دورية أكاديمية
أعرض في EDS

The lack of PI3Kγ favors M1 macrophage polarization and does not prevent kidney diseases progression.

التفاصيل البيبلوغرافية
العنوان: The lack of PI3Kγ favors M1 macrophage polarization and does not prevent kidney diseases progression.
المؤلفون: Amano MT; Laboratory of Transplantation Immunobiology, Department of Immunology, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil; Instituto Sírio-Libanês de Ensino e Pesquisa, Hospital Sírio-Libanês, Sao Paulo, Brazil. Electronic address: mariane.tamano@hsl.org.br., Castoldi A; Laboratory of Transplantation Immunobiology, Department of Immunology, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil., Andrade-Oliveira V; Laboratory of Transplantation Immunobiology, Department of Immunology, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil., Latancia MT; Laboratory of Transplantation Immunobiology, Department of Immunology, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil; Instituto Sírio-Libanês de Ensino e Pesquisa, Hospital Sírio-Libanês, Sao Paulo, Brazil., Terra FF; Laboratory of Transplantation Immunobiology, Department of Immunology, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil., Correa-Costa M; Laboratory of Transplantation Immunobiology, Department of Immunology, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil., Breda CNS; Laboratory of Transplantation Immunobiology, Department of Immunology, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil., Felizardo RJF; Laboratory of Transplantation Immunobiology, Department of Immunology, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil., Pereira WO; School of Medicine, Faculdade Israelita de Ciências da Saúde Albert Einstein, Sao Paulo, Brazil., da Silva MB; Laboratory of Transplantation Immunobiology, Department of Immunology, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil., Miyagi MYS; Laboratory of Transplantation Immunobiology, Department of Immunology, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil., Aguiar CF; Laboratory of Transplantation Immunobiology, Department of Immunology, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil., Hiyane MI; Laboratory of Transplantation Immunobiology, Department of Immunology, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil., Silva JS; Department of Biochemistry and Immunology, Medical School Ribeirão Preto, FMRP, University of Sao Paulo, Sao Paulo, Brazil., Moura IC; INSERM UMR 1163, Laboratory of Cellular and Molecular Mechanisms of Hematological Disorders and Therapeutic Implications, Paris, France; Paris Descartes - Sorbonne Paris Cité University, Paris, France; CNRS ERL 8254, Imagine Institute, Laboratory of Excellence GR-Ex, Paris, France., Camara NOS; Laboratory of Transplantation Immunobiology, Department of Immunology, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil; Laboratory of Renal Pathology, Faculty of Medicine, University of São Paulo, Sao Paulo, Brazil.
المصدر: International immunopharmacology [Int Immunopharmacol] 2018 Nov; Vol. 64, pp. 151-161. Date of Electronic Publication: 2018 Aug 31.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Elsevier Science Country of Publication: Netherlands NLM ID: 100965259 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1878-1705 (Electronic) Linking ISSN: 15675769 NLM ISO Abbreviation: Int Immunopharmacol Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Amsterdam ; New York : Elsevier Science, c2001-
مواضيع طبية MeSH: Cell Polarity*, Acute Kidney Injury/*prevention & control , Class Ib Phosphatidylinositol 3-Kinase/*physiology , Macrophages/*physiology , Renal Insufficiency, Chronic/*prevention & control, Animals ; Disease Progression ; Inflammation/etiology ; Interleukin-12/biosynthesis ; Mice ; Mice, Inbred C57BL ; Ureteral Obstruction/complications
مستخلص: Acute kidney injury (AKI) and chronic kidney disease (CKD) are major concerns in worldwide public health, and their pathophysiology involves immune cells activation, being macrophages one of the main players of both processes. It is suggested that metabolic pathways could contribute to macrophage modulation and phosphatidylinositol‑3 kinase (PI3K) pathway was shown to be activated in kidneys subjected to ischemia and reperfusion as well as unilateral ureteral obstruction (UUO). Although PI3K inhibition is mostly associated with anti-inflammatory response, its use in kidney injuries has been shown controversial results, which indicates the need for further studies. Our aim was to unveil the role of PI3Kγ in macrophage polarization and in kidney diseases development. We analyzed bone-marrow macrophages polarization from wild-type (WT) and PI3Kγ knockout (PI3K KO) animals. We observed increased expression of M1 (CD86, CCR7, iNOS, TNF, CXCL9, CXCL10, IL-12 and IL-23) and decreased of M2 (CD206, Arg-1, FIZZ1 and YM1) markers in the lack of PI3Kγ. And this modulation was accompanied by higher levels of inflammatory cytokines in PI3K KO M1 cells. PI3K KO mice had increased M1 in steady state kidneys, and no protection was observed in these mice after acute and chronic kidney insults. On the contrary, they presented higher levels of protein-to-creatinine ratio and Kim-1 expression and increased tubular injury. In conclusion, our findings demonstrated that the lack of PI3Kγ favors M1 macrophages polarization providing an inflammatory-prone environment, which does not prevent kidney diseases progression.
(Copyright © 2018 Elsevier B.V. All rights reserved.)
فهرسة مساهمة: Keywords: Acute kidney injury; Chronic kidney disease; Macrophage; PI3K
المشرفين على المادة: 187348-17-0 (Interleukin-12)
EC 2.7.1.137 (Class Ib Phosphatidylinositol 3-Kinase)
EC 2.7.1.153 (Pik3cg protein, mouse)
تواريخ الأحداث: Date Created: 20180904 Date Completed: 20190222 Latest Revision: 20190222
رمز التحديث: 20231215
DOI: 10.1016/j.intimp.2018.08.020
PMID: 30176533
قاعدة البيانات: MEDLINE
الوصف
تدمد:1878-1705
DOI:10.1016/j.intimp.2018.08.020