The Interplay Between Apoptosis, Mitophagy and Mitochondrial Biogenesis Induced by Resveratrol Can Determine Activated Hepatic Stellate Cells Death or Survival

Martins, Léo Anderson Meira; Vieira, Moema Queiroz; Ilha, Mariana; Vasconcelos, Mariana de; Biehl, Henrique B.; Lima, Daniela Bonzanini de; Schein, Vanessa; Barbé-Tuana, Florencia Marı́a; Borojević, Radovan; Guma, Fátima Costa Rodrigues

doi:10.1007/s12013-014-0245-5

Cited by 52 publications

(38 citation statements)

References 57 publications

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“…Images from six random fields were acquired, deconvolved using the Interactive 3D plugin and cell fluorescence intensity was analyzed using the software ImageJ (National Institute of Health, Rock Ville Pike, Bethesda, MD, EUA). Colocalization analysis was performed using intensity correlation analysis plugin of ImageJ …”

Section: Methodsmentioning

confidence: 99%

Exogenous expression of caveolin‐1 is sufficient for hepatic stellate cell activation

Ilha

Moraes

Rohden

et al. 2019

J of Cellular Biochemistry

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Caveolin‐1 (Cav‐1) expression is increased in hepatic stellate cells (HSC) upon liver cirrhosis and it functions as an integral membrane protein of lipid rafts and caveolae that regulates and integrates multiple signals as a platform. This study aimed to evaluate the role of Cav‐1 in HSC. Thus, the effects of exogenous expression of Cav‐1 in GRX cells, a model of activated HSC, were determined. Here, we demonstrated through evaluating well‐known HSC activation markers – such as α‐smooth muscle actin, collagen I, and glial fibrillary acidic protein – that up regulation of Cav‐1 induced GRX to a more activated phenotype. GRXEGFP‐Cav1 presented an increased migration, an altered adhesion pattern, a reorganization f‐actin cytoskeleton, an arrested cell cycle, a modified cellular ultrastructure, and a raised endocytic flux. Based on this, GRX EGFP‐Cav1 represents a new cellular model that can be an important tool for understanding of events related to HSC activation. Furthermore, our results reinforce the role of Cav‐1 as a molecular marker of HSC activation.

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Section: Methodsmentioning

confidence: 99%

Exogenous expression of caveolin‐1 is sufficient for hepatic stellate cell activation

Ilha

Moraes

Rohden

et al. 2019

J of Cellular Biochemistry

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“…Thus, the PKA/CREB pathway can play a significant role in the regulation of PGC-1α expression in APPswe M17 cells. Resveratol can induce biogenesis and control the interplay between apoptosis, mitophagy and biogenesis [100]. …”

Section: Mitochondria As a Therapeutic Targetmentioning

confidence: 99%

Abnormal Glucose Metabolism in Alzheimer’s Disease: Relation to Autophagy/Mitophagy and Therapeutic Approaches

et al. 2015

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Diminished glucose metabolism accompanies many neurodegenerative diseases including Alzheimer’s disease. An understanding of the relation of these metabolic changes to the disease will enable development of novel therapeutic strategies. Following a metabolic challenge, cells generally conserve energy to preserve viability. This requires activation of many cellular repair/regenerative processes such as mitophagy/autophagy and fusion/fission. These responses may diminish cell function in the long term. Prolonged fission induces mitophagy/autophagy which promotes repair but if prolonged progresses to mitochondrial degradation. Abnormal glucose metabolism alters protein signaling including the release of proteins from the mitochondria or migration of proteins from the cytosol to the mitochondria or nucleus. This overview provides an insight into the different mechanisms of autophagy/mitophagy and mitochondrial dynamics in response to the diminished metabolism that occurs with diseases, especially neurodegenerative diseases such as Alzheimer's disease. The review discusses multiple aspects of mitochondrial responses including different signaling proteins and pathways of mitophagy and mitochondrial biogenesis. Improving cellular bioenergetics and mitochondrial dynamics will alter protein signaling and improve cellular/mitochondrial repair and regeneration. An understanding of these changes will suggest new therapeutic strategies.

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“…Failure of mitophagy or mitochondrial biogenesis affects hepatocellular function during ischemia/reperfusion and cholestasis . Moreover, interplay between these processes and oxidative metabolism, which may contribute to hepatic cell damage, has been suggested to occur in the steatotic liver . The pathophysiological relevance of mitophagy and mitochondrial biogenesis, and the mechanisms controlling them, are not yet completely understood.…”

Section: Introductionmentioning

confidence: 99%

Melatonin enhances mitophagy and mitochondrial biogenesis in rats with carbon tetrachloride‐induced liver fibrosis

Kang

Hong

Lee

2016

Journal of Pineal Research

201

161

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Liver fibrosis leads to liver cirrhosis and failure, and no effective treatment is currently available. Growing evidence supports a link between mitochondrial dysfunction and liver fibrogenesis and mitochondrial quality control-based therapy has emerged as a new therapeutic target. We investigated the protective mechanisms of melatonin against mitochondrial dysfunction-involved liver fibrosis, focusing on mitophagy and mitochondrial biogenesis. Rats were treated with carbon tetrachloride (CCl4) dissolved in olive oil (0.5 mL/kg, twice a week, i.p.) for 8 wk. Melatonin was administered orally at 2.5, 5, and 10 mg/kg once a day. Chronic CCl4 exposure induced collagen deposition, hepatocellular damage, and oxidative stress, and melatonin attenuated these increases. Increases in mRNA and protein expression levels of transforming growth factor β1 and α-smooth muscle actin in response to CCl4 were attenuated by melatonin. Melatonin attenuated hallmarks of mitochondrial dysfunction, such as mitochondrial swelling and glutamate dehydrogenase release. Chronic CCl4 exposure impaired mitophagy and mitochondrial biogenesis, and melatonin attenuated this impairment, as indicated by increases in mitochondrial DNA and in protein levels of PTEN-induced putative kinase 1 (PINK1); Parkin; peroxisome proliferator-activated receptor-gamma coactivator 1α (PGC-1α); nuclear respiratory factor 1 (NRF1); and transcription factor A, mitochondrial (TFAM). CCl4-mediated decreases in mitochondrial fission- and fusion-related proteins, such as dynamin-related protein 1 (DRP1) and mitofusin 2, were also attenuated by melatonin. Moreover, melatonin induced AMP-activated protein kinase (AMPK) phosphorylation. These results suggest that melatonin protects against liver fibrosis via upregulation of mitophagy and mitochondrial biogenesis, and may be useful as an anti-fibrotic treatment.

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The Interplay Between Apoptosis, Mitophagy and Mitochondrial Biogenesis Induced by Resveratrol Can Determine Activated Hepatic Stellate Cells Death or Survival

Cited by 52 publications

References 57 publications

Exogenous expression of caveolin‐1 is sufficient for hepatic stellate cell activation

Exogenous expression of caveolin‐1 is sufficient for hepatic stellate cell activation

Abnormal Glucose Metabolism in Alzheimer’s Disease: Relation to Autophagy/Mitophagy and Therapeutic Approaches

Melatonin enhances mitophagy and mitochondrial biogenesis in rats with carbon tetrachloride‐induced liver fibrosis

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