Mast cells and type VIII collagen in human diabetic nephropathy

Rüger, Beate M.; Hasan, Qurratulain; Greenhill, Nicholas S.; Davis, Paul F.; Dunbar, P. Rod; Neale, T. J.

doi:10.1007/bf02658509

Cited by 76 publications

(65 citation statements)

References 35 publications

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“…A prominent rise in mast cell number has been established in a variety of renal diseases, including primary and secondary nephritis (16,19,45), acute cellular rejection of renal allografts (23), diabetic nephropathy (46), and nephrosclerosis (25). Furthermore, three patterns of mast cell localization in the kidney have been observed: (1) Mast cells localize in the interstitium contacting fibroblasts; (2) also in the interstitium, mast cells are in close contact with lymphocytes/macrophages; and (3) mast cells infiltrate the tubules (tubulitis), usually the distal tubules (25).…”

Section: Discussionmentioning

confidence: 99%

A Pathogenetic Role for Mast Cells in Experimental Crescentic Glomerulonephritis

Timoshanko¹,

Kitching²,

Semple³

et al. 2006

Journal of the American Society of Nephrology

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Section: Discussionmentioning

confidence: 99%

A Pathogenetic Role for Mast Cells in Experimental Crescentic Glomerulonephritis

Timoshanko¹,

Kitching²,

Semple³

et al. 2006

Journal of the American Society of Nephrology

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“…RNA was reverse transcribed to cDNA and amplified using the Perkin Elmer (Norwalk, CT) rTth RT-PCR kit as described (17)(18)(19)(20)(21). Briefly, a 10-min RT step was followed by 40 cycles of three-stage PCR using temperatures of 94°C for denaturing, 72°C for extension, and specific annealing temperatures for each primer set ( Table 3).…”

Section: Cell Countingmentioning

confidence: 99%

A Novel In Vitro Human Model of Hemangioma

Tan¹,

Hasan²,

Velickovic³

et al. 2000

Modern Pathology

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Hemangioma, the most common tumor of infancy, is characterized by a proliferation of capillary endothelial cells with multilamination of the basement membrane and accumulation of cellular elements, including mast cells. The initial rapid growth is followed by an inevitable but slow involution. The currently available therapies are empirical and unsatisfactory because what is known of the cellular and molecular basis of hemangioma development is rudimentary. Advances in the understanding of its programmed biologic behavior has been hampered by the lack of a valid human model.We report here a novel in vitro culture system that is a useful human model of hemangioma. A small fragment of hemangioma biopsy is embedded in fibrin gel in a well of culture plates and incubated in a serum-free, buffered-salt, minimal medium. A complex network of microvessels grows out from the tissue fragments. Biopsies taken from all three phases of hemangioma development were cultured successfully; proliferative phase samples developed microvessels in 1 to 4 days, involuting phase in 5 to 7 days, and involuted phase in 7 to 12 days. The relative growth rates of the microvessels in the culture of biopsies taken from different stages of hemangioma development reflect the growth patterns seen clinically. This model has been validated using histochemistry, immunohistochemistry, and reverse transcriptase-polymerase chain reaction. Comparison of the number, localization, and phenotype of endothelial and mast cells and the distribution of basement membrane constituents (type IV collagen, perlecan, and laminins) and growth factors (basic fibroblast growth factor, vascular endothelial growth factor, transforming growth factor-␤s) in the biopsy and the tissue after culture shows that many of the characteristics of the original tissues were retained in culture.This in vitro human model of hemangioma overcomes some of the deficiencies associated with earlier models. It offers an opportunity for studying the precise cellular, biochemical, and molecular basis of hemangioma. It may also help to elucidate the mechanisms of action of existing therapies and may lead to the identification of novel treatments for hemangioma.

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“…The MC T MCs are believed to be T cell-dependent and the MC TC MCs are believed to be T cell-independent [38]. In human renal tissue, different results have been reported on MC subtype [11,15,17,[32][33][34]. MC subtype is believed to be disease-dependent [16].…”

Section: Discussionmentioning

confidence: 99%

“…MCs have been detected in a lot of renal diseases [11][12][13][14][15][16][17][18][19][20][21][22]; however, only a few cases were investigated in each kind of renal disease in most of the studies reported. Observation of MCs in the development of renal disease is still scarce.…”

Section: Introductionmentioning

confidence: 99%

“…Evidence provided by previous studies suggests that MCs contribute to renal diseases mainly by promoting tubular interstitial injury; however, their exact role remains poorly understood. Increased numbers of MCs have been reported in diabetic nephropathy [11,13,17], but, again, only a few patients were examined. Evidence of the involvement of MCs in diabetic nephropathy is still scarce, and no observation has been made of MCs during the development of diabetic nephropathy in humans.…”

Section: Introductionmentioning

confidence: 99%

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Pathogenic role of mast cells in the development of diabetic nephropathy: a study of patients at different stages of the disease

et al. 2011

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Aims/hypothesis Increased renal mast cells have been detected in diabetic nephropathy. However, only a few patients have been examined. Evidence of the involvement of mast cells in diabetic nephropathy is still scarce, and no observation of mast cells during the development of diabetic nephropathy has yet been reported in humans. Here, we examined changes in renal mast cells in patients at different stages of diabetic nephropathy and related these to the development of the disease. Methods Eighty patients at different clinical stages of diabetic nephropathy and 16 normal kidney donors were recruited. Immunohistochemical staining for tryptase, chymase, TGF-β1, renin and TNF-α was done on renal sections from patients and control participants. Changes in mast cell number, degranulation, subtype and phenotype were examined. Correlation between mast cells and patients' clinical and pathological indices was analysed. Results With progression of diabetic nephropathy, the number and degranulation level of mast cells increased. Increase in mast cell number and degranulation level correlated significantly with tubular interstitial injury. Almost all renal mast cells in patients with diabetic nephropathy were found to produce chymase, renin, TGF-β1 and TNF-α. The level of TNF-α in mast cells increased with progression of diabetic nephropathy. Conclusions/interpretation This study suggests that mast cells are involved in development of diabetic nephropathy. Through release of bioactive substances, such as tryptase, chymase, TGF-β1, renin and TNF-α, into the tubular interstitium by degranulation, mast cells could promote renal inflammation and fibrosis, and thus contribute to diabetic nephropathy.

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Mast cells and type VIII collagen in human diabetic nephropathy

Cited by 76 publications

References 35 publications

A Pathogenetic Role for Mast Cells in Experimental Crescentic Glomerulonephritis

A Pathogenetic Role for Mast Cells in Experimental Crescentic Glomerulonephritis

A Novel In Vitro Human Model of Hemangioma

Pathogenic role of mast cells in the development of diabetic nephropathy: a study of patients at different stages of the disease

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