دورية أكاديمية
أعرض في EDS

Angiotensin-(1-7) and Alamandine Promote Anti-inflammatory Response in Macrophages In Vitro and In Vivo .

التفاصيل البيبلوغرافية
العنوان: Angiotensin-(1-7) and Alamandine Promote Anti-inflammatory Response in Macrophages In Vitro and In Vivo .
المؤلفون: de Carvalho Santuchi M; Department of Physiology and Biophysics, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Brazil., Dutra MF; Department of Physiology and Biophysics, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Brazil., Vago JP; Department of Clinical and Toxicological Analyses, Faculty of Pharmacy, Federal University of Minas Gerais, Belo Horizonte, Brazil., Lima KM; Department of Clinical and Toxicological Analyses, Faculty of Pharmacy, Federal University of Minas Gerais, Belo Horizonte, Brazil., Galvão I; Department of Biochemistry and Immunology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Brazil., de Souza-Neto FP; Department of Physiology and Biophysics, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Brazil., Morais E Silva M; Department of Physiology and Biophysics, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Brazil., Oliveira AC; Department of Physiology and Biophysics, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Brazil., de Oliveira FCB; Department of Biochemistry and Immunology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Brazil., Gonçalves R; Department of Pathology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Brazil., Teixeira MM; Department of Biochemistry and Immunology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Brazil., Sousa LP; Department of Clinical and Toxicological Analyses, Faculty of Pharmacy, Federal University of Minas Gerais, Belo Horizonte, Brazil., Dos Santos RAS; Department of Physiology and Biophysics, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Brazil., da Silva RF; Department of Physiology and Biophysics, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Brazil.
المصدر: Mediators of inflammation [Mediators Inflamm] 2019 Feb 21; Vol. 2019, pp. 2401081. Date of Electronic Publication: 2019 Feb 21 (Print Publication: 2019).
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Hindawi Pub. Corp Country of Publication: United States NLM ID: 9209001 Publication Model: eCollection Cited Medium: Internet ISSN: 1466-1861 (Electronic) Linking ISSN: 09629351 NLM ISO Abbreviation: Mediators Inflamm Subsets: MEDLINE
أسماء مطبوعة: Publication: 2005- : Sylvania, OH : Hindawi Pub. Corp.
Original Publication: Oxford, UK : Rapid Communications of Oxford Ltd., c1992-
مواضيع طبية MeSH: Angiotensin I/*pharmacology , Anti-Inflammatory Agents/*pharmacology , Macrophages/*drug effects , Macrophages/*metabolism , Oligopeptides/*pharmacology , Peptide Fragments/*pharmacology, Animals ; Cells, Cultured ; Interleukin-4/pharmacology ; Male ; Mice ; Mice, Inbred BALB C ; Proto-Oncogene Mas ; Proto-Oncogene Proteins/metabolism ; Receptors, G-Protein-Coupled/metabolism
مستخلص: The renin-angiotensin system (RAS) peptides play an important role in inflammation. Resolution of inflammation contributes to restore tissue homeostasis, and it is characterized by neutrophil apoptosis and their subsequent removal by macrophages, which are remarkable plastic cells involved in the pathophysiology of diverse inflammatory diseases. However, the effects of RAS peptides on different macrophage phenotypes are still emerging. Here, we evaluated the effects of angiotensin-(1-7) (Ang-(1-7)) and the most novel RAS peptide, alamandine, on resting (M0), proinflammatory M(LPS+IFN- γ ), and anti-inflammatory M(IL-4) macrophage phenotypes in vitro , as well as on specific immune cell populations and macrophage subsets into the pleural cavity of LPS-induced pleurisy in mice. Our results showed that Ang-(1-7) and alamandine, through Mas and MrgD receptors, respectively, do not affect M0 macrophages but reduce the proinflammatory TNF- α , CCL2, and IL-1 β transcript expression levels in LPS+IFN- γ -stimulated macrophages. Therapeutic administration of these peptides in LPS-induced inflammation in mice decreased the number of neutrophils and M1 (F4/80 low Gr1 + CD11b med ) macrophage frequency without affecting the other investigated macrophage subsets. Our data suggested that both Ang-(1-7) and alamandine, through their respective receptors Mas and MrgD, promote an anti-inflammatory reprogramming of M(LPS+IFN- γ )/M1 macrophages under inflammatory circumstances and potentiate the reprogramming induced by IL-4. In conclusion, our work sheds light on the emerging proresolving properties of Ang-(1-7) and alamandine, opening new avenues for the treatment of inflammatory diseases.
