Toll-like receptor 4 and tumor necrosis factor-alpha as diagnostic biomarkers for diabetic peripheral neuropathy

Zhu, Tao; Meng, Qingming; Ji, Jian; Lou, Xiaoli; Zhang, Lijuan

doi:10.1016/j.neulet.2014.11.020

Cited by 55 publications

(36 citation statements)

References 25 publications

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“…In accordance with recent studies [8, 18-20], through measuring plasma levels of VEGF, IL-1β, IL-6, TNF-α, and TLR4 we found that inflammatory factors and VEGF expression were higher in patients with DPN than in DN patients. These findings are in agreement with the theory that DPN may be associated with inflammation and endothelial dysfunction [21].…”

Section: Discussionsupporting

confidence: 92%

“…A combination of chronic hyperglycemia, oxidative stress, inflammation, microangiopathy of nerve blood vessels and a reduction in nerve fiber repair result in damage to the vasa nervorum, the microvessels that supply blood to neural tissue [6, 7]. High glucose can induce oxidative stress and inflammatory responses to activate the Toll-like receptor 4 (TLR4)/nuclear factor-κB (NF-KB) signal pathway, which is believed to play an important role in DPN [8]. Although glycemic control can prevent the progression of DPN, whether it has the capability of reversing the condition has not been established.…”

Section: Introductionmentioning

confidence: 99%

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Expression of Nrf2 Promotes Schwann Cell-Mediated Sciatic Nerve Recovery in Diabetic Peripheral Neuropathy

Tang

Chen

Liu

et al. 2018

Cell Physiol Biochem

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Background/Aims: High glucose-induced oxidative stress and inflammatory responses play an important role in painful diabetic neuropathy by activating the TLR4/NFκB signal pathway. Schwann cells (SCs) are integral to peripheral nerve biology, contributing to saltatory conduction along axons, nerve and axon development, and axonal regeneration. SCs provide a microenvironment favoring vascular regeneration but their low survival ratio in hyperglycemic conditions suppress the function to promote nerve growth. Nuclear factor erythroid 2-related factor 2 (Nrf2) promotes remyelination after peripheral nerve injury. The aim of this study was to identify the role of Nrf2 in SC-mediated functional recovery after sciatic nerve injury. Methods: We compared plasma inflammatory factors in diabetic patients (DN) with/without diabetic peripheral neuropathy (DPN) and assessed whether Nrf2 expression in SCs could repair peripheral nerve injury in a rat model. Nrf2, TLR4/NFκB signal pathway and apoptosis relative protein expression were detected by western blot. Apoptosis and angiogenesis were determined by immunofluorescence and tubule formation assay, respectively. Regenerated nerves were determined by transmission electron microscope. Results: Higher levels of inflammatory factors and VEGF expression were found in DPN patients. Cellular experiments indicate that Nrf2 expression inhibits hyperglycemia-induced apoptosis and promotes angiogenesis by regulating the TLR4/NFκB signal pathway. Animal experiments show that nerve conduction velocity, myelin sheath thickness, and sciatic vasa nervorum are restored with transplantation of SCs overexpressing Nrf2. Conclusions: Taken together, the high survival ratio of SCs in a DPN rat model indicates that overexpression of Nrf2 restores nerve injury.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Expression of Nrf2 Promotes Schwann Cell-Mediated Sciatic Nerve Recovery in Diabetic Peripheral Neuropathy

Tang

Chen

Liu

et al. 2018

Cell Physiol Biochem

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“…The overweight / metabolic syndrome group demonstrated a significant elevation in expression of TLR-2, TLR-4, TNF-α and IL-6 in peripheral monocytes, and increased circulating levels of TNF-α and IL-6 when compared with a overweight healthy group [24]. TLR-4 and TNF-α are potential sensitive diagnostic biomarkers for diabetic peripheral neuropathy in both general population and type 2 diabetic subjects [25]. Patients with acute coronary syndromes have an increased expression of TLR-2 and TLR-4 on circulating monocytes [26,27].…”

Section: Monocyte Surface Biomarkersmentioning

confidence: 99%

Perspectives for Monocyte/Macrophage-Based Diagnostics of Chronic Inflammation

Kzhyshkowska¹,

Gudima

Moganti

et al. 2016

Transfus Med Hemother

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Low-grade chronic inflammation underlies the development of the most dangerous cardiometabolic disorders including type 2 diabetes and its vascular complications. In contrast to acute inflammation induced by bacteria and viruses, chronic inflammation can be driven by abnormal reaction to endogenous factors, including Th2 cytokines, metabolic factors like advanced glycation end products (AGEs), modified lipoproteins, or hyperglycemia. The key innate immune cells that recognize these factors in blood circulation are monocytes. Inflammatory programming of monocytes which migrate into tissues can, in turn, result into generation of tissue macrophages with pathological functions. Therefore, determination of the molecular and functional phenotype of circulating monocytes is a very promising diagnostic tool for the identification of hidden inflammation, which can precede the development of the pathology. Here we propose a new test system for the identification of inflammatory programming of monocytes: surface biomarkers and ex vivo functional system. We summarize the current knowledge about surface biomarkers for monocyte subsets, including CD16, CCR2, CX3CR1, CD64, stabilin-1 and CD36, and their association with inflammatory human disorders. Furthermore, we present the design of an ex vivo monocyte-based test system with minimal set of parameters as a potential diagnostic tool for the identification of personalized inflammatory responses.

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“…Развивающаяся в результате гибели инсулиноцитов стойкая гипергликемия способствует повсеместному накоплению гли-кированных белков, в отношении которых также осуществляются аутоиммунные реакции. Гипер-гликемия приводит к развитию низкоинтенсив-ного системного хронического воспаления, формированию хронических осложнений СД, таких как микроангиопатии, нефропатия, рети-нопатия [1,18,42,45]. Регуляция воспалитель-ных и аутоиммунных реакций иммунокомпе-тентными клетками осуществляется посредством секреции таких провоспалительных цитокинов, как фактор некроза опухолей-альфа (TNFα), ин-терлейкин-1 (IL-1) и интерлейкин-6 (IL-6) [17,35].…”

Section: Introductionunclassified

Cytokine Regulation of Regenerative Processes in Pancreatic Gland in Alloxan-Induced Diabetic Rats, and It Correction by 1,3,4-Thiadiazine Composition and Lipoic Acid

Данилова¹,

Емельянов²,

Гетте³

et al. 2018

Med. immunol.

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Toll-like receptor 4 and tumor necrosis factor-alpha as diagnostic biomarkers for diabetic peripheral neuropathy

Cited by 55 publications

References 25 publications

Expression of Nrf2 Promotes Schwann Cell-Mediated Sciatic Nerve Recovery in Diabetic Peripheral Neuropathy

Expression of Nrf2 Promotes Schwann Cell-Mediated Sciatic Nerve Recovery in Diabetic Peripheral Neuropathy

Perspectives for Monocyte/Macrophage-Based Diagnostics of Chronic Inflammation

Cytokine Regulation of Regenerative Processes in Pancreatic Gland in Alloxan-Induced Diabetic Rats, and It Correction by 1,3,4-Thiadiazine Composition and Lipoic Acid

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