Proinflammatory and atherogenic activity of monocytes in Type 2 diabetes

Gacka, Małgorzata; Dobosz, Tadeusz; Szymaniec, S; Bednarska-Chabowska, Dorota; Adamiec, Rajmund; Sadakierska‐Chudy, Anna

doi:10.1016/j.jdiacomp.2008.07.001

Cited by 19 publications

(18 citation statements)

References 30 publications

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“…Also miR-146a, which is a classical microRNA dampening inflammatory responses and earlier found as down-regulated in monocytes and macrophages of patients with (auto-)inflammatory conditions [38], was not reduced in the monocytes of our T2D Ecuadorian cases as compared to the non-diabetic controls (it was also not identified in the finding cohort). Our current data thus refute the earlier expressed views in literature [15], and by us [21], that circulating monocytes of T2D patients are in general characterized by a pro-inflammatory state.…”

Section: Discussionsupporting

confidence: 89%

“…There is however a relative paucity in reports on the state of activation of circulating monocytes in patients with the MetS [13,14] and T2D [15]. In general this state of activation is thought to be pro-inflammatory and increases in pattern recognition receptors (TLRs, NOD-like receptors), oxidative stress and the machinery for the production of pro-inflammatory cytokines have been described [16,17].…”

Section: Introductionmentioning

confidence: 99%

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Type 2 Diabetes Monocyte MicroRNA and mRNA Expression: Dyslipidemia Associates with Increased Differentiation-Related Genes but Not Inflammatory Activation

et al. 2015

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There is increasing evidence that inflammatory macrophages in adipose tissue are involved in insulin resistance of type 2 diabetes (T2D). Due to a relative paucity of data on circulating monocytes in T2D, it is unclear whether the inflammatory changes of adipose tissue macrophages are reflected in these easily accessible cells.ObjectiveTo study the expression pattern of microRNAs and mRNAs related to inflammation in T2D monocytes.DesignA microRNA finding study on monocytes of T2D patients and controls using array profiling was followed by a quantitative Real Time PCR (qPCR) study on monocytes of an Ecuadorian validation cohort testing the top over/under-expressed microRNAs. In addition, monocytes of the validation cohort were tested for 24 inflammation-related mRNAs and 2 microRNAs previously found deregulated in (auto)-inflammatory monocytes.ResultsIn the finding study, 142 significantly differentially expressed microRNAs were identified, 15 having the strongest power to discriminate T2D patients from controls (sensitivity 66%, specificity 90%). However, differences in expression of these microRNAs between patients and controls were small. On the basis of >1.4 or <0.6-fold change expression 5 microRNAs were selected for further validation. One microRNA (miR-34c-5p) was validated as significantly over-expressed in T2D monocytes. In addition, we found over expression of 3 mRNAs (CD9, DHRS3 and PTPN7) in the validation cohort. These mRNAs are important for cell morphology, adhesion, shape change, and cell differentiation. Classical inflammatory genes (e.g. TNFAIP3) were only over-expressed in monocytes of patients with normal serum lipids. Remarkably, in dyslipidemia, there was a reduction in the expression of inflammatory genes (e.g. ATF3, DUSP2 and PTGS2).ConclusionsThe expression profile of microRNAs/mRNAs in monocytes of T2D patients indicates an altered adhesion, differentiation, and shape change potential. Monocyte inflammatory activation was only found in patients with normal serum lipids. Abnormal lipid values coincided with a reduced monocyte inflammatory state.

