Abnormal expression and function of Dectin-1 receptor in type 2 diabetes mellitus patients with poor glycemic control (HbA1c &gt; 8%)

Cortez-Espinosa, Nancy; García-Hernández, Mariana Haydee; Reynaga-Hernández, Elizabeth; Cortés-García, Juan D.; Corral-Fernández, Nancy E.; Rodríguez-Rivera, Jaime Guillermo; Bravo-Ramírez, Anamaría; González‐Amaro, Roberto; Portales-Pérez, Diana Patricia

doi:10.1016/j.metabol.2012.03.020

Cited by 17 publications

(24 citation statements)

References 42 publications

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“…In addition, it has been reported that Dectin-1 has relationships with not only innate immunity but also autoimmune diseases (67)(68)(69), allergic diseases (29,70), and metabolic diseases (71), indicating that mast cells may contribute to and offer new insights into these diseases.…”

Section: Discussionmentioning

confidence: 99%

Dectin-1-mediated Signaling Leads to Characteristic Gene Expressions and Cytokine Secretion via Spleen Tyrosine Kinase (Syk) in Rat Mast Cells

Kimura

Chihara

Honjoh

et al. 2014

Journal of Biological Chemistry

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Background: ␤-Glucan receptor Dectin-1 in dendritic cells and macrophages plays important roles in antifungal immunity. Results: Dectin-1 is expressed in rat mast cells, and its tyrosine phosphorylation induces characteristic gene expression of transcription factors and cytokines through protein-tyrosine kinase Syk. Conclusion: Dectin-1 functions in rat mast cells. Significance: Dectin-1-mediated signaling in mast cells may contribute to antifungal immunity.

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Section: Discussionmentioning

confidence: 99%

Dectin-1-mediated Signaling Leads to Characteristic Gene Expressions and Cytokine Secretion via Spleen Tyrosine Kinase (Syk) in Rat Mast Cells

Kimura

Chihara

Honjoh

et al. 2014

Journal of Biological Chemistry

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“…It could be hypothesized that CLRs may also be able to recognize similar carbohydrate structures on endogenous (so far unknown) ligands in hyperglycemic/diabetic patients, such as AGEs. Within this respect, it is interesting that expression of the CLR Dectin-1 is increased on circulating monocytes from patients with diabetes as compared to healthy controls [59]. …”

Section: Can Trained Immunity Contribute To Atherosclerosis In Diabetmentioning

confidence: 99%

Diabetes propels the risk for cardiovascular disease: sweet monocytes becoming aggressive?

Diepen

Thiem

Stienstra

et al. 2016

Cell. Mol. Life Sci.

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Diabetes strongly predisposes to cardiovascular disease (CVD), the leading cause of mortality in these patients, as well as in the entire population. Hyperglycemia is an important cardiovascular risk factor as shown by the observation that even transient periods of hyperglycemia, despite return to normoglycemia during follow-up, increase the risk for CVD, a phenomenon termed ‘hyperglycemic memory’. The molecular mechanisms underlying this phenomenon remain largely unknown. As inflammation plays an important role in the pathogenesis of atherosclerosis, we propose that long-term functional reprogramming of monocytes and macrophages, induced by hyperglycemia, plays an important role in the phenomenon of hyperglycemic memory leading to cardiovascular complications in patients with diabetes. In this review, we discuss recent insights showing that innate immune cells possess the capacity to reprogram their function through epigenetically mediated rewiring of gene transcription, a process termed ‘trained immunity’. The long-term reprogramming of monocytes can be induced by microbial as well as metabolic products, and involves a shift in cellular metabolism from oxidative phosphorylation to aerobic glycolysis. We hypothesize that hyperglycemia in diabetes patients induces long-term activation of monocytes and macrophages through similar mechanisms, thereby contributing to plaque development and subsequent macrovascular complications.

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“…Patients with T2D exhibit increased markers of endoplasmic reticulum (ER) stress (i.e. 78 kDa glucose regulated protein (GRP78) and CCAAT/-enhancerbinding protein homologous protein (CHOP); Komura et al 2010;Mozzini et al 2015) and oxidative stress (Avogaro et al 2003;Farah et al 2008;Huang et al 2011;Cortez-Espinosa et al 2012;He et al 2013;Mandal et al 2013;Paneni et al 2015) in circulating monocytes and peripheral blood mononuclear cells (PBMCs). A potential mechanism by which monocyte-derived ROS are increased in T2D is ER stress (Lenin et al 2012).…”

Section: Introductionmentioning

confidence: 99%

Increased monocyte‐derived reactive oxygen species in type 2 diabetes: role of endoplasmic reticulum stress

Restaino

Deo

Parrish

et al. 2017

Experimental Physiology

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Recent evidence suggests that exposure of human monocytes to glucolipotoxic media to mimic the composition of plasma of patients with type 2 diabetes (T2D) results in the induction of endoplasmic reticulum stress markers and formation of reactive oxygen species (ROS). The extent to which these findings translate to patients with T2D remains unclear. Thus, we first measured ROS (dihydroethidium fluorescence) in peripheral blood mononuclear cells (PBMCs) from whole blood of T2D patients (n=8) and compared to age matched healthy controls (n=8). T2D patients exhibited greater basal intracellular ROS (mean±SD, +3.4±1.4 fold; p<0.05) compared to controls. Next, increased ROS in PBMCs isolated from T2D patients was partially recapitulated in cultured human monocytes (THP-1 cells) exposed to plasma from T2D patients for 36 hours (+1.3±0.08 fold vs. plasma from controls; p<0.05). In addition, we found that increased ROS formation in THP-1 cells treated with T2D plasma was NADPH oxidase-derived and led to increased endothelial cell adhesion (+1.8±0.5 fold; p<0.05) and lipid uptake (+1.3±0.3 fold; p<0.05). Notably, we found that T2D plasma-induced monocyte ROS and downstream functional effects were abolished by treating cells with tauroursodeoxycholic acid, a chemical chaperone known to inhibit ER stress. Collectively, these data indicate that monocyte ROS production with T2D can be, in part, attributed to signals from the circulating environment. Furthermore, an interplay between ER stress and NADPH oxidase activity contributes to ROS production and may be a mechanism mediating endothelial cell adhesion and foam cell formation in T2D.

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Abnormal expression and function of Dectin-1 receptor in type 2 diabetes mellitus patients with poor glycemic control (HbA1c > 8%)

Cited by 17 publications

References 42 publications

Dectin-1-mediated Signaling Leads to Characteristic Gene Expressions and Cytokine Secretion via Spleen Tyrosine Kinase (Syk) in Rat Mast Cells

Dectin-1-mediated Signaling Leads to Characteristic Gene Expressions and Cytokine Secretion via Spleen Tyrosine Kinase (Syk) in Rat Mast Cells

Diabetes propels the risk for cardiovascular disease: sweet monocytes becoming aggressive?

Increased monocyte‐derived reactive oxygen species in type 2 diabetes: role of endoplasmic reticulum stress

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