References: J Hypertens. 1999 Apr;17(4):537-45. (PMID: 10404956)
ScientificWorldJournal. 2011;11:2391-402. (PMID: 22194670)
Sci Rep. 2015 Feb 03;5:8209. (PMID: 25644821)
Neuropharmacology. 2013 Aug;71:154-63. (PMID: 23583926)
Clin Transl Med. 2014 Nov 21;3(1):63. (PMID: 25635207)
PLoS One. 2017 Dec 12;12(12):e0189535. (PMID: 29232407)
J Immunol. 2016 Feb 15;196(4):1922-32. (PMID: 26800869)
Eur J Clin Invest. 2017 Feb;47(2):117-128. (PMID: 27930810)
Curr Protoc Immunol. 2008 Nov;Chapter 14:14.2.1-14.2.8. (PMID: 19016446)
J Immunol. 2005 Jul 1;175(1):342-9. (PMID: 15972667)
Thromb Haemost. 2014 Apr 1;111(4):736-47. (PMID: 24499778)
Br J Pharmacol. 2015 May;172(9):2330-42. (PMID: 25559763)
Cell Death Dis. 2018 Jun 4;9(6):665. (PMID: 29867198)
Eur J Immunol. 2011 Feb;41(2):366-79. (PMID: 21268007)
J Leukoc Biol. 2010 May;87(5):895-904. (PMID: 20103769)
J Immunol. 2014 Oct 1;193(7):3654-63. (PMID: 25165151)
J Immunol. 2010 Nov 1;185(9):5569-76. (PMID: 20935211)
Circ Res. 2013 Apr 12;112(8):1104-11. (PMID: 23446738)
Blood. 2011 Dec 22;118(26):e192-208. (PMID: 22012065)
Int J Biol Sci. 2014 May 01;10(5):520-9. (PMID: 24910531)
J Clin Invest. 2007 Jan;117(1):175-84. (PMID: 17200717)
Circ Res. 2010 Oct 1;107(7):888-97. (PMID: 20671240)
Front Immunol. 2017 Nov 20;8:1596. (PMID: 29209329)
Eur Rev Med Pharmacol Sci. 2014;18(7):985-91. (PMID: 24763878)
Clin Transl Med. 2015 Feb 14;4:5. (PMID: 25852821)
Life Sci. 2018 Aug 1;206:106-116. (PMID: 29679702)
FASEB J. 2009 Mar;23(3):844-54. (PMID: 18971259)
Am J Physiol Cell Physiol. 2018 Jun 1;314(6):C702-C711. (PMID: 29443552)
J Leukoc Biol. 2012 Aug;92(2):249-58. (PMID: 22493082)
Clin Sci (Lond). 2014 Jul;127(1):19-31. (PMID: 24383472)
Proc Natl Acad Sci U S A. 2016 Dec 6;113(49):14109-14114. (PMID: 27872279)
Nat Methods. 2012 Jun 28;9(7):676-82. (PMID: 22743772)
J Atheroscler Thromb. 2016;23(1):10-7. (PMID: 26412584)
Braz J Med Biol Res. 2017 Jan 09;50(1):e5594. (PMID: 28076452)
Trends Immunol. 2004 Dec;25(12):677-86. (PMID: 15530839)
PLoS One. 2015 Jun 19;10(6):e0129744. (PMID: 26091535)
Blood. 2017 May 25;129(21):2896-2907. (PMID: 28320709)
Int J Exp Pathol. 2014 Aug;95(4):290-5. (PMID: 24953785)
Br J Pharmacol. 2017 Nov;174(22):4055-4069. (PMID: 27935022)
Peptides. 2014 Jan;51:65-73. (PMID: 24262271)
Front Pharmacol. 2016 Dec 15;7:482. (PMID: 28018220)
Immunity. 2014 Jul 17;41(1):14-20. (PMID: 25035950)
FASEB J. 2011 Apr;25(4):1145-55. (PMID: 21148418)
Peptides. 2011 Oct;32(10):2141-50. (PMID: 21945916)
Clin Exp Immunol. 2015 Jul;181(1):126-32. (PMID: 25707554)
Front Immunol. 2016 Apr 26;7:160. (PMID: 27199985)
Am J Physiol Heart Circ Physiol. 2019 Jan 1;316(1):H123-H133. (PMID: 30339496)
Curr Hypertens Rep. 2018 Mar 14;20(2):17. (PMID: 29541937)
Mol Immunol. 2009 Jan;46(3):355-61. (PMID: 19041135)
Biochem Pharmacol. 2009 Aug 15;78(4):396-405. (PMID: 19422809)
Front Immunol. 2012 Jan 31;3:4. (PMID: 22566890)
Int J Cardiol. 2018 Nov 1;270:221-227. (PMID: 29884291)
Am J Physiol Lung Cell Mol Physiol. 2014 Apr 15;306(8):L709-25. (PMID: 24508730)
J Immunol. 2015 May 15;194(10):4940-50. (PMID: 25876761)
Blood. 2008 Nov 15;112(10):4117-27. (PMID: 18779392)
Curr Opin Pharmacol. 2013 Aug;13(4):555-64. (PMID: 23747023)
Shock. 2014 Apr;41(4):331-6. (PMID: 24430551)
Neuroscience. 2017 Mar 27;346:267-277. (PMID: 28147245)
EMBO J. 2009 Jul 22;28(14):2114-27. (PMID: 19536133)
J Cell Physiol. 2012 May;227(5):2117-22. (PMID: 21769868)
J Exp Med. 2007 May 14;204(5):1057-69. (PMID: 17485518)
المشرفين على المادة: 0 (Anti-Inflammatory Agents)
0 (Mrgprd protein, mouse)
0 (Oligopeptides)
0 (Peptide Fragments)
0 (Proto-Oncogene Mas)
0 (Proto-Oncogene Proteins)
0 (Receptors, G-Protein-Coupled)
0 (alamandine)
207137-56-2 (Interleukin-4)
9041-90-1 (Angiotensin I)
IJ3FUK8MOF (angiotensin I (1-7))
تواريخ الأحداث: Date Created: 20190329 Date Completed: 20190722 Latest Revision: 20231006
رمز التحديث: 20240628
مُعرف محوري في PubMed: PMC6409041
DOI: 10.1155/2019/2401081
PMID: 30918468
قاعدة البيانات: MEDLINE
الوصف
تدمد:1466-1861
DOI:10.1155/2019/2401081