In vivo hyperexpression of transforming growth factor-β1 in humans: Stimulation by cyclosporine

Shin, Gyu‐Tae; Khanna, Ashwani; Sharma, Vijay Kumar; Ding, Ruchuang; Azizlerli, S.; Li, B.; Suthanthiran, Manikkam

doi:10.1016/s0041-1345(96)00094-2

Cited by 75 publications

(75 citation statements)

References 5 publications

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“…TGF-ß1 is a pro-fibrotic cytokine. It was demonstrated by several investigators (37)(38)(39) that cyclosporine promotes hyperexpression of this cytokine both in vitro and in vivo.…”

Section: Discussionmentioning

confidence: 99%

Determination of renal function in long-term heart transplant patients by measurement of urinary retinol-binding protein levels

Chinen

Câmara

Nishida

et al. 2006

Braz J Med Biol Res

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Significant improvements have been noted in heart transplantation with the advent of cyclosporine. However, cyclosporine use is associated with significant side effects, such as chronic renal failure. We were interested in evaluating the incidence of long-term renal dysfunction in heart transplant recipients. Fifty-three heart transplant recipients were enrolled in the study. Forty-three patients completed the entire evaluation and follow-up. Glomerular (serum creatinine, creatinine clearance measured, and creatinine clearance calculated) and tubular functions (urinary retinol-binding protein, uRBP) were reanalyzed after 18 months. At the enrollment time, the prevalence of renal failure ranged from 37.7 to 54% according to criteria used to define it (serum creatinine ≥1.5 mg/dL and creatinine clearance <60 mL/min). Mean serum creatinine was 1.61 ± 1.31 mg/dL (range 0.7 to 9.8 mg/dL) and calculated and measured creatinine clearances were 67.7 ± 25.9 and 61.18 ± 25.04 mL min -1 (1.73 m 2 ) -1 , respectively. Sixteen of the 43 patients who completed the follow-up (37.2%) had tubular dysfunction detected by increased levels of uRBP (median 1.06, 0.412-6.396 mg/dL). Eleven of the 16 patients (68.7%) with elevated uRBP had poorer renal function after 18 months of followup, compared with only eight of the 27 patients (29.6%) with normal uRBP (RR = 3.47, P = 0.0095). Interestingly, cyclosporine trough levels were not different between patients with or without tubular and glomerular dysfunction. Renal function impairment is common after heart transplantation. Tubular dysfunction, assessed by uRBP, correlates with a worsening of glomerular filtration and can be a useful tool for early detection of renal dysfunction.

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“…TGF-ß1 is a pro-fibrotic cytokine. It was demonstrated by several investigators (37)(38)(39) that cyclosporine promotes hyperexpression of this cytokine both in vitro and in vivo.…”

Section: Discussionmentioning

confidence: 99%

Determination of renal function in long-term heart transplant patients by measurement of urinary retinol-binding protein levels

Chinen

Câmara

Nishida

et al. 2006

Braz J Med Biol Res

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“…This suggests that TGFb enhances collagen synthesis (Riser et al, 1998). Angiotensin II, high salt diet, and cyclosporine stimulate TGF-b expression in the kidney and endothelium (Shin et al, 1998;Wolf, 1998;Ying & Sanders, 1999). Both high salt intake and high glucose also enhance NO synthesis (Ying & Sanders, 1999;Trachtman et al, 1998), whereas NO blocks TGF-b synthesis and suppresses matrix protein synthesis by mesangial cells (Craven et al, 1997;Studer et al, 1999).…”

Section: Transforming Growth Factor-b No and Hypertensionmentioning

confidence: 99%

Long-chain polyunsaturated fatty acids interact with nitric oxide, superoxide anion, and transforming growth factor-β to prevent human essential hypertension

Das¹

2004

Eur J Clin Nutr

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Patients with uncontrolled essential hypertension have elevated concentrations of superoxide anion (O 2 ÀK ), hydrogen peroxide (H 2 O 2 ), lipid peroxides, endothelin, and transforming growth factor-b (TGF-b) with a simultaneous decrease in endothelial nitric oxide (eNO), superoxide dismutase (SOD), vitamin E, and long-chain polyunsaturated fatty acids (LCPUFAs). Physiological concentrations of angiotensin II activate NAD(P)H oxidase and trigger free radical generation (especially that of O 2 ÀK ). Normally, angiotensin II-induced oxidative stress is abrogated by adequate production and release of eNO, which quenches O 2 ÀK to restore normotension. Angiotensin II also stimulates the production of endothelin and TGF-b. TGF-b enhances NO generation, which in turn suppresses TGF-b production. Thus, NO has a regulatory role on TGF-b production and is also a physiological antagonist of endothelin. Antihypertensive drugs suppress the production of O 2 ÀK and TGF-b and enhance eNO synthesis to bring about their beneficial actions. LCPUFAs suppress angiotensin-converting enzyme (ACE) activity, reduce angiotensin II formation, enhance eNO generation, and suppress TGF-b expression. Perinatal supplementation of LCPUFAs decreases insulin resistance and prevents the development of hypertension in adult life, whereas deficiency of LCPUFAs in the perinatal period results in raised blood pressure later in life. Patients with essential hypertension have low concentrations of various LCPUFAs in their plasma phospholipid fraction. Based on this, it is proposed that LCPUFAs serve as endogenous regulators of ACE activity, O 2 ÀK , eNO generation, and TGF-b expression. Further, LCPUFAs have actions similar to statins, inhibit (especially o-3 fatty acids) cyclooxygenase activity and suppress the synthesis of proinflammatory cytokines, and activate the parasympathetic nervous system, all actions that reduce the risk of major vascular events. Hence, it is proposed that availability of adequate amounts of LCPUFAs during the critical periods of growth prevents the development of hypertension in adulthood.

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“…36 It is known that TGF-␤ is a potent cell-growth modulator and affects cell-extracellular matrix interactions in a dose-dependent manner. Although both CyA 37 and tacrolimus 38 increase TGF-␤ transcription rates in humans in vivo, comparative studies suggest that this may be more prevalent with CyA. 39 …”

Section: Role Of Immunosuppressionmentioning

confidence: 99%

De novo malignancies after liver transplantation: A major cause of late death

Fung

Jain

Kwak

et al. 2001

Liver Transplantation

181

145

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In vivo hyperexpression of transforming growth factor-β1 in humans: Stimulation by cyclosporine

Cited by 75 publications

References 5 publications

Determination of renal function in long-term heart transplant patients by measurement of urinary retinol-binding protein levels

Determination of renal function in long-term heart transplant patients by measurement of urinary retinol-binding protein levels

Long-chain polyunsaturated fatty acids interact with nitric oxide, superoxide anion, and transforming growth factor-β to prevent human essential hypertension

De novo malignancies after liver transplantation: A major cause of late death

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