Advanced glycation endproducts induce podocyte apoptosis by activation of the FOXO4 transcription factor

Chuang, Peter Y.; Yu, Qianqian; Fang, Wei; Uribarri, Jaime; He, John Cijiang

doi:10.1038/sj.ki.5002456

Cited by 140 publications

(129 citation statements)

References 38 publications

Supporting

Mentioning

121

Contrasting

Order By: Relevance

“…28 The vpr, tat, and nef constructs as well as a control green fluorescence protein-containing construct and a Stat3 dominant negative mutant (a gift from Dr. C.M. Horvath, The Rockefeller University, New York, NY) were individually introduced into wild-type conditionally immortalized podocytes maintained at 33°C via nucleofection (Amaxa Biosystems, Cologne, Germany), and the cells were transferred to 37°C for 3 d. 29 The transfection efficiency was evaluated by fluorescence microscopy confirming 70 to 80% efficiency.…”

Section: Hiv-1 Constructsmentioning

confidence: 99%

HIV-1 Upregulates VEGF in Podocytes

Korgaonkar

Feng²,

Ross³

et al. 2008

Journal of the American Society of Nephrology

View full text Add to dashboard Cite

Section: Hiv-1 Constructsmentioning

confidence: 99%

HIV-1 Upregulates VEGF in Podocytes

Korgaonkar

Feng²,

Ross³

et al. 2008

Journal of the American Society of Nephrology

View full text Add to dashboard Cite

“…Similarly, glycated albumin can stimulate p38 phosphorylation in cultured fibroblasts [18]. Activation of p38 induces apoptosis of rat mesangial cells exposed to methylglyoxal [19] and apoptosis of mouse podocytes following stimulation with TGF-β [20] and AGE [21,22]. In addition, p38 signalling can contribute to proinflammatory and profibrotic responses.…”

Section: Introductionmentioning

confidence: 99%

Role of MKK3–p38 MAPK signalling in the development of type 2 diabetes and renal injury in obese db/db mice

et al. 2008

View full text Add to dashboard Cite

Aims/hypothesis Obesity and diabetes are associated with increased intracellular p38 mitogen-activated protein kinase (MAPK) signalling, which may promote tissue inflammation and injury. Activation of p38 MAPK can be induced by either of the immediate upstream kinases, MAP kinase kinase (MKK)3 or MKK6, and recent evidence suggests that MKK3 has non-redundant roles in the pathology attributed to p38 MAPK activation. Therefore, this study examined whether MKK3 signalling influences the development of obesity, type 2 diabetes and diabetic nephropathy. Methods Wild-type and Mkk3 (also known as Map2k3) gene-deficient db/db mice were assessed for the development of obesity, type 2 diabetes and renal injury from 8 to 32 weeks of age. Results Mkk3+/+ db/db and Mkk3 −/− db/db mice developed comparable obesity and were similar in terms of incidence and severity of type 2 diabetes. At 32 weeks, diabetic Mkk3 +/+ db/db mice had increased kidney levels of phospho-p38 and MKK3 protein. In comparison, kidney levels of phospho-p38 in diabetic Mkk3 −/− db/db mice remained normal, despite a fourfold compensatory increase in MKK6 protein levels. The reduced levels of p38 MAPK signalling in the diabetic kidneys of Mkk3 −/− db/ db mice was associated with protection against the following: declining renal function, increasing albuminuria, renal hypertrophy, podocyte loss, mesangial cell activation and glomerular fibrosis. Diabetic Mkk3 −/− db/db mice were also significantly protected from tubular injury and interstitial fibrosis, which was associated with reduced Ccl2 mRNA expression and interstitial macrophage accumulation. Conclusions/interpretation MKK3-p38 MAPK signalling is not required for the development of obesity or type 2 diabetes, but plays a distinct pathogenic role in the progression of diabetic nephropathy in db/db mice.

show abstract

“…The postmitotic podocyte is the primary glomerular target for both immune and metabolic toxins, which have the potential to induce reactive oxygen species (ROS) and/or injury in podocytes [3] . Podocyte damage plays a crucial role in the mechanisms of many glomerular diseases, including focal segmental glomerulosclerosis (FSGS), diabetic nephropathy (DN), minimal change disease (MCD), and membranous nephropathy (MN) [4][5][6] .…”

Section: Introductionmentioning

confidence: 99%

Ginsenoside Rg1 protects mouse podocytes from aldosterone-induced injury in vitro

Ma¹,

Cheng²,

Shi³

et al. 2014

Acta Pharmacol Sin

View full text Add to dashboard Cite

Aim: Aldosterone is elevated in many diseases such as hypertension, diabetic nephropathy and chronic kidney disease, etc. The aim of this study was to investigate the effects of aldosterone on intracellular ROS production and autophagy in podocytes in vitro, and to explore the possibility of ginsenoside Rg1 (Rg1) being used for protecting podocytes from aldosterone-induced injury. Methods: MPC5 mouse podocyte cells were tested. Autophagosome and autophagic vacuole formation were examined under confocal microscopy with MDC and acridine orange staining, respectively. ROS were detected with flow cytometry. Malondialdehyde content and superoxide dismutase (T-SOD) activity were measured using commercial kits. The expression of LC3-II, beclin-1, SOD2 and catalase was measured by Western blotting. Results: Treatment with aldosterone (10 nmol/L) significantly increased ROS generation and the expression of SOD2 and catalase in MPC5 cells. Furthermore, treatment with aldosterone significantly increased the conversion of LC3-I to LC3-II, beclin-1 expression and autophagosome formation. Co-treatment with rapamycin (1 ng/mL) or chloroquine (10 μmol/L) further increased aldosterone-induced autophagosome formation. Co-treatment with Rg1 (80 ng/mL) effectively relieved oxidative stress and increased T-SOD activity at the early stage and subsequently decreased autophagy in aldosterone-treated podocytes. Co-treatment with 3-MA (4 mmol/L) or NAC (50 mmol/L) exerted similar effects against aldosterone-induced autophagy in podocytes. Conclusion: Aldosterone enhances ROS generation and promotes autophagy in podocytes in vitro. Ginsenoside-Rg1 effectively relieves aldosterone-induced oxidative stress, thereby indirectly inhibiting aldosterone-induced podocyte autophagy.

show abstract

Advanced glycation endproducts induce podocyte apoptosis by activation of the FOXO4 transcription factor

Cited by 140 publications

References 38 publications

HIV-1 Upregulates VEGF in Podocytes

HIV-1 Upregulates VEGF in Podocytes

Role of MKK3–p38 MAPK signalling in the development of type 2 diabetes and renal injury in obese db/db mice

Ginsenoside Rg1 protects mouse podocytes from aldosterone-induced injury in vitro

Contact Info

Product

Resources

About