Oleic Acid Protects from Arsenic-Induced Cardiac Hypertrophy via AMPK/FoxO/NFATc3 Pathway

Samanta, Jayeeta; Mondal, Arunima; Saha, Srimoyee; Chakraborty, Santanu; Sengupta, Arunima

doi:10.1007/s12012-019-09550-9

Cited by 32 publications

(26 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In contrast, overexpression of FoxO1 rescued abnormal growth of the heart 18 . Recently, oleic acid was shown to activate AMPK and increase FoxO1 nuclear translocation, thus reducing NFATc3 expression and attenuating arsenic‐induced cardiac hypertrophy 36 . These findings suggest that AMPK protects against cardiac hypertrophy by regulating the transcription factor FoxO1.…”

Section: Role and Molecular Mechanism Of Foxo1 In Cardiac Hypertrophymentioning

confidence: 98%

“…Recent advancements demonstrated that AMPK protects against cardiac hypertrophy by inhibiting protein synthesis through many transcriptional regulation factors, including FoxOs, NFAT, and PPARα. 18,36,39 Activation of AMPK by 5-aminoimidazole-4carboxamide ribonucleoside (AICAR, a specific AMPK activator) attenuates hypertrophy of cardiomyocytes by regulating FoxO1/MuRF1 signalling. 39 Notably, mutation of AMPKγ2 subunit inactivated FoxO1 and stimulated proliferation and hypertrophy of cardiomyocytes.…”

Section: Foxo1 and The Ampk Pathwaymentioning

confidence: 99%

See 1 more Smart Citation

The role and molecular mechanism of FoxO1 in mediating cardiac hypertrophy

Chen

Cheng

2020

ESC Heart Failure

View full text Add to dashboard Cite

Cardiac hypertrophy can lead to heart failure and cardiovascular events and has become a research hotspot in the field of cardiovascular disease. Despite extensive and in-depth research, the pathogenesis of cardiac hypertrophy is far from being fully understood. Increasing evidence has shown that the transcription factor forkhead box protein O 1 (FoxO1) is closely related to the occurrence and development of cardiac hypertrophy. This review summarizes the current literature on the role and molecular mechanism of FoxO1 in cardiac hypertrophy. We searched the database MEDLINE via PubMed for available evidence on the effect of FoxO1 on cardiac hypertrophy. FoxO1 has many effects on multiple diseases, including cardiovascular diseases, diabetes, cancer, aging, and stem cell activity. Recent studies have shown that FoxO1 plays a critical role in the development of cardiac hypertrophy. Evidence for this relationship includes the following. (i) FoxO1 can regulate cardiac growth/protein synthesis, calcium homeostasis, cell apoptosis, and autophagy and (ii) is controlled by several upstream signalling molecules (e.g. phosphatidylinositol 3-kinase/Akt, AMP-activated protein kinase, and sirtuins) and regulates many downstream transcription proteins (e.g. ubiquitin ligases muscle RING finger 1/muscle atrophy F-box, calcineurin/nuclear factor of activated T cells, and microRNAs). In response to stress or external stimulation (e.g. low energy, oxidative stress, or growth factor signalling), FoxO1 undergoes post-translational modification and transfers from the cytoplasm to nucleus, thus regulating the expression of a series of target genes in myocardium that are involved in cardiac growth/protein synthesis, calcium homeostasis, cell apoptosis, and autophagy. (iii) Finally, targeted regulation of FoxO1 is an effective method of intervening in myocardial hypertrophy. The information reviewed here should be significant for understanding the roles of FoxO1 in cardiac hypertrophy and should contribute to the design of further studies related to FoxO1 and the hypertrophic response. It should also shed light on a potential treatment for cardiac hypertrophy.

show abstract

Section: Role and Molecular Mechanism Of Foxo1 In Cardiac Hypertrophymentioning

confidence: 98%

Section: Foxo1 and The Ampk Pathwaymentioning

confidence: 99%

The role and molecular mechanism of FoxO1 in mediating cardiac hypertrophy

Chen

Cheng

2020

ESC Heart Failure

View full text Add to dashboard Cite

show abstract

“…AMPK has been reported to counter cardiac hypertrophy through the inhibition of p70S6K, thus limiting protein synthesis (Mailleux et al, 2018; B. Wang et al, 2016). AMPK can also regulate the transcriptional activity, such as the suppression of hypertrophic gene transcription by increased nuclear FoxO1 localization (Gélinas et al, 2018; Samanta et al, 2019), and suppress cardiac hypertrophy by regulating microRNA expression, such as increasing mir‐133a levels (Kuwabara et al, 2015). Additionally, AMPK can inhibit cardiac hypertrophy by increasing the density and inhibiting the accumulation of microtubules (Fassett et al, 2013), alleviating energy deficiency (Dong et al, 2018), regulating autophagy (Z. P. Wang et al, 2019), and inhibiting endoplasmic reticulum stress (W. W. Lu et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

Bone marrow mesenchymal stem cells inhibit cardiac hypertrophy by enhancing FoxO1 transcription

