Role of CD2-associated protein in podocyte apoptosis and proteinuria induced by angiotensin II

Huang, Li Jun; You, Yu-Sheng; Wu, Wei

doi:10.3109/0886022x.2014.934177

Cited by 5 publications

(4 citation statements)

References 18 publications

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“…The apoptosis assays performed on podocytes under HG and ANG II treatments also reinforced observations previously confirmed by other authors ( 16 , 19 , 20 ). Complementing these results, morphological analyses of treated podocytes showed an increase in apoptosis characteristic features in cells exposed to both treatments.…”

Section: Discussionsupporting

confidence: 89%

The Rab-Rabphilin system in injured human podocytes stressed by glucose overload and angiotensin II

Martínez-Arroyo

Ortega

Perez-Hernandez

et al. 2020

American Journal of Physiology-Renal Physiology

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Kidney injury in hypertension and diabetes entails, among in other structures, damage in a key cell of the glomerular filtration barrier, the podocyte. Podocytes are polarized and highly differentiated cells in which vesicular transport, partly driven by Rab GTPases, is a relevant process. The aim of the present study was to analyze Rab GTPases of the Rab-Rabphilin system in human immortalized podocytes and the impact of high glucose and angiotensin II. Furthermore, alterations of the system in urine cell pellets from patients with hypertension and diabetes were studied. Apoptosis was analyzed in podocytes, and mRNA level quantification, Western blot analysis, and immunofluorescence were developed to quantify podocyte-specific molecules and Rab-Rabphilin components (Rab3A, Rab27A, and Rabphilin3A). Quantitative RT-PCR was performed on urinary cell pellet from patients. The results showed that differentiated cells had reduced protein levels of the Rab-rabphillin system compared with undifferentiated cells. After glucose overload and angiotensin II treatment, apoptosis was increased and podocyte-specific proteins were reduced. Rab3A and Rab27A protein levels were increased under glucose overload, and Rabphilin3A decreased. Furthermore, this system exhibited higher levels under stress conditions in a manner of angiotensin II dose and time treatment. Immunofluorescence imaging indicated different expression patterns of podocyte markers and Rab27A under treatments. Finally, Rab3A and Rab27A were increased in patient urine pellets and showed a direct relationship with albuminuria. Collectively, these results suggest that the Rab-Rabphilin system could be involved in the alterations observed in injured podocytes and that a mechanism may be activated to reduce damage through the vesicular transport enhancement directed by this system.

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Section: Discussionsupporting

confidence: 89%

The Rab-Rabphilin system in injured human podocytes stressed by glucose overload and angiotensin II

Martínez-Arroyo

Ortega

Perez-Hernandez

et al. 2020

American Journal of Physiology-Renal Physiology

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“…These results demonstrated that MiR-30a may regulate cardiomyocyte autophagy through Beclin-1, during injury induced by Ang II. 23,24…”

Section: Discussionmentioning

confidence: 99%

“…These results demonstrated that MiR-30a may regulate cardiomyocyte autophagy through Beclin-1, during injury induced by Ang II. 23,24 Our rat study results demonstrated that MiR-30a plays an important role by regulating the Beclin-1 protein during Ang II damage, so it became possible to control the autophagy under a beneficial threshold by regulating MiR-30a expression, to protect cardiomyocytes against injury induced by Ang II. The ratio of Beclin-1/LC3-I in different groups: It was found that Beclin-1 was up-regulated by IR (n = 10 each, p = 0 < 0.05).…”

Section: Discussionmentioning

confidence: 99%

Role of MiR-30a in cardiomyocyte autophagy induced by Angiotensin II

Huang

Luo

et al. 2014

J Renin Angiotensin Aldosterone Syst

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Objective: The aim of this study was to investigate whether MiR-30a regulates autophagy by regulating the Beclin-1 protein, which is the marker for autophagosomes during myocardial injury, when induced by angiotensin II (Ang II). Methods: We randomly assigned 20 rats into two equal groups: Control group and Ang II group. We detected the expression of MiR-30a by quantitative real-time polymerase chain reaction (RT-PCR), and we employed western blotting to detect the protein expression of Beclin-1. Results: In this study, we found that Ang II induced cardiomyocyte autophagy, together with down-regulation of MiR-30a and upregulation of the Beclin-1 protein. We also found that the Beclin-1 protein is regulated by MiR-30a, by transferring a MiR-30a mimic or AMO-204 into the cardiomyocytes. Conclusion: These studies provided evidence that MiR-30a plays an important role in regulating autophagy through the Beclin-1 protein, during myocardial injury induced by Ang II.

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“…2 Anesthetic agents administered can cause apoptosismediated neurodegeneration and synapse loss, whereas they increase synaptogenesis later in neurodevelopment. [3][4][5] Recent studies based on rodents had demonstrated that maternal anesthesia in the second trimester pregnancy for several hours can induce neurodegeneration of the fetal rats. In the second trimester of pregnancy, both the rodent and human fetus show similar neurodevelopmental profiles.…”

Section: Introductionmentioning

confidence: 99%