Autophagy is involved in aldosterone-induced mesangial cell proliferation

Wang, Bin; Miao, Lei; Xu, Xianlin; He, Xiaozhou

doi:10.3892/mmr.2016.5807

Cited by 4 publications

(4 citation statements)

References 28 publications

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“…Autophagy is known to be a self-degradative process that is important for balancing sources of energy at critical times during development, and in response to nutrient stress ( 32 ). Studies have demonstrated that autophagy is involved in a number of general processes, including proliferation, development, apoptosis and cell death ( 33 , 34 ). LC3BII, Beclin1 and P62 are closely associated with the formation of autophagosomes, serving as markers of autophagy ( 35 ).…”

Section: Discussionmentioning

confidence: 99%

Dexamethasone-induced production of reactive oxygen species promotes apoptosis via endoplasmic reticulum stress and autophagy in MC3T3-E1 cells

Liu

Zhao

et al. 2018

Int J Mol Med

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Apoptosis of osteoblasts, triggered by prolonged or excessive use of glucocorticoids (GCs), has been identified as a dominant contributor to the development of osteoporosis and osteonecrosis. However, the molecular mechanisms underlying GC-induced apoptosis are multifaceted and remain to be fully elucidated. The present study aimed to explore the correlation between dexamethasone (DEX)-induced reactive oxygen species (ROS), autophagy and apoptosis in MC3T3-E1 osteoblast-like cells. Cell viability was assessed using a Cell Counting Kit-8 assay, and flow cytometry was performed to assess cellular apoptosis, cell cycle and ROS production. Immunofluorescence and western blot analysis were respectively used to detect autophagic vacuoles and the expression of proteins, including cyclin D kinase (CDK)2, poly[ADP ribose] polymerase, caspase-3, activating transcription factor (ATF)4, CCAAT/enhancer-binding protein homologous protein (CHOP), Beclin1, microtubule-associated proteins 1A/1B light chain (LC)3B and P62. It was revealed that DEX not only reduced cell viability, but also promoted apoptosis via the activation of endoplasmic reticulum (ER) stress. In addition, DEX induced cell cycle arrest at G0/G1 phase via inhibition of the expression of CDK2, and the production of ROS was activated. Of note, the DEX-mediated changes in viability and apoptosis were attenuated in MC3T3-E1 cells after treatment with 3-methyladenine, which is an autophagy inhibitor. Treatment with the antioxidant N-acetylcysteine abolished the effect of DEX on the proliferation, apoptosis, ER stress and autophagy of MC3T3-E1 cells. In conclusion, the present results indicated that DEX promoted the production of ROS, which enhanced apoptosis through activation of autophagy and ER stress in MC3T3-E1 cells.

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Section: Discussionmentioning

confidence: 99%

Dexamethasone-induced production of reactive oxygen species promotes apoptosis via endoplasmic reticulum stress and autophagy in MC3T3-E1 cells

Liu

Zhao

et al. 2018

Int J Mol Med

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“…The findings are consistent with the fact that the site of contact of mitochondria with the endoplasmic reticulum induced the formation of autophagosomes. 54 Autophagy is a self-protective cellular mechanism limiting toxicity to promote cell survival, 55,56 and autophagy could control inflammatory signaling by regulating the secretion of inflammatory mediators. 57,58 Evidence indicates that autophagy is closely related to the inflammatory response, 59 which is consistent with our findings that DEHPexposed quail had increased levels of TNF-α and the formation of typical autophagosomes.…”

Section: Discussionmentioning

confidence: 99%

Gap Junction Protein Connexin 43 as a Target Is Internalized in Astrocyte Neurotoxicity Caused by Di-(2-ethylhexyl) Phthalate

