The Role of Macrophages in Diabetic Glomerulosclerosis

Furuta, Takahisa; Saito, Takao; Ootaka, Tetsuya; Soma, Jun; Obara, Koji; Abe, Keishi; Yoshinaga, Kaoru

doi:10.1016/s0272-6386(12)80393-3

Cited by 286 publications

(221 citation statements)

References 20 publications

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“…The cellular response of the interstitium in diabetic nephropathy, which often includes large numbers of lymphocytes, was indistinguishable from that observed in other forms of chronic renal disease ( 19). Some investigations have revealed that the interstitial cellular infiltrates in tubulo-interstitial disease, glomerulonephritis, systemic disease, and DMwere predominantly T cells, whereas the B cell population accounted for less than 20% of the infiltrates (19)(20)(21). In the present case, interstitial infiltration of mononuclear cells comprised mostly T cells.…”

Section: Discussioncontrasting

confidence: 46%

Type II Diabetes Mellitus and Primary Sjoegren's Syndrome Complicated by Pleural Effusion.

et al. 2000

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A 73-year-old manwas admitted to our hospital because of pleural effusion and nephrotic syndrome. Sjogren's syndrome (Sjs) was diagnosed based on a positive test for antibodies to Ro and La, and the result of labial salivary gland biopsy. The pleural effusion showed a high number of lymphocytes and high titers of antibodies to Ro and La. By immunohistochemistry, it was determined that infiltrating CD3+ cells predominated over infiltrating CD20+cells in the pleura. Nephrotic syndromewasalso present, which, as confirmed by renal biopsy was due to advanced diabetic nephropathy. Here, wereport a case of Type II diabetes mellitus and primary Sjs complicated by pleural effusion, discuss the available treatment for pleural effusion. (Internal Medicine 39: 979-984, 2000)

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Section: Discussioncontrasting

confidence: 46%

Type II Diabetes Mellitus and Primary Sjoegren's Syndrome Complicated by Pleural Effusion.

et al. 2000

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“…The macrophage has been presumed to be a critical mediator of diabetic nephropathy [36][37][38], and blockade of the MCP-1/CC chemokine receptor 2 system in diabetic mice leads to reduced albuminuria, mesangial expansion and macrophage infiltration [39][40][41][42]. Secretory factors from macrophages may cause histological and functional changes in glomeruli.…”

Section: Discussionmentioning

confidence: 99%

Exacerbation of diabetic nephropathy by hyperlipidaemia is mediated by Toll-like receptor 4 in mice

et al. 2012

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Aims/hypothesis Hyperlipidaemia is an independent risk factor for the progression of diabetic nephropathy, but its molecular mechanism remains elusive. We investigated in mice how diabetes and hyperlipidaemia cause renal lesions separately and in combination, and the involvement of Toll-like receptor 4 (TLR4) in the process. Methods Diabetes was induced in wild-type (WT) and Tlr4 knockout (KO) mice by intraperitoneal injection of streptozotocin (STZ). At 2 weeks after STZ injection, normal diet was substituted with a high-fat diet (HFD). Functional and histological analyses were carried out 6 weeks later. Results Compared with treatment with STZ or HFD alone, treatment of WT mice with both STZ and HFD markedly aggravated nephropathy, as indicated by an increase in albuminuria, mesangial expansion, infiltration of macrophages and upregulation of pro-inflammatory and extracellularmatrix-associated gene expression in glomeruli. In Tlr4 KO mice, the addition of an HFD to STZ had almost no effects on the variables measured. Production of protein S100 calcium binding protein A8 (calgranulin A; S100A8), a potent ligand for TLR4, was observed in abundance in macrophages infiltrating STZ-HFD WT glomeruli and in glomeruli of diabetic nephropathy patients. High-glucose and fatty acid treatment synergistically upregulated S100a8 gene expression in macrophages from WT mice, but not from KO mice. As putative downstream targets of TLR4, phosphorylation of interferon regulatory factor 3 (IRF3) was enhanced in kidneys of WT mice co-treated with STZ and HFD. Conclusions/interpretation Activation of S100A8/TLR4 signalling was elucidated in an animal model of diabetic glomerular injury accompanied with hyperlipidaemia, which may provide novel therapeutic targets in progressive diabetic nephropathy.

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“…This final common pathway is initially characterized by the triggering of interstitial infiltration of inflammatory cells, which trigger further tubular damage, and interstitial fibrosis, which correlates with the rate of progression of renal disease. This seems to hold true, even in what are considered to be non-inflammatory diseases such as diabetic nephropathy, with recent studies suggesting that macrophage-derived proinflammatory cytokines acting upon resident cells may represent key events in progressive nephropathy (14,48). The data presented in this article provide insight into how alterations in HA synthesis in the renal cortex may be involved in modulation of the interaction between infiltrating inflammatory cells and resident cells and furthermore suggest a mechanism by which the known antiinflammatory and antifibrotic effects of BMP-7 in renal disease may be mediated.…”

Section: Discussionmentioning

confidence: 99%

BMP-7 Modulates Hyaluronan-Mediated Proximal Tubular Cell-Monocyte Interaction

Selbi¹,

Motte²,

Hascall³

et al. 2004

Journal of the American Society of Nephrology

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Abstract. Increased synthesis of hyaluronan (HA) in the renal corticointerstitium has been documented in renal injury, although the functional significance of this is unclear. The aim of the work presented in the current study was to examine the role of HA in monocyte binding by proximal tubular cells (PTC). Using the PTC line HK-2, the authors show that unstimulated cells formed pericellular HA cable-like structures that bound mononuclear leukocytes via their cell surface CD44. Stimulation with bone morphogenic protein-7 (BMP-7) led to increased formation of HA cable-like structures and also a dosedependent increase in CD44-dependent binding of radiolabeled

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The Role of Macrophages in Diabetic Glomerulosclerosis

Cited by 286 publications

References 20 publications

Type II Diabetes Mellitus and Primary Sjoegren's Syndrome Complicated by Pleural Effusion.

Type II Diabetes Mellitus and Primary Sjoegren's Syndrome Complicated by Pleural Effusion.

Exacerbation of diabetic nephropathy by hyperlipidaemia is mediated by Toll-like receptor 4 in mice

BMP-7 Modulates Hyaluronan-Mediated Proximal Tubular Cell-Monocyte Interaction

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