Fusaric acid-induced epigenetic modulation of hepatic H3K9me3 triggers apoptosis in vitro and in vivo.
Terisha GhaziSavania NagiahShanel DhaniAnil Amichund ChuturgoonPublished in: Epigenomics (2020)
Aim: To determine the effect of the food-borne mycotoxin, fusaric acid (FA) on miR-200a, SUV39H1-mediated H3K9me3, genome integrity and apoptosis in human liver (HepG2) cells and C57BL/6 mice livers. Materials & methods: MiR-200a, Sirt1, SUV39H1-mediated H3K9me3, genome integrity and apoptosis was measured in HepG2 cells and C57BL/6 mice livers using qPCR, western blot, DNA electrophoresis and luminometry. Results: FA: upregulated miR-200a and decreased Sirt1 expression in HepG2 cells and mice livers; decreased expression of SUV39H1 and KDM4B, thus decreasing H3K9me3 and increasing H3K9me1; increased cell mortality via apoptosis. Conclusion: FA induced apoptosis by upregulating miR-200a and decreasing SUV39H1-mediated H3K9me3 in HepG2 cells and mice livers.
Keyphrases
- endoplasmic reticulum stress
- oxidative stress
- induced apoptosis
- long non coding rna
- cell proliferation
- poor prognosis
- cell cycle arrest
- high fat diet induced
- long noncoding rna
- cell death
- dna methylation
- gene expression
- ischemia reperfusion injury
- cardiovascular events
- signaling pathway
- insulin resistance
- metabolic syndrome
- stem cells
- cell therapy
- binding protein
- risk assessment
- cardiovascular disease
- risk factors
- south africa
- genome wide
- skeletal muscle
- cell free
- human health