Hypoxia and high glucose cause exaggerated mesangial cell growth and collagen synthesis: role of osteopontin

Sodhi, Chhinder P.; Phadke, Sarojini A.; Batlle, Daniel; Sahai, Atul

doi:10.1152/ajprenal.2001.280.4.f667

Cited by 77 publications

(72 citation statements)

References 34 publications

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“…Extensive studies have recently clarified that OPN is widespread and localized in several pathological organs and has important roles in ectopic calcification [6,8], wound healing [4], several types of cancer [15,18], and vascular remodeling, including diabetic condition [7][8][9][10][11][12][13][14], granulomatous inflammation [3], and glomerulonephritis [5,19]. Although the clinical implications of these findings have yet to be fully clarified, it is more likely that OPN can, at least, evolve as a major player in the injury/repair cascades.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, several investigators have recently revealed that OPN can play multiple roles in the progression of atherosclerotic plaque [7][8][9][10][11][12][13][14] including diabetic vascular complications [12][13][14]. Particularly in diabetes, OPN has the potential to promote both the growth and migration of vascular wall cells such as VSMCs [9,10,12,14] and mesangial cells [13], depending on the glucose concentration.…”

mentioning

confidence: 99%

“…Particularly in diabetes, OPN has the potential to promote both the growth and migration of vascular wall cells such as VSMCs [9,10,12,14] and mesangial cells [13], depending on the glucose concentration. This implies that OPN can directly contribute not only to the tissue calcification process but also to the development of diabetic vascular complications.…”

mentioning

confidence: 99%

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Progression of Diabetic Nephropathy Enhances the Plasma Osteopontin Level in Type 2 Diabetic Patients

et al. 2004

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Abstract. Osteopontin (OPN) is thought to play multiple roles in the progression of atherosclerotic plaque including diabetic vascular complications. However, it still remains unclear whether the level of OPN in vivo is indeed clinically associated with the progression of diabetic complications. This study evaluated whether the levels of OPN in plasma and urine are correlated with the progression of diabetic complications, such as retinopathy, neuropathy, and nephropathy in patients with type 2 diabetes. In 229 patients with type 2 diabetes, OPN level in plasma and urine was evaluated by both the severity of diabetic complications, such as retinopathy, neuropathy, and nephropathy, and the clinical characteristics and the substantial laboratory findings. Plasma OPN level increased significantly with aging and the progression of diabetic nephropathy, especially at the stage of renal failure (p<0.05). However, the level was not related to the progression of retinopathy or neuropathy, or to laboratory findings, such as HbA1c or serum lipids. In contrast, urinary OPN level was not associated with diabetic complications in any of the subjects. There was no correlation between the plasma and urinary values of OPN. The results established that the plasma OPN was elevated in proportion to the progression of diabetic nephropathy, indicating that the plasma concentration may be a potential diagnostic predictor of diabetic end-stage renal disease.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

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Progression of Diabetic Nephropathy Enhances the Plasma Osteopontin Level in Type 2 Diabetic Patients

et al. 2004

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“…In addition, regional expression of osteopontin in vascular smooth muscle cells promotes medial thickening, neointima formation, and mesangioproliferative responses (55,56). Moreover, even though the modest metabolic changes observed (trend for decrease in glucose, percentage of body fat, and leptin levels) were not of statistical significance, the experimental design was underpowered for these specific parameters and may contribute to net physiological responses.…”

Section: Pth(1-34) and Opn Suppress In Vitro Osteogenic Mineralizatiomentioning

confidence: 99%

Teriparatide (Human Parathyroid Hormone (1–34)) Inhibits Osteogenic Vascular Calcification in Diabetic Low Density Lipoprotein Receptor-deficient Mice

