Ubiquitination-dependent CARM1 degradation facilitates Notch1-mediated podocyte apoptosis in diabetic nephropathy

Kim, Dong-Il; Lim, Seul-Ki; Park, Min-Jung; Choi, Joo-Hee; Kim, Jongchoon; Han, Ho Jae; Yoon, Kyung-Chul; Kim, Kwonseop; Lim, Jae-Hyang; Park, Soo-Hyun

doi:10.1016/j.cellsig.2014.04.008

Cited by 61 publications

(45 citation statements)

References 37 publications

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“…HA and HA-CARM1 were described previously [16]. Transient transfection was performed with Lipofectamine™ 2000 (Invitrogen), as instructed by the manufacturers.…”

Section: Dna Transfectionmentioning

confidence: 99%

High-glucose-induced CARM1 expression regulates apoptosis of human retinal pigment epithelial cells via histone 3 arginine 17 dimethylation: Role in diabetic retinopathy

Kim¹,

Park²,

Lim³

et al. 2014

Archives of Biochemistry and Biophysics

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“…HA and HA-CARM1 were described previously [16]. Transient transfection was performed with Lipofectamine™ 2000 (Invitrogen), as instructed by the manufacturers.…”

Section: Dna Transfectionmentioning

confidence: 99%

High-glucose-induced CARM1 expression regulates apoptosis of human retinal pigment epithelial cells via histone 3 arginine 17 dimethylation: Role in diabetic retinopathy

Kim¹,

Park²,

Lim³

et al. 2014

Archives of Biochemistry and Biophysics

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“…Under diabetic conditions, oxidative stress caused by various stressors such as high glucose, angiotensin II and advanced glycation end products enhances apoptosis of glomerular mesangial cells, podocytes and renal tubular cells (44)(45)(46). Reportedly, SIRT1 deacetylates several apoptosis-related proteins, such as p53, Smad7, FOXO3 and FOXO4, protecting renal cells against damage-induced apoptosis (47-51).…”

Section: Sirt1 Inhibits Apoptosis By Targeting P53 Smad7 Foxo3 and mentioning

confidence: 99%

Sirtuin 1: A Target for Kidney Diseases

Kong

Zhou

et al. 2015

Mol Med

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Sirtuin 1 (SIRT1) is an evolutionarily conserved NAD + -dependent histone deacetylase that is necessary for caloric restriction-related lifespan extension. SIRT1, as an intracellular energy sensor, detects the concentration of intracellular NAD + and uses this information to adapt cellular energy output to cellular energy requirements. Previous studies on SIRT1 have confirmed its beneficial effects on cellular immunity to oxidative stress, reduction of fibrosis, suppression of inflammation, inhibition of apoptosis, regulation of metabolism, induction of autophagy and regulation of blood pressure. All of the above biological processes are involved in the pathogenesis of kidney diseases. Therefore, the activation of SIRT1 may become a therapeutic target to improve the clinical outcome of kidney diseases. In this review, we give an overview of SIRT1 and its molecular targets as well as SIRT1-modulated biological processes, with a particular focus on the role of SIRT1 in kidney diseases.

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“…In recent years, a series of studies have demonstrated that in diabetic nephropathy podocyte apoptosis plays an essential role in the pathogenesis of proteinuria and deteriorated renal function [15,16]. However, the mechanisms of podocyte apoptosis in diabetes are still not fully elucidated.…”

Section: Discussionmentioning

confidence: 99%

VEGF-A Inhibition Ameliorates Podocyte Apoptosis via Repression of Activating Protein 1 in Diabetes

Bai

Geng²,

Li³

et al. 2014

Am J Nephrol

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Background/Aims: Vascular endothelial growth factor-A (VEGF-A) upregulation and podocyte apoptosis have been documented in diabetes. This study was designed to investigate whether inhibiting VEGF-A could ameliorate podocyte apoptosis in diabetes and the underlying mechanisms. Methods: In vitro, small interfering RNAs (siRNAs) of VEGF-A and activator protein 1 (AP-1, c-fos and c-jun), bevacizumab (VEGF-A inhibitor) and SP600125 (AP-1 inhibitor) were added to high glucose (30 mM) induced podocytes. Luciferase reporter assay was used to investigate whether AP-1 was a direct target of VEGF-A. In vivo, bevacizumab and SP600125 were administered to 12-week-old streptozotocin-induced male Sprague Dawley rats. The level of VEGF-A, c-fos, c-jun and bcl-2 were examined using immunostaining and Western blot analysis. Podocyte apoptosis was detected using the terminal deoxynucleotidyl transferase-mediated uridine 5′-triphosphate-biotin nick end labeling (TUNEL) assay, electron microscopy and flow cytometry. Results: Silencing VEGF-A or AP-1 upregulated bcl-2 and ameliorated podocyte apoptosis. Silencing VEGF-A decreased the level of c-fos and c-jun and bevacizumab and SP600125 treatment attenuated podocyte apoptosis. Luciferase reporter activity of VEGF-A-3′-UTR constructs was significantly provoked when stimulated with TGF-β1. In diabetic rat kidneys, VEGF-A co-localized with bcl-2 in podocytes. With bevacizumab and SP600125 treatment, the level of VEGF-A and AP-1 decreased while bcl-2 increased. Podocyte apoptotic rate was reduced with condensed podocyte nuclei less frequently observed. The urine albumin excretion rate (UAER) and albumin/creatinine were improved. Conclusion: This study demonstrates VEGF-A inhibition ameliorates podocyte apoptosis by regulating AP-1 and bcl-2 signaling. AP-1 is a direct target of VEGF-A and a novel player in podocyte apoptosis.

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Ubiquitination-dependent CARM1 degradation facilitates Notch1-mediated podocyte apoptosis in diabetic nephropathy

Cited by 61 publications

References 37 publications

High-glucose-induced CARM1 expression regulates apoptosis of human retinal pigment epithelial cells via histone 3 arginine 17 dimethylation: Role in diabetic retinopathy

High-glucose-induced CARM1 expression regulates apoptosis of human retinal pigment epithelial cells via histone 3 arginine 17 dimethylation: Role in diabetic retinopathy

Sirtuin 1: A Target for Kidney Diseases

VEGF-A Inhibition Ameliorates Podocyte Apoptosis via Repression of Activating Protein 1 in Diabetes

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