Association of monocyte chemoattractant protein-1 with renal tubular damage in diabetic nephropathy

Morii, Tsukasa; Fujita, Hiroki; Narita, Takuma; Shimotomai, Takashi; Fujishima, Hiromi; Yoshioka, Naomi; Imai, Hirokazu; Kakei, Masafumi; Ito, Seiki

doi:10.1016/s1056-8727(02)00176-9

Cited by 165 publications

(155 citation statements)

References 21 publications

Supporting

Mentioning

135

Contrasting

Unclassified

Order By: Relevance

“…In diabetic kidneys, Ccl2 expression increases with macrophage accumulation and disease progression [4] and appears to be dependent on both the diabetic milieu [18] and activation of the renin-angiotensin system [19]. In addition, urine MCP-1 levels correlate with albuminuria during human diabetic nephropathy [18,20]. Therefore, MCP-1 may play a key role in the development of both type 2 diabetes and its associated nephropathy.…”

mentioning

confidence: 99%

Monocyte chemoattractant protein-1-induced tissue inflammation is critical for the development of renal injury but not type 2 diabetes in obese db/db mice

et al. 2006

View full text Add to dashboard Cite

Aims/hypothesis Tissue macrophage accumulation is thought to induce insulin resistance during obesity and stimulate the progression of diabetic nephropathy. Monocyte chemoattractant protein-1 (MCP-1) is a potent stimulator of macrophage recruitment. It is increased in adipose tissue during obesity and in diabetic kidneys, suggesting that inflammation of these tissues may be MCP-1-dependent. Based on these findings, the aim of this study was to examine whether a deficiency in MCP-1 would alter the development of type 2 diabetes and its renal complications. Materials and methods The role of MCP-1 in the progression of type 2 diabetes and its associated renal injury was assessed in obese db/db mice that were deficient in the gene encoding MCP-1 (Ccl2). Results The incidence and development of type 2 diabetes were similar in Ccl2 +/+ and Ccl2 −/− db/db mice between 8 and 32 weeks of age. Body mass, hyperglycaemia, hyperinsulinaemia, glucose and insulin tolerance, plasma triacylglycerol and serum NEFA were not different between these strains. Pathological changes in epididymal adipose tissue, including increases in macrophage accumulation and Tnfa mRNA and reductions in Adipoq mRNA, were unaffected by the absence of MCP-1. In contrast, kidney macrophage accumulation and the progression of diabetic renal injury (albuminuria, histopathology, renal fibrosis) were substantially reduced in Ccl2 −/− compared with Ccl2 +/+ db/db mice with equivalent diabetes. Conclusions/interpretation Our study demonstrates that MCP-1 promotes type 2 diabetic renal injury but does not influence the development of obesity, insulin resistance or type 2 diabetes in db/db mice. MCP-1 plays a critical role in inflammation of the kidney, but not adipose tissue, during the progression of type 2 diabetes.

show abstract

mentioning

confidence: 99%

Monocyte chemoattractant protein-1-induced tissue inflammation is critical for the development of renal injury but not type 2 diabetes in obese db/db mice

et al. 2006

View full text Add to dashboard Cite

show abstract

“…It has been reported that both plasma MCP-1 and urinary MCP-1 levels rise along with progression of nephropathy (8,9) and that a rise in MCP-1 correlates with renal tubular injuries (10 -13). It is thought that macrophages and MCP-1 play an important role in renal damages of various causes (32).…”

Section: Discussionmentioning

confidence: 99%

“…It is thought that macrophages and MCP-1 play an important role in renal damages of various causes (32). In diabetic nephropathy, a large number of macrophages accumulate in renal tubules, thereby causing local inflammations (7)(8)(9)(10)(11)(12)(13)(14)32). It is postulated that urinary MCP-1 may reflect renal tubular inflammations.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Reduced Albuminuria with Sarpogrelate Is Accompanied by a Decrease in Monocyte Chemoattractant Protein-1 Levels in Type 2 Diabetes

