Abstract
Carnitine palmitoyltransferase-2 (CPT2) is a mitochondrial enzyme involved in long-chain fatty acid entry into mitochondria for their β-oxidation and energy production. Two phenotypes are associated with the extremely reduced CPT2 activity in genetically deficient patients: neonatal lethality or, in milder forms, myopathy. Resveratrol (RSV) is a phytophenol produced by grape plant in response to biotic or abiotic stresses that displays anti-oxidant properties, in particular through AP-1, NFκB, STAT-3, and COX pathways. Some beneficiary effects of RSV are due to its modulation of microRNA (miRNA) expression. RSV can enhance residual CPT2 activities in human fibroblasts derived from CPT2-deficient patients and restores normal fatty acid oxidation rates likely through stimulation of mitochondrial biogenesis. Here, we report changes in miRNA expression linked to CPT2-deficiency, and we identify miRNAs whose expression changed following RSV treatment of control or CPT2-deficient fibroblasts isolated from patients. Our findings suggest that RSV consumption might exert beneficiary effects in patients with CPT2-deficiency.
Highlights
Resveratrol (RSV, trans-3,5,40 -trihydroxystilbene) is a phytoalexin produced by numerous plants in response to abiotic or biotic stress [1,2,3]
Increasing Parametric p Value miRNAs upregulated in Carnitine palmitoyltransferase-2 (CPT2)-deficient fibroblasts: 449b miRNAs miRNAs upregulated in CPT2-deficient fibroblasts: 10b miRNAs downregulated in CPT2-deficient fibroblasts: let-7d let-7a3
Twelve miRNAs were upregulated and 24 miRNAs downregulated in control fibroblasts, versus 8 miRNAs upregulated and 16 miRNAs downregulated in CPT2-deficient fibroblasts
Summary
Resveratrol (RSV, trans-3,5,40 -trihydroxystilbene) is a phytoalexin produced by numerous plants in response to abiotic or biotic stress [1,2,3]. This polyphenol compound admittedly protects humans against various diseases (cardiovascular and inflammation-associated pathologies, infection, cancer, neurodegenerescence, aging, etc.) through the modulation of several signaling pathways, including those mediated by transcription factors AP-1 [4], NFκB, and STAT-3 [5] or the COX enzyme [6]. MiRNA primarily controls mRNA translation and stability Due to their ability to regulate several hundred transcripts directly or indirectly through targeting components of key regulatory pathways, miRNAs behave as master regulators that impact all aspects of cell homeostasis and functions. Many miRNAs are considered either as tumor suppressor or onco-miRs, depending on the cellular context [8]
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