CD36 mediates proximal tubular binding and uptake of albumin and is upregulated in proteinuric nephropathies

Baines, Richard; Chana, Ravinder S.; Hall, Matthew; Febbraio, Maria; Kennedy, David J.; Brunskill, Nigel J.

doi:10.1152/ajprenal.00021.2012

Cited by 45 publications

(41 citation statements)

References 45 publications

(52 reference statements)

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“…For example, intrarenal CD36 has been identified as a novel mediator in renal diseases associated with proteinuria and renal dysfunction (35). The elevated level of serum/plasma/urinary Fabp4 is considered a predictor or biomarker for renal dysfunction in diabetes and cardiovascular diseases (23)(24)(25)(26)(27).…”

Section: Articlesmentioning

confidence: 99%

“…We observed that BSA-PA stimulated both CD36 and Fabp4 protein expression in a dose-dependent manner in IRPTCs. CD36 has been shown to mediate PTC apoptosis (36) and to influence the binding and uptake of albumin in PTCs to promote proteinuria (35). The activated CD36 in PTCs targets JNK, ROS, and inflammatory cytokines to facilitate renal dysfunction (22).…”

Section: Articlesmentioning

confidence: 99%

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Post-weaning high-fat diet accelerates kidney injury, but not hypertension programmed by maternal diabetes

et al. 2015

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Background:The aim of this study was to establish the underlying mechanisms by which a post-weaning high-fat diet (HFD) accelerates the perinatal programming of kidney injury occurring in the offspring of diabetic mothers. Methods: Male mice, offspring of nondiabetic and diabetic dams were fed with normal diet (ND) or HFD from 4 to 20 wk of age. Rat renal proximal tubular cells were used in vitro. results: On ND, the offspring of dams with severe maternal diabetes had an intrauterine growth restriction (IUGR) phenotype and developed mild hypertension and evidence of kidney injury in adulthood. Exposing the IUGR offspring to HFD resulted in rapid weight gain, catch-up growth, and later to profound kidney injury with activation of renal TGFβ1 and collagen type IV expression, increased oxidative stress, and enhanced renal lipid deposition, but not systemic hypertension. Given our data, we speculate that HFD or free fatty acids may accelerate the process of perinatal programming of kidney injury, via increased CD36 and fatty acid-binding protein 4 expression, which may target reactive oxygen species, nuclear factor-kappa B, and TGFβ1 signaling in vivo and in vitro. conclusion: Early postnatal exposure to overnutrition with a HFD increases the risk of development of kidney injury, but not hypertension, in IUGR offspring of dams with maternal diabetes.d iabetes during pregnancy, whether gestational or pregestational diabetes (type 1 or type 2), results in offspring at high risk of developing hypertension, cardiovascular disease, and chronic kidney disease in adult life. This phenomenon, termed perinatal programming, in which intrauterine events are associated with later adverse changes, has attracted much attention (1-3). Substantial epidemiologic data have also suggested that the offspring whose mothers were diabetic during pregnancy are susceptible to metabolic disturbances induced by postnatal overnutrition, as seen with high-fat diet (HFD) or with increased caloric intake in early life (1)(2)(3)(4).Women who have diabetes during pregnancy and/or are obese and hyperinsulinemic are at risk of delivering macrosomic newborns (high birth weight), and both shortand long-term outcomes of macrosomic neonates are influenced by postnatal overnutrition (1-4). In high-birth-weight neonates, subsequent growth in infancy and risk of becoming obese or diabetic are directly and linearly linked-e.g., the higher the birth weight, the greater the risk of overweight and metabolic disturbances later in life (1-4). In contrast, pregnant women with severe, uncontrolled diabetes or diabetic complications, such as diabetic nephropathy and/or retinopathy, are at high risk of having a microsomic fetus (i.e., a fetus with intrauterine growth restriction (IUGR)) (5,6). Such infants may be markedly small for dates; but many develop excessive weight gain and increased fat deposition in early infancy, a proxy for neonatal overnutrition (7,8). However, the long-term outcome of IUGR offspring who experience overnutrition in early life is incomplet...

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Section: Articlesmentioning

confidence: 99%

Section: Articlesmentioning

confidence: 99%

Post-weaning high-fat diet accelerates kidney injury, but not hypertension programmed by maternal diabetes

et al. 2015

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“…Current studies suggest a role for CD36 in mediating cardiovascular disease associated with type II diabetes, insulin resistance, and obesity in rodent models [16] and in hypertensive humans [17]. Human genetic studies also support a role for CD36 in dyslipidemia, obesity and metabolic diseases [18–20], and CD36 protein expression is increased in kidney proximal convoluted tubule cells (PCT) in patients with proteinuria [21]. …”

Section: Introductionmentioning

confidence: 99%

Antagonism of scavenger receptor CD36 by 5A peptide prevents chronic kidney disease progression in mice independent of blood pressure regulation

Souza

Bocharov

Baranova

et al. 2016

Kidney International

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Scavenger receptor CD36 participates in lipid metabolism and inflammatory pathways important for cardiovascular disease and chronic kidney disease (CKD). Few pharmacological agents are available to slow the progression of CKD. However, apolipoprotein AI-mimetic peptide 5A antagonizes CD36 in vitro. To test the efficacy of 5A, and to test the role of CD36 during CKD, we compared wild type to CD36 knockout mice and wild type mice treated with 5A, in a progressive CKD model that resembles human disease. Knockout and 5A-treated wild type mice were protected from CKD progression without changes in blood pressure and had reductions in cardiovascular risk surrogate markers that are associated with CKD. Treatment with 5A did not further protect CD36 knockout mice from CKD progression, implicating CD36 as its main site of action. In a separate model of kidney fibrosis, 5A-treated wild type mice had less macrophage infiltration and interstitial fibrosis. Peptide 5A exerted anti-inflammatory effects in the kidney and decreases renal expression of inflammasome genes. Thus, CD36 is a new therapeutic target for CKD and its associated cardiovascular risk factors. Peptide 5A may be a promising new agent to slow CKD progression.

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“…The proximal tubule is known to endocytose a number of low-molecular-weight proteins, [3][4][5] and the molecular size of BTP is similar to light chains (w25,000 Da) that are filtered and metabolized by the kidney. 6 We agree that further investigations are needed to define renal handling of BTP; for example, determining whether proximal tubular cells uptake BTP in vitro 7,8 and additional measurements of BTP clearance in vivo using methods that do not rely on radioactive labels. 125 I in the urine suggests that the 125 I-labelled BTP is freely filtered and then 125 I is released from the BTP, presumably as BTP is metabolized."…”

Section: Interpreting the Evidencementioning

confidence: 93%

Renal Handling of β-Trace Protein: Interpreting the Evidence

Shafi

Pluznick

2015

American Journal of Kidney Diseases

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CD36 mediates proximal tubular binding and uptake of albumin and is upregulated in proteinuric nephropathies

Abstract: Baines RJ, Chana RS, Hall M, Febbraio M, Kennedy D, Brunskill NJ. CD36 mediates proximal tubular binding and uptake of albumin and is upregulated in proteinuric nephropathies. Am J Physiol

Cited by 45 publications

References 45 publications

Post-weaning high-fat diet accelerates kidney injury, but not hypertension programmed by maternal diabetes

Post-weaning high-fat diet accelerates kidney injury, but not hypertension programmed by maternal diabetes

Antagonism of scavenger receptor CD36 by 5A peptide prevents chronic kidney disease progression in mice independent of blood pressure regulation

Renal Handling of β-Trace Protein: Interpreting the Evidence

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