Proinflammatory monocyte polarization in type 2 diabetes mellitus and coronary heart disease

Nikita G. Nikiforov , Karina O. Galstyan , Liudmila V. Nedosugova , Natalia V. Elizova , Kira I. Kolmychkova , Ekaterina A. Ivanova

Vessel Plus ›› 2017, Vol. 1 ›› Issue (1) : 192 -5.

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Vessel Plus ›› 2017, Vol. 1 ›› Issue (1) :192 -5. DOI: 10.20517/2574-1209.2017.21
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Proinflammatory monocyte polarization in type 2 diabetes mellitus and coronary heart disease

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Abstract

Aim: Type 2 diabetes mellitus (T2DM) is associated with rapid progression of atherosclerosis. There is no doubt that inflammation is involved in atherogenesis. Recent studies showed the relationship between the development of atherosclerotic plaque formation and the amount of pro-inflammatory (M1) activated macrophages in situ.

Methods: The authors studied the ability of circulating monocytes isolated from patients with diabetes (n = 28), coronary heart disease (CHD) (n = 27) and healthy subjects (n = 50) to be activated into M1 phenotype in vitro.

Results: Increased levels of basal and stimulated secretion of tumor necrosis factor alpha (TNF-α) was observed in diabetic patients compared with healthy subjects. On the contrary, in patients with CHD, decreased secretion of the pro-inflammatory cytokine, TNF-α, was found. A direct correlation between glycated hemoglobin (HbA1c) levels in T2DM patients and basal secretion of TNF-α from monocytes was observed.

Conclusion: The authors found diametrically different responses of monocytes from T2DM and CHD under pro-inflammatory stimuli.

Keywords

Type 2 diabetes mellitus / coronary heart disease / M1/M2 monocyte polarization / oxidative stress / atherosclerosis / inflammatory

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Nikita G. Nikiforov, Karina O. Galstyan, Liudmila V. Nedosugova, Natalia V. Elizova, Kira I. Kolmychkova, Ekaterina A. Ivanova. Proinflammatory monocyte polarization in type 2 diabetes mellitus and coronary heart disease. Vessel Plus, 2017, 1(1): 192-5 DOI:10.20517/2574-1209.2017.21

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References

[1]

IDF Diabetes Atlas 7th Edition (2015). Available from: http://www.idf.org/e-library/epidemiology-research/diabetes-atlas.html. [Last accessed on 29 Sep 2017]

[2]

Kanter JE.Inflammation and diabetes-accelerated atherosclerosis: myeloid cell mediators..Trends Endocrinol Metab2013;24:137-44 PMCID:PMC3578033

[3]

Coutinho M,Wang Y.The relationship between glucose and incident of cardiovascular events. A meta regression analysis of published data from 20 studies of 93,7883 individuals followed for 12.5 years..Diabetes Care1999;22:233-40

[4]

Brownlee M.Biochemistry and molecular cell biology of diabetic complications..Nature2001;414:813-20

[5]

Evans JL,Maddux BA.Oxidative stress and stress-activated signaling pathways: a unifying hypothesis of type 2 diabetes..Endocr Rev2002;23:599-622

[6]

Lankin VZ,Arzamastseva NE,Nedosugova LV,Tikhaze AK,Kukharchuk VV.Oxidative stress in atherosclerosis and diabetes..Bull Exp Biol Med2005;140:41-3

[7]

Lavi S,Rihal CS,Mathew V,Lerman A.Local production of lipoprotein-associated phospholipase A2 and lysophosphatidylcholine in the coronary circulation: association with early coronary atherosclerosis and endothelial dysfunction in humans..Circulation2007;115:2715-21

[8]

Tousoulis D,Stefanadis C,Ambrose JA.Inflammatory and thrombotic mechanisms in coronary atherosclerosis..Heart2003;89:993-7 PMCID:PMC1767836

[9]

Bonizzi G.The two NF-kappaB activation pathways and their role in innate and adaptive immunity..Trends Immunol2004;25:280-8

[10]

Lawrence T.Chronic inflammation: a failure of resolution?.Int J Exp Pathol2007;88:85-94 PMCID:PMC2517296

[11]

MantovaniA,Locati M,Sica A.Macrophage polarization: tumor-associated macrophages as a paradigm for polarized M2 mononuclear phagocytes..Trends Immunol2002;2:549-55

[12]

Arzamastseva NE,Konovalova GG,Ageev FT,Narusov OY,Belenkov YN.Oxidative stress in patients with chronic heart failure and type 2 diabetes mellitus..Bull ExpBiol Med2007;143:207-9

[13]

Wellen KE.Inflammation, stress, and diabetes..J Clin Invest2005;115:1111-9 PMCID:PMC1087185

[14]

Neels JG.Inflamed fat: what starts the fire?.J Clin Invest2006;116:33-5 PMCID:PMC1323268

[15]

Sobenin IA,Grechko AV.Small dense and desialylated low density lipoprotein in diabetic patients..Vessel Plus2017;1:29-37

[16]

Fernandez-Real JM.Insulin resistance and chronic cardiovascular inflammatory syndrome..Endocr Rev2003;24:278-301

[17]

Xia P,Kern TS,Oates PJ.Characterisation of the mechanism for the chronic activation of diacylglycerol-protein kinase C in diabetes and hypergalactosaemia..Diabetes1994;43:1122-9

[18]

Ceolotto G,Miola M,Trevisan R,Semplicini A.Protein kinase C activity is acutely regulated by plasma glucose concentration in human monocytes in vivo..Diabetes1999;48:1316-22

[19]

Jin X,Zhou Z,Zhang S,Shen C.Advanced glycation end products enhance macrophages polarization into M1 phenotype through activating RAGE/NF-kB pathway..Bio Med Res Int2015;2015:732450

[20]

Bouhlel MA,Rigamonti E,Brozek J,Zawadzki C,Torpier G,Staels B.PPARgamma activation primes human monocytes into alternative M2 macrophages with anti-inflammatory properties..Cell Metab2007;6:137-43

[21]

Kraakman MJ,Jandeleit-Dahm K.Macrophage polarization in obesity and type 2 diabetes: weighing down our understanding of macrophage function?.Front Immunol2014;470:1-6

[22]

Ivanova EA.Monocyte activation in immunopathology: cellular test for development of diagnostics and therapy..J Immunol Res2016;2016:4789279

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