Identification of megakaryocytes as a target of advanced glycation end products in diabetic complications in bone marrow

Wang, Benfang; Yu, Jianjiang; Wang, Ting; Shen, Ying; Lin, Dandan; Xu, Xin

doi:10.1007/s00592-018-1109-z

Cited by 5 publications

(3 citation statements)

References 49 publications

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“…This appears to be a plausible explanation since microvascular damage in DM is likely to impact perfusion to the bone marrow as well as abnormal levels of cytokines related to widespread inflammation in DM [ 61 , 67 , 68 ]. Notably, some evidence shows that the accumulation of advanced glycation end products (AGEs) in DM can also influence hematopoiesis in the bone marrow [ 69 ]. Whether or not this mechanism directly affects RBC progenitors is unknown.…”

Section: Multifactorial Mechanisms Of Rbc Dysfunction and Anemia In D...mentioning

confidence: 99%

Pathophysiology of Red Blood Cell Dysfunction in Diabetes and Its Complications

et al. 2023

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Diabetes Mellitus (DM) is a complex metabolic disorder associated with multiple microvascular complications leading to nephropathy, retinopathy, and neuropathy. Mounting evidence suggests that red blood cell (RBC) alterations are both a cause and consequence of disturbances related to DM-associated complications. Importantly, a significant proportion of DM patients develop varying degrees of anemia of confounding etiology, leading to increased morbidity. In chronic hyperglycemia, RBCs display morphological, enzymatic, and biophysical changes, which in turn prime them for swift phagocytic clearance from circulation. A multitude of endogenous factors, such as oxidative and dicarbonyl stress, uremic toxins, extracellular hypertonicity, sorbitol accumulation, and deranged nitric oxide metabolism, have been implicated in pathological RBC changes in DM. This review collates clinical laboratory findings of changes in hematology indices in DM patients and discusses recent reports on the putative mechanisms underpinning shortened RBC survival and disturbed cell membrane architecture within the diabetic milieu. Specifically, RBC cell death signaling, RBC metabolism, procoagulant RBC phenotype, RBC-triggered endothelial cell dysfunction, and changes in RBC deformability and aggregation in the context of DM are discussed. Understanding the mechanisms of RBC alterations in DM provides valuable insights into the clinical significance of the crosstalk between RBCs and microangiopathy in DM.

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Section: Multifactorial Mechanisms Of Rbc Dysfunction and Anemia In D...mentioning

confidence: 99%

Pathophysiology of Red Blood Cell Dysfunction in Diabetes and Its Complications

et al. 2023

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“…It has been shown that two different models of diabetes in rats show different phenotypes of platelet response . Also, recently published report on alterations in profile of protein expression in megakaryocytes and platelet generation in STZ‐induced diabetic and in ob/ob diabetic mice revealed that these two models differ in this aspect . It implicates that platelet hyperreactivity in diabetes is a complex phenomenon, which is influenced by a plethora of factors which vary with the type of diabetes and its associated alterations.…”

Section: Discussionmentioning

confidence: 99%

“…How diabetes influences expression of COX‐1 in platelets remains to be elucidated. It has been recently published that bovine serum albumin modified by advanced glycation end products significantly altered expression of certain proteins including platelet factor 4 in cultured megakaryocytes . It suggests that long‐term hyperglycaemia can indirectly affect protein profile in platelets produced by megakaryocytes.…”

Section: Discussionmentioning

confidence: 99%

Effects of three‐month streptozotocin‐induced diabetes in mice on blood platelet reactivity, COX‐1 expression and adhesion potential

Przygodzki

Kassassir

Talar

et al. 2019

Int J Experimental Path

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Diabetes is associated with an increased risk of cardiovascular disease. This is partially attributed to an altered activation status of blood platelets in this disease. Previously, alterations have been shown in COX-1 and protease activated receptor (PAR)-3 receptor expression in platelets in two animal models of diabetes, there have not been studies which address expression of these proteins in mice with long-term streptozotocin (STZ)-induced diabetes. We have also addressed the effect of diabetes on platelet adhesion under flow conditions. With the use of flow cytometry, we have shown that certain markers of platelet basal activation, such as active form of α IIb β 3 and of CD40L were increased in STZ-induced diabetic mice. Platelets from STZ-induced diabetic mice were also more reactive when stimulated with PAR-4 activating peptide as revealed by higher expression of active form of α IIb β 3 , membrane-bound on vWillebrand Factor and binding of exogenous fluorescein isothyanate-labelled fibrinogen.Expression of COX-1 and production of thromboxane A 2 in platelets of STZ-induced diabetic mice were higher than in control animals. We observed no effect of diabetes on ability of platelets to form stable adhesions with fibrinogen in flow conditions. We conclude that although certain similarities exist between patterns of activation of platelets in animal models of diabetes, the differences should also be taken into account. K E Y W O R D Scell adhesion, diabetes, platelets, prostanoids 42 | PRZYGODZKI et al.

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