Zhao

Tang

Sun

et al. 2022

J. Agric. Food Chem.

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phthalate (DEHP) is widely used as a plasticizer in plastic products, consumer products, and packaging materials. It is of great health concern in both animals and humans as it released into the environment and entered into the body from plastic products over time, thereby resulting in neurotoxicity. As a pivotal regulator of the central nervous system (CNS), astrocytes, are crucial for maintaining brain homeostasis. Nevertheless, the underlying reason for astrocyte neurotoxicity due to DEHP exposure remains incompletely understood. Here, using an in vivo model of neurotoxicity in quail, this study summarizes that Cx43 is internalized by phosphorylation and translocated to the nucleus as a consequence of DEHP exposure in astrocytes. This study further demonstrated that astrocytes transformed to pro-inflammatory status and induced the formation of autophagosomes. Of note, integrated immunofluorescent codetection approaches revealed an overexpression of the glial fibrillary acidic protein (GFAP) and down-expression of Cx43 in astrocytes. Therefore, in terms of neurotoxicity, this experiment in vivo models directly linked Cx43 internalization to autophagy and neuroinflammation and ultimately locked these changes to the astrocytes of the brain. These findings unveil a potential approach targeting Cx43 internalization for the treatment of neurodegeneration caused by DEHP exposure in astrocytes.

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“…Conversely, inhibition of PI3K/Akt signaling inhibits the phosphorylation of mTOR, thereby enhancing autophagy ( Wang et al, 2015 ). Besides, autophagy can also be induced by RAS/RAF/MEK/ERK signaling pathway ( Zhang et al, 2017 ; Sooro et al, 2018 ) and aldosterone ( Yang et al, 2016 ; Luo et al, 2017 ).…”

Section: Introductionmentioning

confidence: 99%

“…( Chen et al, 2015 ; Chen and Sun 2019 ). Aldosterone may induce autophagy to cause an aggravation of diseases ( Yang et al, 2016 ; Luo et al, 2017 ), and KL (+/-) mice showed elevated serum levels of aldosterone. These results suggest that Klotho deficiency may decrease elastin levels in smooth muscle cells by upregulating aldosterone and thereby inducing autophagy ( Chen et al, 2015 ).…”

Section: Introductionmentioning

confidence: 99%

Klotho as Potential Autophagy Regulator and Therapeutic Target

Zhou

et al. 2021

Front. Pharmacol.

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The protein Klotho can significantly delay aging, so it has attracted widespread attention. Abnormal downregulation of Klotho has been detected in several aging-related diseases, such as Alzheimer’s disease, kidney injury, cancer, chronic obstructive pulmonary disease (COPD), vascular disease, muscular dystrophy and diabetes. Conversely, many exogenous and endogenous factors, several drugs, lifestyle changes and genetic manipulations were reported to exert therapeutic effects through increasing Klotho expression. In recent years, Klotho has been identified as a potential autophagy regulator. How Klotho may contribute to reversing the effects of aging and disease became clearer when it was linked to autophagy, the process in which eukaryotic cells clear away dysfunctional proteins and damaged organelles: the abovementioned diseases involve abnormal autophagy. Interestingly, growing evidence indicates that Klotho plays a dual role as inducer or inhibitor of autophagy in different physiological or pathological conditions through its influence on IGF-1/PI3K/Akt/mTOR signaling pathway, Beclin 1 expression and activity, as well as aldosterone level, which can help restore autophagy to beneficial levels. The present review examines the role of Klotho in regulating autophagy in Alzheimer’s disease, kidney injury, cancer, COPD, vascular disease, muscular dystrophy and diabetes. Targeting Klotho may provide a new perspective for preventing and treating aging-related diseases.

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Autophagy is involved in aldosterone-induced mesangial cell proliferation

Cited by 4 publications

References 28 publications

Dexamethasone-induced production of reactive oxygen species promotes apoptosis via endoplasmic reticulum stress and autophagy in MC3T3-E1 cells

Dexamethasone-induced production of reactive oxygen species promotes apoptosis via endoplasmic reticulum stress and autophagy in MC3T3-E1 cells

Gap Junction Protein Connexin 43 as a Target Is Internalized in Astrocyte Neurotoxicity Caused by Di-(2-ethylhexyl) Phthalate

Klotho as Potential Autophagy Regulator and Therapeutic Target

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