Role of T Cells in Type 2 Diabetic Nephropathy

Wu, Chia Chao; Sytwu, Huey Kang; Lu, Kuo Cheng; Lin, Yuh Feng

doi:10.1155/2011/514738

Cited by 69 publications

(63 citation statements)

References 106 publications

(142 reference statements)

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“…Circulating leukocytes use endothelial cell transmembrane ICAM-1 as an anchor to transmigrate and cause inflammation (Nayak, 2005). Activation of renal endothelial cell ICAM-1 expression by hyperglycemia along with subsequent leukocyte infiltration has been suggested to be an important event in the pathophysiology of tubular inflammation in DN (Fornoni et al, 2008;Soetikno et al, 2011;Wu et al, 2011;Lin et al, 2012). We observed that suramin intervention after induction of diabetes decreased phosphorylation of p65, blocked ICAM-1 expression, and decreased leukocyte infiltration.…”

Section: Downloaded Fromsupporting

confidence: 48%

Diabetes-Induced Renal Injury in Rats Is Attenuated by Suramin

Korrapati

Shaner²,

Neely³

et al. 2012

J Pharmacol Exp Ther

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Progression of hyperglycemia-induced renal injury is a contributing factor for diabetic nephropathy (DN)-induced end-stage renal disease (ESRD), and development of novel therapeutic strategies that act early to prevent progression of DN and ESRD are important. We examined the efficacy and mechanism(s) of suramin on hyperglycemia-induced renal injury before development of overt histological damage. Two groups of male Sprague-Dawley rats received streptozotocin (STZ) and one group received saline. Three weeks later, one STZ group received suramin (10 mg/kg). All animals were euthanized 1 week later (4 weeks). Although there was a decrease in creatinine clearance between control and STZ Ϯ suramin rats, there was no difference in creatinine clearance between STZ rats Ϯ suramin intervention. Liquid chromatography-tandem mass spectroscopy-based analysis revealed increases in urinary proteins that are early indicators of DN (e.g., cystatin C, clusterin, cathepsin B, retinol binding protein 4, and peroxiredoxin-1) in the STZ group, which were blocked by suramin. Endothelial intracellular adhesion molecule-1 (ICAM-1) activation, leukocyte infiltration, and inflammation; transforming growth factor-␤1 (TGF-␤1) signaling; TGF-␤1/SMAD-3-activated fibrogenic markers fibronectin-1, ␣-smooth muscle actin, and collagen 1A2; activation of proinflammatory and profibrotic transcription factors nuclear factor-B (NF-B) and signal transducer and activator of transcription factor-3 (STAT-3), respectively, were all increased in STZ rats and suramin blocked these changes. In conclusion, delayed administration of suramin attenuated 1) urinary markers of DN, 2) inflammation by blocking NF-B activation and ICAM-1-mediated leukocyte infiltration, and 3) fibrosis by blocking STAT-3 and TGF-␤1/ SMAD-3 signaling. These results support the potential use of suramin in DN.

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Section: Downloaded Fromsupporting

confidence: 48%

Diabetes-Induced Renal Injury in Rats Is Attenuated by Suramin

Korrapati

Shaner²,

Neely³

et al. 2012

J Pharmacol Exp Ther

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“…Recently it is believed that DM is a chronic inflammatory disease, and anti-inflammation may prevent the progression of the complications such as DN [6,7]. Studies have shown that P-selectin may be involved in the pathogenesis of DN, and may become a novel target of DN therapy [8,9].…”

Section: Introductionmentioning

confidence: 99%

Effects of Magnoline on P-Selectin's Expression in Diabetic Rats and its Reno-Protection

Zhou

Wang

Hao

et al. 2013

Kidney Blood Press Res

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Background and Objective: Magnoline is an active ingredient of magnolia fargesii with anti-inflammatory and anti-platelet effects. The objective is to explore the renoprotection of magnoline in diabetic rats and its effects on P-selectin. Methods: Thirty-six rats were randomized into 4 groups—normal control group (C), diabetic group (D), small-dose magnoline treatment group (M1) and large-dose magnoline treatment group (M2) (n=9 in each group). Streptozotocin was selected to construct diabetic rat model, and group M1 and group M2 were treated with magnoline 0.5mg/Kg.d and 2mg/Kg.d respectively. Urinary albumin excretion rate, renal function, levels of P-selectin and TGF-β1 were observed after 16 weeks. Results: Levels of albuminuria and serum creatinine of group M1 (1078.9 ± 77.3μg/24h, 29.7 ± 3.9μmol/L) and M2 (852.9 ± 80.1μg/24h, 30.9 ± 2.9μmol/L) were lower than group D (1572.8 ± 176.2μg/24h, 39.4 ± 4.1μmol/L) (P <0.05). Serum levels of P-selectin in group M1 and M2 were lower than group D (P <0.05). The renal expression of P-selectin and TGF-β1 in group M1 and M2 were significantly attenuated respectively. Conclusions: Magnoline has reno-protective effects on diabetic rats which may be related to the inhibition of P-selectin.

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“…It is highly probable that hemodynamic factors in DN may trigger the inflammatory responses and cytokine production [21]. Hemodynamic factors imply the activation of various vasoactive hormone systems, such as the renin-angiotensin-aldosterone and endothelin systems.…”

Section: Hemodynamic Factorsmentioning

confidence: 99%

Microinflammation as a Candidate for Diabetic Nephropathy

hafez

2014

Interdiscip J Microinflammation

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Diabetic Nephropathy (DN) is a major cause of mortality in patients with Type 1 and 2 diabetes throughout the world. This review draws attention to the important role of microinflammation and the complex pathways implicated in the development and progression of DN. These pathways include the collaboration of metabolic, hemodynamic and hormonal factors with oxidative stress in patients with genetic susceptibility to create an inflammatory milieu. The key role of inflammatory cells in the kidney, particularly infiltrating macrophages and T-lymphocytes is highlighted. The major inflammatory cytokines and chemokines, receptors, adhesion molecules as well as transcription factors and transduction pathways involved in the pathogenesis of DN are also discussed. Understanding of these inflammatory pathways guides important therapeutic appliances and improves the discovery of new therapeutic targets that can be translated into clinical treatments for DN.

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Role of T Cells in Type 2 Diabetic Nephropathy

Cited by 69 publications

References 106 publications

Diabetes-Induced Renal Injury in Rats Is Attenuated by Suramin

Diabetes-Induced Renal Injury in Rats Is Attenuated by Suramin

Effects of Magnoline on P-Selectin's Expression in Diabetic Rats and its Reno-Protection

Microinflammation as a Candidate for Diabetic Nephropathy

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