Qiu

Xiao

Zhou

et al. 2020

Cell Biology International

View full text Add to dashboard Cite

Bone marrow–derived mesenchymal stem cells (BMSCs) have therapeutic potential for certain heart diseases. Previous studies have shown that stem cells inhibit cardiac hypertrophy; however, it is necessary to explore the mechanisms underlying this effect. This study aimed to investigate the possible mechanism underlying the inhibitory effect of BMSCs on cardiomyocyte hypertrophy. We induced cardiomyocyte hypertrophy in cultured rat cells through isoproterenol (ISO) treatment with or without BMSC coculture. A microarray was performed to analyze messenger RNA expression in response to ISO treatment and BMSC coculture. Pathway enrichment analysis showed that the expression of differential genes was closely related to the 5′‐adenosine monophosphate‐activated protein kinase (AMPK) signaling pathway and that the expression of forkhead box O 1 (FoxO1) was significantly increased in the presence of BMSCs. Furthermore, we determined the expression levels of p‐AMPK/AMPK and p‐FoxO1/FoxO1 by western blot analysis. The expression of p‐AMPK/AMPK was upregulated, whereas that of p‐FoxO1/FoxO1 was downregulated upon coculturing with BMSCs. The AMPK‐specific antagonist Compound C inhibited the downregulation of p‐FoxO1/FoxO1 induced by the BMSC coculture. Furthermore, treatment with the specific FoxO1 antagonist AS1842856 reduced the inhibitory effects of BMSCs on cardiomyocyte hypertrophy in vivo and in vitro. Our present study demonstrates the inhibition of cardiomyocyte hypertrophy by BMSCs, which occurs partly through the AMPK–FoxO1 signaling pathway.

show abstract

“…They attributed this finding to decreased activity of adenosine monophosphate-activated protein kinase and forkhead box transcription factor along with increased expression of nuclear factor of activated T-cells, cytoplasmic 3. 37 Whether these effects can be translated into in vivo studies remains to be investigated, and thus future studies are essential to provide confirming evidence. Hormetic Effect of Arsenic on Pulpal Cells Nassar et al…”

Section: Discussionmentioning

confidence: 99%

The Hormetic Effect of Arsenic Trioxide on Rat Pulpal Cells: An In Vitro Preliminary Study

et al. 2020

View full text Add to dashboard Cite

Objectives Despite the agreement that there is no longer any indication for arsenic use in modern endodontics, some concerns are surfacing about the minute amount of arsenic trioxide (As2O3) released from Portland cement-based materials. The present study investigated the effect of different concentrations of As2O3 on rat pulpal cells and the efficacy of N-acetylcysteine (NAC) in preventing As2O3-mediated toxicity. Materials and Methods Cytotoxicities of 50, 10, or 5 µm As2O3 and the effect of cells co-treatment with 50 µm As2O3 and 5,000 µm NAC or 500 µm NAC were tested at 24 hours or 3 days. Cell viability was assessed by means of MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay and cellular morphological changes were observed under phase contrast microscope. Statistical Analysis Two-way analysis of variance with Tukey’s post-hoc test was used to evaluate differences between the groups (α = 0.05). Results At both exposure times, 50 µm As2O3 resulted in lower optical density (OD) values when compared with 10 or 5 µm As2O3. At 24 hours, 10 µm As2O3 resulted in a higher OD value compared with the control; however, at 3 days the difference was statistically insignificant. At each exposure time, the OD value of 5 µm As2O3 group was comparable to the control and 10 µm As2O3 group. There were no significant differences between 50 µm As2O3 group and 500 NAC+50 µm As2O3 group; however, these two groups had lower OD values when compared with 5,000 NAC + 50 µm As2O3 group at 24 hours and 3 days. The latter group showed significantly lower OD value in comparison with the control at 24 hours and 3 days. Control cells were polygonal-shaped while 50 µm As2O3-treated cells exhibited contracted and spherical morphology with increased intercellular spaces. At 24 hours, 10 μm and 5 µm As2O3-treated cells were slightly hypertrophic. Cells co-treated with NAC and As2O3 showed increased intercellular spaces and lower cellular density compared with the control. Conclusions As2O3 displayed a hormetic effect on pulpal cells; however, the proliferative effect induced by low As2O3 concentrations should be interpreted with caution. NAC did not prevent As2O3-mediated toxicity; however, it demonstrated potential for ameliorating this toxicity.

show abstract

Oleic Acid Protects from Arsenic-Induced Cardiac Hypertrophy via AMPK/FoxO/NFATc3 Pathway

Cited by 32 publications

References 38 publications

The role and molecular mechanism of FoxO1 in mediating cardiac hypertrophy

The role and molecular mechanism of FoxO1 in mediating cardiac hypertrophy

Bone marrow mesenchymal stem cells inhibit cardiac hypertrophy by enhancing FoxO1 transcription

The Hormetic Effect of Arsenic Trioxide on Rat Pulpal Cells: An In Vitro Preliminary Study

Contact Info

Product

Resources

About