Curcumin attenuates high glucose-induced podocyte apoptosis by regulating functional connections between caveolin-1 phosphorylation and ROS

Sun, Lina; Liu, Xiang-chun; Chen, Xiangjun; Guan, Guangju; Liu, Gang

doi:10.1038/aps.2015.159

Cited by 48 publications

(42 citation statements)

References 44 publications

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“…In this study, we found that citral inhibits high glucose induced ROS production in the HepG2 cells [Table/ Fig-2]. It has been previously reported that curcumin, an active phytochemical effectively attenuated high glucose induced oxdative damage through inhibiting ROS generation in cultured mouse podocytes [31].…”

Section: Discussionmentioning

confidence: 72%

Citral, A Monoterpene Protect Against High Glucose Induced Oxidative Injury in HepG2 Cell In Vitro-An Experimental Study

Subramaniyan

Natarajan

2017

JCDR

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Introduction: Diabetes mellitus, a major metabolic disorder associated with hyperglycaemia is one of the leading cause of death in many developed countries. However, use of natural phytochemicals have been proved to have a protective effect against oxidative damage. Aim:To investigate the effect of citral, a monoterpene on high glucose induced cytotoxicity and oxidative stress in human hepatocellular liver carcinoma (Hep G2) cell line. Materials and Methods:Cells were treated with 50 mM con centration of glucose for 24 hours incubation following citral (30 μM) was added to confluent HepG2 cells. Cell viability, Reactive Oxygen Species (ROS) generation, DNA damage, lipid peroxidation, antioxidants and Mitogen Activated Protein Kinases (MAPKs) signaling were assessed in citral and/or high glucose induced HepG2 cells.

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Section: Discussionmentioning

confidence: 72%

Citral, A Monoterpene Protect Against High Glucose Induced Oxidative Injury in HepG2 Cell In Vitro-An Experimental Study

Subramaniyan

Natarajan

2017

JCDR

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“…Unbalanced apoptotic cell death leads to renal cell loss and has been observed in podocytes, tubular cells, and endothelial cells in experimental diabetic nephropathy [8]. Diabetic nephropathy is the most frequent cause of end-stage renal disease in developed countries.…”

Section: Discussionmentioning

confidence: 99%

Association of Vitamin D deficiency, cellular hypoxia, and caspase-3 with renal disease in pediatric diabetic nephropathy

Maidannyk¹,

Burlaka²

2016

J Transl Sci

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The increased prevalence of Type I Diabetes (T1D) has also led to an increase in the number of macro-and microvascular complications of diabetes such as coronary heart disease, stroke, visual impairment, diabetic nephropathy (DN), and end stage renal disease (ESRD). Additionally, diabetes remains the most common reason for progressing to end stage renal disease.The aim of the study was to investigate the level of hypoxic disorders, condition of apoptosis controlling system and Vitamin D3 levels in children with diabetic nephropathy.The study involved 36 children with T1D and diabetic nephropathy (aged 6 to 17 years). The levels of the marker of cellular hypoxia HIF-1alfa, levels of the apoptotic factor caspase-3 studied by Western Blotting, Vitamin D3 levels were analyzed using ELISA assay.Stage-dependent manner of the cellular hypoxia and apoptotic effector caspase-3 levels increase documented. Both markers detected at significantly higher rate in DN patients as compared to T1D. Vitamin D3 deficiency documented in patients with DN.Thus, the development of DN in children is associated with the formation of cellular hypoxia and activation of apoptosis, as one of the basic mechanisms of kidney damage in DN. All mentioned above disorders accompanied by Vitamin D3 deficiency.

