Short-chain fatty acids induced autophagy serves as an adaptive strategy for retarding mitochondria-mediated apoptotic cell death

Tang, Yong; Chen, Y; Jiang, Hongmei; Nie, Daotai

doi:10.1038/cdd.2010.117

Cited by 163 publications

(143 citation statements)

References 37 publications

(39 reference statements)

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“…25 Additionally, in cancer cells, butyrate treatment induced autophagy as a defense strategy to retard mitochondrial apoptosisinduced cell death. 26 We observed lower apoptosis levels and higher levels of the ATG-7 protein after acetate treatment, suggesting that acetate could induce autophagy and thereby retard apoptosis.…”

Section: Discussionmentioning

confidence: 73%

Gut Bacteria Products Prevent AKI Induced by Ischemia-Reperfusion

Andrade-Oliveira

Amano

Corrêa-Costa

et al. 2015

Journal of the American Society of Nephrology

402

330

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Short-chain fatty acids (SCFAs) are fermentation end products produced by the intestinal microbiota and have anti-inflammatory and histone deacetylase-inhibiting properties. Recently, a dual relationship between the intestine and kidneys has been unraveled. Therefore, we evaluated the role of SCFA in an AKI model in which the inflammatory process has a detrimental role. We observed that therapy with the three main SCFAs (acetate, propionate, and butyrate) improved renal dysfunction caused by injury. This protection was associated with low levels of local and systemic inflammation, oxidative cellular stress, cell infiltration/activation, and apoptosis. However, it was also associated with an increase in autophagy. Moreover, SCFAs inhibited histone deacetylase activity and modulated the expression levels of enzymes involved in chromatin modification. In vitro analyses showed that SCFAs modulated the inflammatory process, decreasing the maturation of dendritic cells and inhibiting the capacity of these cells to induce CD4 + and CD8 + T cell proliferation. Furthermore, SCFAs ameliorated the effects of hypoxia in kidney epithelial cells by improving mitochondrial biogenesis. Notably, mice treated with acetate-producing bacteria also had better outcomes after AKI. Thus, we demonstrate that SCFAs improve organ function and viability after an injury through modulation of the inflammatory process, most likely via epigenetic modification.

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Section: Discussionmentioning

confidence: 73%

Gut Bacteria Products Prevent AKI Induced by Ischemia-Reperfusion

Andrade-Oliveira

Amano

Corrêa-Costa

et al. 2015

Journal of the American Society of Nephrology

402

330

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“…Under chronic or irreversible ER stress, cells undergo apoptosis, where the Bcl-2 protein family plays a crucial role at the mitochondria to trigger cytochrome c release and formation of apoptosome (Rodriguez et al 2011). The ability of ABT-737 (Malik et al 2011) as well as HDACi (Shao et al 2004;Tang et al 2011) to induce autophagy has already been documented. Our results could be in favour of inducing autophagy by NaBu.…”

Section: Discussionmentioning

confidence: 99%

“…In addition to mitochondrial apoptosis, butyrate can induce another types of cell death namely autophagy (Shao et al 2004;Tang et al 2011).…”

Section: Introductionmentioning

confidence: 99%

ABT-737 accelerates butyrate-induced death of HL-60 cells. Involvement of mitochondrial apoptosis pathway

Stefanikova

Kliková²,

Hatok³

et al. 2013

gpb

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Abstract. The aim of presented study was to determine effect of NaBu in combination with ABT-737 on cell survival of leukemic cell line HL-60. In addition, analysis of molecular mechanism of NaBu action with a focus on mitochondrial apoptosis was performed. Both NaBu and ABT-737 are inducing death of HL-60 cells with different kinetics. ABT-737-induced cell death is fast while NaBu-induced death preceded by cell cycle arrest in G2 phase is rather slow. Cell viability was significantly decreased after 48 hours of incubation with 2 and 5 mmol/l of NaBu while it was significantly decreased after 24 hours of incubation with 1 μmol/l of ABT-737 combined with 2 and 5 mmol/l of NaBu. Incubation of HL-60 cells with NaBu was associated with increased level of pro-apoptotic protein BIM EL and decreased levels of anti-apoptotic proteins of Bcl-2 family as well as GRP78 involved in ER stress signalling. It seems that ABT-737 accelerates NaBu-induced death of HL-60 cells due to mitochondrial apoptosis resulting from ABT-737-mediated inhibition of functions and NaBu-induced decrease of the levels of anti-apoptotic Bcl-2 family proteins as well as due to accelerated decrease of GRP78 observed after the treatment of cells with combination of NaBu and ABT-737. The effect of combination of both drugs on survival of HL-60 cells seems to be synergistic at high concentrations of NaBu (2 and 5 mmol/) while it is rather antagonistic at concentrations of NaBu less than 1 mmol/l. Finally, it might be assumed that NaBu is capable to induce cell death with mechanisms independent from mitochondrial apoptosis.

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“…In addition, another short-chain fatty acid, propionate, was shown to inhibit HDAC activity (Davie 2003). Both compounds induce autophagy with the up-regulation of LAM-2 (lysosomal-associated membrane protein 2) expression and LC3 conversion (Tang et al 2011). However, considering the low stability of this compound, its use is limited to in vitro studies.…”

Section: Hdac Inhibitors Of Natural and Dietary Originsmentioning

confidence: 99%

Histone deacetylase modulators provided by Mother Nature

et al. 2012

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Protein acetylation status results from a balance between histone acetyltransferase and histone deacetylase (HDAC) activities. Alteration of this balance leads to a disruption of cellular integrity and participates in the development of numerous diseases, including cancer. Therefore, modulation of these activities appears to be a promising approach for anticancer therapy. Histone deacetylase inhibitors (HDACi) are epigenetically active drugs that induce the hyperacetylation of lysine residues within histone and non-histone proteins, thus affecting gene expression and cellular processes such as proteinprotein interactions, protein stability, DNA binding and protein sub-cellular localization. Therefore, HDACi are promising anti-tumor agents as they may affect the cell cycle, inhibit proliferation, stimulate differentiation and induce apoptotic cell death. Over the last 30 years, numerous synthetic and natural products, including a broad range of dietary compounds, have been identified as HDACi. This review focuses on molecules from natural origins modulating HDAC activities and presenting promising anticancer activities.

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Short-chain fatty acids induced autophagy serves as an adaptive strategy for retarding mitochondria-mediated apoptotic cell death

Cited by 163 publications

References 37 publications

Gut Bacteria Products Prevent AKI Induced by Ischemia-Reperfusion

Gut Bacteria Products Prevent AKI Induced by Ischemia-Reperfusion

ABT-737 accelerates butyrate-induced death of HL-60 cells. Involvement of mitochondrial apoptosis pathway

Histone deacetylase modulators provided by Mother Nature

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