Ogawa

Mori

Nako

et al. 2008

Clinical Journal of the American Society of Nephrology

View full text Add to dashboard Cite

Background and objectives: Sarpogrelate has been shown to reduce albuminuria in diabetic nephropathy. For examination of whether this is based on the same mechanisms as angiotensin II receptor blockers or thiazolidinedione, effects of sarpogrelate on atherosclerotic inflammatory molecules and their relations to albuminuria in patients who had diabetes and had already been treated with angiotensin II receptor blockers and with or without thiazolidinedione were examined.Design, setting, participants, & measurements: Forty patients who had diabetes with nephropathy and arteriosclerosis obliterans and had already been treated with angiotensin II receptor blocker (n ‫؍‬ 40) were randomly assigned to sarpogrelate (300 mg/d; n ‫؍‬ 20) or aspirin group (100 mg/d; n ‫؍‬ 20). Plasma monocyte chemoattractant protein-1 and urinary albumin-tocreatinine ratio and monocyte chemoattractant protein-1 were measured at baseline and 16 wk after administration.Results: Only the sarpogrelate group showed increases in plasma adiponectin and decreases in both plasma and urinary monocyte chemoattractant protein-1 and albumin-to-creatinine ratio levels. Moreover, percentage change of monocyte chemoattractant protein-1 level correlated positively to that of albumin-to-creatinine ratio. Even when the sarpogrelate group was further divided into two groups with (n ‫؍‬ 9) or without thiazolidinedione (n ‫؍‬ 11), changes in monocyte chemoattractant protein-1 or albumin-to-creatinine ratio did not differ.Conclusions: Sarpogrelate can reduce albuminuria and plasma and urinary monocyte chemoattractant protein-1 levels while increasing plasma adiponectin in diabetic nephropathy. These effects seem to be mediated via mechanisms that are different from those of angiotensin II receptor blocker or thiazolidinedione.

show abstract

“…Reactive oxygen species, induced by hyperglycemia, cause both direct and indirect endothelial damage by modifying extracellular matrix pro-teins and by escalating the inflammatory response [9,10]. Nuclear factor kappa B is triggered by reactive oxygen species and induces monocyte chemotactic protein-1 (MCP-1), a pro-inflammatory chemokine, which contributes to renal deterioration by recruiting macrophages [11][12][13][14].…”

Section: Diabetic Nephropathymentioning

confidence: 99%

Effect of cilostazol in treating diabetes-associated microvascular complications

Asal

Wojciak

2017

Endocrine

View full text Add to dashboard Cite

Purpose Cilostazol (Pletal), a phosphodiesterase-3 inhi-bitor, was approved in the United States in 1999 to reduce symptoms of intermittent claudication. Cyclic adenosine monophosphate levels increase from inhibition of phos-phodiesterase resulting in anti-platelet, anti-inflammatory, and vasodilatory effects. Diabetes mellitus is a chronic disease that causes endothelial and platelet dysfunction leading to both microvascular and macrovascular compli-cations. This mini-review highlights the emerging evidence suggesting benefits of using cilostazol in treating micro-vascular complications associated with diabetes mellitus. Methods A review of literature was conducted using PubMed and Embase databases focusing on cilostazol use in diabetes mellitus. Results Cilostazol demonstrated renoprotective effects in patients with diabetic nephropathy by reducing serum soluble adhesion molecule-1 and monocyte chemoattractant protein-1. Cilostazol's anti-inflammatory actions predictably attenuate glomerular damage from increased leukocyte adherence. Additionally, cilostazol delayed renal dysfunc-tion secondary to type 2 diabetes mellitus as albuminuria was reduced most likely resulting from inhibition of nuclear factor kappa-induced inflammatory and endothelial mar-kers. Cilostazol's antiinflammatory actions in addition to its vasodilatory actions relieved retinal hypoxia and decreased excessive production of retinal blood vessels suggesting benefit in diabetic retinopathy. Cilostazol did not improve

show abstract

Association of monocyte chemoattractant protein-1 with renal tubular damage in diabetic nephropathy

Cited by 165 publications

References 21 publications

Monocyte chemoattractant protein-1-induced tissue inflammation is critical for the development of renal injury but not type 2 diabetes in obese db/db mice

Monocyte chemoattractant protein-1-induced tissue inflammation is critical for the development of renal injury but not type 2 diabetes in obese db/db mice

Reduced Albuminuria with Sarpogrelate Is Accompanied by a Decrease in Monocyte Chemoattractant Protein-1 Levels in Type 2 Diabetes

Effect of cilostazol in treating diabetes-associated microvascular complications

Contact Info

Product

Resources

About