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“…Oxidative stress occurs when ROS affect the balance between oxidative pressure and antioxidant defense (23). SOD is an enzymatic scavenger of ROS, which can com bat the accumulation of ROS and limit oxidative injury (24).…”

Section: Overexpressed Mir-130a-3p/301a-3p Inhibited Hg-induced Mpc5 mentioning

confidence: 99%

Overexpression of miR‑130a‑3p/301a‑3p attenuates high glucose‑induced MPC5 podocyte dysfunction through suppression of TNF‑α signaling

Jiang

Wang²,

Liu

et al. 2017

Exp Ther Med

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Abstract. Tumor necrosis factor (TNF)-α has been reported to be important in glomerulonephritis, which is closely associated with podocyte dysfunction and apoptosis. However, the precise mechanisms by which TNF-α expression are regulated remain unclear. The purpose of the present study was to investigate the role of microRNA (miR)-130a-3p/301a-3p in the post-transcriptional control of TNF-α expression and high glucose (HG)-induced podocyte dysfunction. Mice MPC5 podocytes were incubated with HG and transfected with miR-130a-3p/301a-3p mimics or inhibitors, reactive oxygen species (ROS) levels were measured by flow cytometry assay, and the mRNA and protein levels were assayed by using reverse transcription-quantitative polymerase chain reaction and western blotting, respectively. The targeted genes were predicted by a bioinformatics algorithm and verified using a dual luciferase reporter assay. It was observed that miR-130a-3p/301a-3p was a novel regulator of TNF-α in mouse podocytes. miR-130a-3p/301a-3p mimics inhibited TNF-α 3'-untranslated region luciferase reporter activity, in addition to endogenous TNF-α protein expression. Furthermore, forced expression of miR-130a-3p or miR-301a-3p resulted in the downregulation of ROS and malondialdehyde (MDA) and the upregulation of superoxide dismutase (SOD) 1 in the presence of HG. Inhibition of TNF-α level prevented a remarkable reduc tion in SOD activity and a marked increase in ROS and MDA levels in HG-treated podocytes. Furthermore, TNF-α loss-of-function significantly reversed HG-induced podocyte apoptosis. These data demonstrated a novel up-stream role for miR-130a-3p/301a-3p in TNF-α-mediated podocyte dysfunction and apoptosis in the presence of HG. IntroductionGlomerular podocytes are highly differentiated cells that play a key role in maintaining the integrity of the glomerular filtration barrier (1). In glomerular diseases, podocyte damage leads to increased glomerular barrier pore size, allowing the passage of proteins or other mediators to the tubular lumen, which results in proteinuria and progressive loss of kidney function (2). Accumulating evidence indicates that hyperglycemia contributes to podocyte lesions (3). Clinical data demonstrate that podocyte integrity is impaired, and the decreased podocyte number is confirmed in individuals with type 1 (T1DM) and 2 diabetes mellitus (T2DM) (4,5). In cultured podocytes, high glucose induces apoptosis, epithelial-mesenchymal transition (EMT), mitochondrial fission and autophagy through different signaling pathways (6-9). However, the underlying molecular mechanisms of high glucose-induced MPC5 podocytes dysfunction remain to be fully elucidated.MicroRNAs (miRs) are endogenous, noncoding, short, single-stranded RNAs (18-25 nucleotides) that are evolutionarily highly conserved, believed to regulate the translation of target messenger RNAs (mRNAs) by binding to its 3'-untranslated regions (3'-UTRs) and verified to play a role in controlling a variety of biological processes (10). Recently, several studies have h...

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Curcumin attenuates high glucose-induced podocyte apoptosis by regulating functional connections between caveolin-1 phosphorylation and ROS

Cited by 48 publications

References 44 publications

Citral, A Monoterpene Protect Against High Glucose Induced Oxidative Injury in HepG2 Cell In Vitro-An Experimental Study

Citral, A Monoterpene Protect Against High Glucose Induced Oxidative Injury in HepG2 Cell In Vitro-An Experimental Study

Association of Vitamin D deficiency, cellular hypoxia, and caspase-3 with renal disease in pediatric diabetic nephropathy

Overexpression of miR‑130a‑3p/301a‑3p attenuates high glucose‑induced MPC5 podocyte dysfunction through suppression of TNF‑α signaling

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