Association of podocyte autophagosome numbers with idiopathic membranous nephropathy and secondary membranous nephropathy

Jin, Juan; Zhan, Huifang; Lin, Bo; Li, Yiwen; Zhang, Wei; He, Qiang

doi:10.1007/s11255-017-1555-5

Cited by 12 publications

(10 citation statements)

References 17 publications

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“…The conversion of LC3-I to LC3-II indicates autophagosome formation [ 16 ] and enhanced autophagy [ 17 ]. Additionally, TEM is the frequently used to monitor autophagosomes in addition to LC3 [ 18 , 19 ]. We observed increased LC3-II and LC3-II/LC3-I ratio in the cisplatin group compared to the control group suggesting that autophagy was activated in response to cisplatin.…”

Section: Discussionmentioning

confidence: 99%

Panax notoginseng saponins mitigate cisplatin induced nephrotoxicity by inducing mitophagy via HIF-1α

et al. 2017

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We investigated the role of HIF-1α in the mitigation of cisplatin-induced nephrotoxicity by Panax notoginseng saponins (PNS) in a rat model. Serum creatinine (Scr), blood urea nitrogen (BUN) and urinary N-acetyl-β-D-glucosaminidase (NAG) levels were all elevated in cisplatin treated rats. PNS reduced Scr, BUN and NAG levels in the presence or absence of the HIF-1α inhibitor 2-methoxyestradiol (2ME2). PNS also reduced the high tubular injury scores, which corresponded to renal tubular damage in cisplatin-treated rats and which were exacerbated by 2ME2. Renal tissues from PNS-treated rats showed increased HIF-1α mRNA and nuclear localized HIF-1α protein. Moreover, PNS treatment increased BNIP3 mRNA as well as LC3-II, BNIP3 and Beclin-1 proteins and the LC3-II/LC3-I ratio in rat renal tissues. This suggested that PNS treatment enhanced HIF-1α, which in turn increased autophagy. This was confirmed in transmission electron micrographs of renal tissues that showed autophagosomes in PNS-treated renal tissues. These findings demonstrate that PNS mitigates cisplatin-induced nephrotoxicity by enhancing mitophagy via a HIF-1α/BNIP3/Beclin-1 signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Panax notoginseng saponins mitigate cisplatin induced nephrotoxicity by inducing mitophagy via HIF-1α

et al. 2017

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“…They are highly specialized cells involved in the charge and size filtration characteristics of the glomerulus. When stimulated with pathogens, podocytes might protect themselves through autophagy [24]. In this study, cultured human podocytes were treated primarily by autoantibodies from serum from patients with LN, inducing autophagy flux and producing foot process injury.…”

Section: Discussionmentioning

confidence: 99%

Vitamin D protects podocytes from autoantibodies induced injury in lupus nephritis by reducing aberrant autophagy

Qiao

et al. 2019

Arthritis Res Ther

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SubjectThe aim of this study was to investigate whether vitamin D plays a protective role in podocyte injury induced by autoantibodies purified from the serum of patients with lupus nephritis (LN) via reducing aberrant autophagy.MethodsAutophagic activities of renal tissues of patients with LN were evaluated under transmission electronic microscope (TEM). Immunoglobulin G (IgG) from patients with LN was purified to induce human podocyte injury, and the role of vitamin D in injury was observed. Podocytes were observed under TEM, autophagic activity was evaluated by western blot analysis and quantitative real-time polymerase chain reaction, and mRFP-GFP-LC3B adenovirus was infected into human podocytes in vitro.ResultsSignificantly higher autophagic levels were observed in patients with LN (P <0.05), and apparently greater autophagic levels in podocytes were shown (P <0.05). Among different classifications of LN, class V (n = 5), III + V (n = 5), and IV + V (n = 5) gained higher autophagic levels than class III (n = 5) and IV (n = 5). Induced autophagy, which was evident by increased LC3B-II and Beclin 1 level, caused consumption of p62, more autophagosomes observed under TEM, and more LC3B dots observed under confocal microscope in the IgG group, along with decreased nephrin expression, which suggests podocyte injury. Reduction of autophagy as well as alleviated podocyte injury was observed in the IgG+ vitamin D group.ConclusionThis study demonstrates that vitamin D plays a protective role in podocyte injury induced by autoantibodies from patients with LN and appears to be a novel therapy target in LN.

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“…Moreover, Cina et al reported that autophagy may play a fundamental role in mouse podocyte differentiation and recovery from puromycin aminonucleoside (PAN)-induced injury [10]. In addition, we previously found that autophagy participated in idiopathic membranous nephropathy (IMN)-induced podocyte injury, and the number of autophagosomes in podocytes was related to the level of pathology [11].…”

Section: Introductionmentioning

confidence: 98%

Rapamycin Reduces Podocyte Apoptosis and is Involved in Autophagy and mTOR/ P70S6K/4EBP1 Signaling

Jin

et al. 2018

Cell Physiol Biochem

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Background/Aims: The purpose of this study was to investigate the impact of rapamycin (RAP) on autophagy in podocytes and the therapeutic effects of RAP on idiopathic membranous nephropathy (IMN). Methods: We established an in vitro model of IMN by preconditioning mouse podocytes with puromycin aminonucleoside (PAN). A Cell Counting Kit-8 was used to detect the proliferation of each group of podocytes. Podocyte apoptosis was analyzed by flow cytometry via annexin V/propidium iodide dual staining. Subsequently, we observed the number of autophagosomes by transmission electron microscopy. Western blotting was used to detect the levels of LC3, mTOR, p-mTOR, 4EBP1, p-4EBP1, P70S6K, and p-P70S6K in each group. Results: The number of podocytes in the PAN + 100 ng/mL RAP group, PAN + 200 ng/mL RAP group, and PAN + 300 ng/mL RAP group was significantly increased (P < 0.01). The apoptotic rate of podocytes was significantly different between the PAN group and the PAN + RAP group (P < 0.001). There were fewer autophagic corpuscles in the PAN group and more autophagosomes were observed in the PAN + RAP group. LC3 protein expression was down-regulated in the PAN group, while its expression was up-regulated in the PAN + RAP group. In the PAN group, the levels of phosphorylated mTOR, 4EBP1, and P70S6K were increased, while in the PAN + RAP group, protein phosphorylation was reduced. Conclusions: RAP can effectively inhibit the mTOR/P70S6K/4EBP1 signaling pathway, and activate podocyte autophagy, consequently reducing podocyte apoptosis. Therefore, RAP could be used for the treatment of idiopathic membranous nephropathy.

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Association of podocyte autophagosome numbers with idiopathic membranous nephropathy and secondary membranous nephropathy

Abstract: The results indicated that the autophagy participated in the podocyte injury in IMN and sMN and the number of autophagosomes in podocytes was related to the pathological classification.

Cited by 12 publications

References 17 publications

Panax notoginseng saponins mitigate cisplatin induced nephrotoxicity by inducing mitophagy via HIF-1α

Panax notoginseng saponins mitigate cisplatin induced nephrotoxicity by inducing mitophagy via HIF-1α

Vitamin D protects podocytes from autoantibodies induced injury in lupus nephritis by reducing aberrant autophagy

Rapamycin Reduces Podocyte Apoptosis and is Involved in Autophagy and mTOR/ P70S6K/4EBP1 Signaling

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