دورية أكاديمية
Temporal changes in glucose metabolism reflect polarization in resident and monocyte-derived macrophages after myocardial infarction.
| العنوان: | Temporal changes in glucose metabolism reflect polarization in resident and monocyte-derived macrophages after myocardial infarction. |
|---|---|
| المؤلفون: | Mouton AJ; Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, United States.; Mississippi Center for Obesity Research, University of Mississippi Medical Center, Jackson, United States., Aitken NM; Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, United States., Moak SP; Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, United States., do Carmo JM; Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, United States.; Mississippi Center for Obesity Research, University of Mississippi Medical Center, Jackson, United States., da Silva AA; Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, United States.; Mississippi Center for Obesity Research, University of Mississippi Medical Center, Jackson, United States., Omoto ACM; Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, United States.; Mississippi Center for Obesity Research, University of Mississippi Medical Center, Jackson, United States., Li X; Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, United States.; Mississippi Center for Obesity Research, University of Mississippi Medical Center, Jackson, United States., Wang Z; Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, United States.; Mississippi Center for Obesity Research, University of Mississippi Medical Center, Jackson, United States., Schrimpe-Rutledge AC; Department of Chemistry and Center for Innovative Technology, Vanderbilt University, Nashville, TN, United States., Codreanu SG; Department of Chemistry and Center for Innovative Technology, Vanderbilt University, Nashville, TN, United States., Sherrod SD; Department of Chemistry and Center for Innovative Technology, Vanderbilt University, Nashville, TN, United States., McLean JA; Department of Chemistry and Center for Innovative Technology, Vanderbilt University, Nashville, TN, United States., Hall JE; Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, United States.; Mississippi Center for Obesity Research, University of Mississippi Medical Center, Jackson, United States. |
| المصدر: | Frontiers in cardiovascular medicine [Front Cardiovasc Med] 2023 May 05; Vol. 10, pp. 1136252. Date of Electronic Publication: 2023 May 05 (Print Publication: 2023). |
| نوع المنشور: | Journal Article |
| اللغة: | English |
| بيانات الدورية: | Publisher: Frontiers Media S.A Country of Publication: Switzerland NLM ID: 101653388 Publication Model: eCollection Cited Medium: Print ISSN: 2297-055X (Print) Linking ISSN: 2297055X NLM ISO Abbreviation: Front Cardiovasc Med Subsets: PubMed not MEDLINE |
| أسماء مطبوعة: | Original Publication: Lausanne : Frontiers Media S.A., [2014]- |
| مستخلص: | Introduction: Metabolic reprogramming from glycolysis to the mitochondrial tricarboxylic acid (TCA) cycle and oxidative phosphorylation may mediate macrophage polarization from the pro-inflammatory M1 to the anti-inflammatory M2 phenotype. We hypothesized that changes in cardiac macrophage glucose metabolism would reflect polarization status after myocardial infarction (MI), ranging from the early inflammatory phase to the later wound healing phase. Methods: MI was induced by permanent ligation of the left coronary artery in adult male C57BL/6J mice for 1 (D1), 3 (D3), or 7 (D7) days. Infarct macrophages were subjected to metabolic flux analysis or gene expression analysis. Monocyte versus resident cardiac macrophage metabolism was assessed using mice lacking the Ccr2 gene (CCR2 KO). Results: By flow cytometry and RT-PCR, D1 macrophages exhibited an M1 phenotype while D7 macrophages exhibited an M2 phenotype. Macrophage glycolysis (extracellular acidification rate) was increased at D1 and D3, returning to basal levels at D7. Glucose oxidation (oxygen consumption rate) was decreased at D3, returning to basal levels at D7. At D1, glycolytic genes were elevated (Gapdh, Ldha, Pkm2), while TCA cycle genes were elevated at D3 (Idh1 and Idh2) and D7 (Pdha1, Idh1/2, Sdha/b). Surprisingly, Slc2a1 and Hk1/2 were increased at D7, as well as pentose phosphate pathway (PPP) genes (G6pdx, G6pd2, Pgd, Rpia, Taldo1), indicating increased PPP activity. Macrophages from CCR2 KO mice showed decreased glycolysis and increased glucose oxidation at D3, and decreases in Ldha and Pkm2 expression. Administration of dichloroacetate, a pyruvate dehydrogenase kinase inhibitor, robustly decreased pyruvate dehydrogenase phosphorylation in the non-infarcted remote zone, but did not affect macrophage phenotype or metabolism in the infarct zone. Discussion: Our results indicate that changes in glucose metabolism and the PPP underlie macrophage polarization following MI, and that metabolic reprogramming is a key feature of monocyte-derived but not resident macrophages. Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. (© 2023 Mouton, Aitken, Codreanu, Sherrod, McLean, Moak, do Carmo, da Silva, Omoto, Li, Wang, Schrimpe-Rutledge and Hall.) |
| References: | Int J Mol Sci. 2020 May 08;21(9):. (PMID: 32397287) Basic Res Cardiol. 2018 Jun 4;113(4):26. (PMID: 29868933) Biochim Biophys Acta. 2013 Apr;1833(4):945-53. (PMID: 22982064) Nat Med. 2015 Mar;21(3):263-9. (PMID: 25686106) J Clin Invest. 2018 May 1;128(5):2127-2143. (PMID: 29664017) Circ Res. 2019 Jan 18;124(2):263-278. (PMID: 30582448) Proc Natl Acad Sci U S A. 2014 Nov 11;111(45):16029-34. (PMID: 25349429) Proc Natl Acad Sci U S A. 2018 May 15;115(20):E4661-E4669. (PMID: 29712858) Circ Res. 2020 Mar 13;126(6):789-806. (PMID: 32163341) Circulation. 1997 Jan 21;95(2):313-5. (PMID: 9008441) Immunity. 2014 Jan 16;40(1):91-104. (PMID: 24439267) Front Immunol. 2015 Apr 08;6:164. (PMID: 25904920) JACC Basic Transl Sci. 2019 Jun 24;4(3):385-400. (PMID: 31312761) Eur J Nucl Med Mol Imaging. 2015 Apr;42(5):771-80. (PMID: 25389013) Circ Res. 2014 Jul 7;115(2):284-95. (PMID: 24786973) Cell Metab. 2012 Jun 6;15(6):813-26. (PMID: 22682222) J Mol Cell Cardiol. 2013 Sep;62:24-35. (PMID: 23644221) Immunity. 2015 Mar 17;42(3):419-30. (PMID: 25786174) Am J Physiol Heart Circ Physiol. 2021 Dec 1;321(6):H1056-H1073. (PMID: 34623181) Metabolites. 2020 Mar 30;10(4):. (PMID: 32235559) Biomedicines. 2022 Mar 12;10(3):. (PMID: 35327464) Discoveries (Craiova). 2015 Jan-Mar;3(1):. (PMID: 26273700) Blood. 2020 Sep 24;136(13):1535-1548. (PMID: 32556090) J Immunol. 2015 Jun 15;194(12):6082-9. (PMID: 25964487) Cell Metab. 2019 Feb 5;29(2):443-456.e5. (PMID: 30595481) Toxicol Sci. 2019 Feb 1;167(2):604-617. (PMID: 30371859) Cardiovasc Res. 2014 Jan 1;101(1):30-8. (PMID: 24048945) Cell. 2011 Sep 16;146(6):980-91. (PMID: 21925319) Front Immunol. 2019 Jul 03;10:1462. (PMID: 31333642) J Mol Cell Cardiol. 2021 Sep;158:38-48. (PMID: 34023353) Cardiovasc Res. 2012 May 1;94(2):359-69. (PMID: 22436846) Am J Physiol Heart Circ Physiol. 2008 Sep;295(3):H939-H945. (PMID: 18660443) Basic Res Cardiol. 2018 Aug 21;113(5):40. (PMID: 30132266) Basic Res Cardiol. 2019 Jan 11;114(2):6. (PMID: 30635789) Nat Commun. 2016 May 18;7:11635. (PMID: 27189088) Cell Rep. 2017 Aug 15;20(7):1654-1666. (PMID: 28813676) J Mol Cell Biol. 2020 Jul 1;12(7):543-555. (PMID: 31900478) Nat Immunol. 2017 Sep;18(9):985-994. (PMID: 28714978) Am J Physiol Heart Circ Physiol. 2018 Jul 1;315(1):H71-H79. (PMID: 29600895) J Exp Med. 2021 Sep 6;218(9):. (PMID: 34325467) Front Cardiovasc Med. 2022 Apr 25;9:889963. (PMID: 35548425) Proc Natl Acad Sci U S A. 2013 May 7;110(19):7820-5. (PMID: 23610393) Circulation. 2022 Feb 22;145(8):e153-e639. (PMID: 35078371) Front Immunol. 2019 May 07;10:944. (PMID: 31134063) Am J Pathol. 2004 Aug;165(2):439-47. (PMID: 15277218) Nat Immunol. 2019 Jan;20(1):29-39. (PMID: 30538339) JCI Insight. 2020 Sep 3;5(17):. (PMID: 32879134) PLoS One. 2017 Jun 23;12(6):e0180115. (PMID: 28644903) Transl Res. 2018 Jan;191:15-28. (PMID: 29106912) Circ Res. 2018 Apr 13;122(8):1084-1093. (PMID: 29440071) Cell. 2016 Oct 6;167(2):457-470.e13. (PMID: 27667687) |
| معلومات مُعتمدة: | P20 GM104357 United States GM NIGMS NIH HHS; R01 DK121411 United States DK NIDDK NIH HHS; R01 HL163076 United States HL NHLBI NIH HHS; U54 GM115428 United States GM NIGMS NIH HHS |
| فهرسة مساهمة: | Keywords: glycolysis; heart failure; immunometabolism; inflammation; macrophage |
| تواريخ الأحداث: | Date Created: 20230522 Latest Revision: 20240604 |
| رمز التحديث: | 20240604 |
| مُعرف محوري في PubMed: | PMC10196495 |
| DOI: | 10.3389/fcvm.2023.1136252 |
| PMID: | 37215542 |
| قاعدة البيانات: | MEDLINE |
Full Text Finder كن أول من يترك تعليقا!