BL/6 BMMs. Further investigations on signaling pathways in C57BL/6 BMMs demonstrated that up-regulation of Prx 5 and 6 by LPS and IFNγ was associated with the activation of multiple protein kinases, most notably JAK2, PI3K, and p38 MAPK. Our experiments also revealed a contribution of inducible NO synthase-derived nitric oxide to the increase in Prx 1, 2, 4, and 6 mRNA expression, whereas NADPH oxidase-derived superoxide was not involved. Furthermore, we could show that LPS- and IFNγ-induced gene expression of Prx 6 was also regulated in an NO-independent manner by cyclooxygenases and prostaglandin E2. Taken together our results indicate a possible role for Prxs in defense mechanisms of activated macrophages against oxidative stress during inflammation or infection. |
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