000095748 001__ 95748
000095748 005__ 20210902121817.0
000095748 0247_ $$2doi$$a10.1038/s41598-020-72342-7
000095748 0248_ $$2sideral$$a120185
000095748 037__ $$aART-2020-120185
000095748 041__ $$aeng
000095748 100__ $$aHotter, G.
000095748 245__ $$aThe influenza virus NS1A binding protein gene modulates macrophages response to cytokines and phagocytic potential in inflammation
000095748 260__ $$c2020
000095748 5060_ $$aAccess copy available to the general public$$fUnrestricted
000095748 5203_ $$aMacrophages show remarkable phenotypic plasticity in response to environmental signals. Although it is generally less considered, cytoskeletal changes in macrophages influence their phenotype, including phagocytosis and secretion of soluble cytokines. Influenza virus NS1A-binding protein (Ivns1abp) belongs to the Kelch family of proteins that play a central role in actin cytoskeleton dynamics by directly associating with F-actin and by protecting against actin derangement. Due to its role in cytoskeleton preservation, the Ivns1abp gene might be a critical regulator of the macrophage phenotype and function under inflammatory conditions. In this study, we determine that the modulation of the Ivns1abp gene in macrophages could modify resistance to macrophages against inflammation and maintain functional phagocytosis. Our results indicate that inflammatory insults inhibit the Ivns1abp gene, whereby phagocytosis is inhibited and the ability of macrophages to induce proliferation and repair of damaged cells is compromised. Furthermore, our results show that inflammatory insults alter the activity of the transcription factor c-myc, a factor which directly modulates the expression of the Ivns1abp gene. In conclusion, this study demonstrates a central role of lvns1abp in promoting and preserving a reparative macrophage phenotype and resistance to this inflammatory environment.
000095748 536__ $$9info:eu-repo/grantAgreement/EUR/ERDF/A way to build Europe$$9info:eu-repo/grantAgreement/ES/FIS/PI17-01411$$9info:eu-repo/grantAgreement/ES/MINECO/SAF2015-67770-R
000095748 540__ $$9info:eu-repo/semantics/openAccess$$aby$$uhttp://creativecommons.org/licenses/by/3.0/es/
000095748 590__ $$a4.379$$b2020
000095748 591__ $$aMULTIDISCIPLINARY SCIENCES$$b17 / 73 = 0.233$$c2020$$dQ1$$eT1
000095748 592__ $$a1.24$$b2020
000095748 593__ $$aMultidisciplinary$$c2020$$dQ1
000095748 655_4 $$ainfo:eu-repo/semantics/article$$vinfo:eu-repo/semantics/publishedVersion
000095748 700__ $$aMastora, C.
000095748 700__ $$aJung, M.
000095748 700__ $$aBrüne, B.
000095748 700__ $$aCarbonell, T.
000095748 700__ $$0(orcid)0000-0002-8328-9836$$aJosa, C.$$uUniversidad de Zaragoza
000095748 700__ $$0(orcid)0000-0003-2361-9941$$aPérez-Calvo, J.I.$$uUniversidad de Zaragoza
000095748 700__ $$aCruzado, J.M.
000095748 700__ $$aGuiteras, R.
000095748 700__ $$aSola, A.
000095748 7102_ $$11007$$2610$$aUniversidad de Zaragoza$$bDpto. Medicina, Psiqu. y Derm.$$cArea Medicina
000095748 773__ $$g10, 1 (2020), 15302 [16 pp]$$pSci. rep.$$tScientific Reports$$x2045-2322
000095748 8564_ $$s2143433$$uhttps://zaguan.unizar.es/record/95748/files/texto_completo.pdf$$yVersión publicada
000095748 8564_ $$s429414$$uhttps://zaguan.unizar.es/record/95748/files/texto_completo.jpg?subformat=icon$$xicon$$yVersión publicada
000095748 909CO $$ooai:zaguan.unizar.es:95748$$particulos$$pdriver
000095748 951__ $$a2021-09-02-10:05:27
000095748 980__ $$aARTICLE