Shao

Cheng

Charlton-Kachigian

et al. 2003

Journal of Biological Chemistry

165

149

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Over a century ago, the pathologist Rudolph Virchow recognized the involvement of calcified tissues in the pathobiology of vascular diseases (1). Coining the term "endarteritis deformans" he descriptively denoted the histological character of the atherosclerotic plaque as exhibiting features of a progressively calcified scar tissue that forms in response to a vascular inflammatory state. Since then, a minimum of three histoanatomic variants of macrovascular calcification, atherosclerosis, calcific valvular sclerosis, and medial artery calcification, have been shown arise in response to metabolic, mechanical, infectious, or inflammatory diseases (2-4). Both early and recent studies point to cellular processes that resemble bone formation at the histological level. However, Demer and co-workers (5) were the first to provide direct evidence for active osteogenic regulation of vascular calcification. They identified BMP2, 1 a powerful bone morphogenetic protein, as a key component of the mineralized atherosclerotic plaque (5). Thus, rather than being a passive process, vascular calcification is in part subject to active regulation. Once thought benign, the deleterious clinical consequences of calcific vasculopathy are now becoming clearer (6 -10). Patients with diabetes have increased mortality and 3-fold increased risk for lower extremity amputation in the setting of medial artery calcification (11). In patients with asymptomatic aortic stenosis, a moderate to severe echocardiographic valve calcification score is the single best predictor of vascular disease progression, again exceeding blood pressure control, lipid control, and diabetes control in positive predictive value (12). Risk for stroke, particularly notable in post-menopausal women, is increased in the presence of aortic arch calcification (13). Multiple metabolic stimuli contribute to calcific vascular disease initiation and progression in patients with diabetes, hypercholesterolemia, poor glycemic control, and phosphate retention associated with renal failure contributing to vascular calcium accumulation (2). A fundamental understanding the molecular physiology of vascular calcification will provide insights useful for developing strategies to prevent and treat this macrovascular disease process.Metabolic contributions to vascular calcification are well known and include hypercholesterolemia, diabetes, hyperphosphatemia, vitamin D toxicosis, magnesium deficiency, and chronic renal insufficiency (2). The mechanisms whereby the metabolic insults of diabetes initiate and propagate vascular calcification are beginning to be examined in detail. Hyperglycemia, hyperlipidemia, and oxidative stress (3, 14) up-regulate the expression of vascular signaling molecules that promote mineral deposition in a process that resembles craniofacial bone formation (15). Hyperglycemia and hyperlipidemia have

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“…Vascular damage due to mechanical injury induced by pressure or volume loads [13], or hypoxia [14], or intervened with angiotension II [15], was the initially proposed mechanism that may stimulate OPN expressions. Subsequently, studies revealed that OPN may regulate extracellular matrix remodeling by inhibiting interleukin-1ß-stimulated increases in the activities of matrix metalloproteinases 2 and 9 and expression in adult rat cardiac fibroblasts [16].…”

Section: Discussionmentioning

confidence: 99%

Osteopontin expression and its possible functions in the aortic disorders and coronary artery disease

Yuan¹,

Wang²,

Huang³

et al. 2011

Rev Bras Cir Cardiovasc

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Background: Osteopontin (OPN) has been verified to be closely associated with oncogenesis and remodeling processes. But this cytokine was rarely assessed in the presence of aortopathies, especially acute aortic dissection. The aim of the present study was to evaluate the expressions of OPN by way of molecular biological approaches so as to offer a better understanding of the possible mechanisms of the aortopathies.Methods: Consecutive patients with type A acute aortic dissection (20 patients), aortic aneurysm (nine patients) or coronary artery disease (21 patients) referred to this hospital for surgical operations were enrolled into this study. Blood samples of the surgical patients after systematic heparinization, and control fast morning blood samples drawn from 21 young healthy volunteers who had no evidence of any healthy problems were investigated for enzyme linked immunosorbent assay (ELISA). The surgical specimens of the aortic tissues collected from the surgical patients during the operations were obtained for quantitative realtime reverse transcription polymerase chain reaction (RT-PCR) for OPN mRNA, western blot assay for OPN protein, and for immunohistochemical staining of OPN. Ascending aortic tissues from the autopsies of the healthy individuals dying of accident were obtained as controls of immunohistochemistry.Results: By quantitative RT-PCR, the expressions of OPN mRNA were all upregulated in all three surgical groups. The quantitative results did not reveal any intergroup

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Hypoxia and high glucose cause exaggerated mesangial cell growth and collagen synthesis: role of osteopontin

Cited by 77 publications

References 34 publications

Progression of Diabetic Nephropathy Enhances the Plasma Osteopontin Level in Type 2 Diabetic Patients

Progression of Diabetic Nephropathy Enhances the Plasma Osteopontin Level in Type 2 Diabetic Patients

Teriparatide (Human Parathyroid Hormone (1–34)) Inhibits Osteogenic Vascular Calcification in Diabetic Low Density Lipoprotein Receptor-deficient Mice

Osteopontin expression and its possible functions in the aortic disorders and coronary artery disease

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