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Section: Discussionsupporting

confidence: 89%

Section: Introductionmentioning

confidence: 99%

Type 2 Diabetes Monocyte MicroRNA and mRNA Expression: Dyslipidemia Associates with Increased Differentiation-Related Genes but Not Inflammatory Activation

et al. 2015

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“…Granulocytes and monocytes contribute to progression of atherosclerotic plaques (Hatanaka et al 2006;Weber et al 2008), and activation of monocytes has been demonstrated to occur in both type 1 and type 2 diabetes (Cipolletta et al 2005). Production of reactive oxygen species in monocytes is increased in patients with type 2 diabetes compared with that in non-diabetic people (Chang and Shaio 1995), and expression levels of inflammatory cytokines, such as tumor necrosis factor-␣, interleukin (IL)-1, IL-6 and IL-8, are higher in patients with type 2 diabetes than in nondiabetic people (Gacka et al 2008;Giulietti et al 2007). Intracellular signal transducers, including nuclear factor-B (NF-B) and extracellular signal-regulated kinase (ERK), are known to be involved in production of the above cytokines in leukocytes (Ghosh and Hayden 2008;Giraldo et al 2010;Guha and Mackman 2001;Li and Verma 2002;Vallabhapurapu and Karin 2009).…”

Section: Introductionmentioning

confidence: 99%

Attenuated phagocytic activity of monocytes in type 2 diabetic Goto–Kakizaki rats

2011

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“…Multiple studies have postulated different mechanism pathways explaining the potential association between established diabetes and periodontal diseases [27][28][29][30][31][32] . Patients with diabetic mellitus have a higher risk for periodontitis development, probably because of vascular changes, neutrophil dysfunction, altered systemic inflammatory responses 33 , altered collagen synthesis, microbiotic factors or genetic predisposition 34,35 .…”

Section: Discussionmentioning

confidence: 99%

Potential association between prediabetic conditions and gingival and/or periodontal inflammation

Andriankaja¹,

Joshipura²

2013

J of Diabetes Invest

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Aims/Introduction Prediabetic conditions, which include impaired fasting glucose (IFG) and impaired glucose tolerance (IGT), might be associated with chronic gingival and/or periodontal inflammation. However, the occurrence of this oral inflammation in prediabetic conditions is poorly understood. The present study aimed to assess the association between prediabetes and gingival and/or periodontal inflammation. Materials and Methods A total of 94 Puerto Rican men and women aged 40–65 years, who were residents of San Juan, Puerto Rico, and free of diabetes, were included in the study. All participants had at least one tooth site with clinical attachment loss ≥3 mm. Fasting and 2-h plasma glucose were collected. Gingival/periodontal inflammation was assessed by bleeding on gentle probing of the sulcus at six sites per tooth. Results Participants with the percentage of teeth with bleeding on probing (BOP) equal to or greater than the median were compared with those with the percentage of teeth with BOP less than median. Participants with high BOP tended to present higher IFG (odds ratio [OR] 5.5, 95% confidence interval [CI] 1.2–25.3) and/or prediabetic condition (OR 3.6, 95% CI 1.0–13.2) than those with a low percentage of BOP, adjusting for age, sex, smoking, alcohol consumption, waist circumference and number of missing teeth. Using the continuous form of the outcome, the corresponding adjusted least squares means of percentage of BOP were 26.8 (standard error of the mean [SEM] 2.3) and 43.8 (SEM 6.0) in normal and IFG, respectively (P = 0.01), and 27.0 (SEM 2.4) and 39.0 (SEM 5.3) among healthy and prediabetic individuals, respectively (P = 0.05). Conclusion IFG and/or prediabetes are strongly associated with BOP, a marker of chronic gingival/periodontal inflammation.

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Proinflammatory and atherogenic activity of monocytes in Type 2 diabetes

Cited by 19 publications

References 30 publications

Type 2 Diabetes Monocyte MicroRNA and mRNA Expression: Dyslipidemia Associates with Increased Differentiation-Related Genes but Not Inflammatory Activation

Type 2 Diabetes Monocyte MicroRNA and mRNA Expression: Dyslipidemia Associates with Increased Differentiation-Related Genes but Not Inflammatory Activation

Attenuated phagocytic activity of monocytes in type 2 diabetic Goto–Kakizaki rats

Potential association between prediabetic conditions and gingival and/or periodontal inflammation

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