Caffeic acid phenethyl ester induces adrenoleukodystrophy (Abcd2) gene in human X-ALD fibroblasts and inhibits the proinflammatory response in Abcd1/2 silenced mouse primary astrocytes
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X-linked adrenoleukodystrophy (X-ALD) is a peroxisomal disorder caused by mutations in the ABCD1 gene. Accumulation of very long chain fatty acids (VLCFA) that have been attributed to reduced peroxisomal VLCFA β-oxidation activity are the hallmark of the disease. Overexpression of ABCD2 gene, the closest homolog of ABCD1, has been shown to compensate for ABCD1, thus correcting the VLCFA derangement. The accumulation of VLCFA leads to a neuroinflammatory disease process associated with demyelination of the cerebral white matter. The present study underlines the importance of caffeic acid phenethyl ester (CAPE) in inducing the expression of ABCD2 (ALDRP), and normalizing the peroxisomal β-oxidation as well as the levels of saturated and monounsaturated VLCFAs in cultured human skin fibroblasts of X-ALD patients. The expression of ELOVL1, the single elongase catalyzing the synthesis of both saturated VLCFA (C26:0) and mono-unsaturated VLCFA (C26:1), was also reduced by CAPE treatment. Importantly, CAPE upregulated Abcd2 expression and peroxisomal β-oxidation and lowered the VLCFA levels in Abcd1-deficient U87 astrocytes and B12 oligodendrocytes. In addition, using Abcd1/Abcd2-silenced mouse primary astrocytes we examined the effects of CAPE in VLCFA-induced inflammatory response. CAPE treatment decreased the inflammatory response as the expression of inducible nitric oxide synthase, inflammatory cytokine, and activation of NF-κB in Abcd1/Abcd2-silenced mouse primary astrocytes was reduced. The observations indicate that CAPE corrects both the metabolic disease of VLCFA as well as secondary inflammatory disease; therefore, it may be a potential drug candidate to be tested for X-ALD therapy in humans.
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In a model based on knock-down of Abcd1 mRNA in rat B12 oligodendrocytes, elevated Elovl1 mRNA levels were reported to coincide with increased VLCFA levels, indicating an association between VLCFA levels and regulation of Elovl1 expression.
“In a model based on knock-down of Abcd1 mRNA in rat B12 oligodendrocytes, elevated Elovl1 mRNA levels were reported to coincide with increased VLCFA levels [65] indicating an association between VLCFA levels and the regulation of Elovl1 expression.”
From Abcd2 Is a Strong Modifier of the Metabolic Impairments in Peritoneal Macrophages of Abcd1-Deficient Mice (2014) · cites this paper as [65]
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“levels [65] indicating an association between VLCFA levels and the regulation of Elovl1 expression.”
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Self-citation
- Authors
- Singh, J., Khan, M., & Singh, I.
- Affiliations
- Medical University of South Carolina (US)
- Corresponding author
- Singh, Inderjit
- Venue
- Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids
- Publisher
- Elsevier BV
- Published
- 2013-04
- Volume
- 1831
- Issue
- 4
- Pages
- 747-758
- ISSN
- 1388-1981 (ISSN-L)
- PMC
- PMC3607212
- OpenAlex
- W2094168063
- Cited by
- 21
- References
- 68
- Citations by year
- 2025: 1 · 2024: 2 · 2023: 1 · 2021: 2 · 2018: 2 · 2017: 2 · 2016: 2 · 2015: 2 · 2014: 5 · 2013: 2
- FWCI
- 2.45
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- U.S. Department of Veterans Affairs (I01 BX001072)
- Medical University of South Carolina
- Coordenação de Aperfeiçoamento de Pessoal de Nível Superior
- National Institutes of Health (1c06rr015455-01a1, 1c06rr018823-01)
- National Institute of Neurological Disorders and Stroke (NS-22576, NS 37766, R01NS037766, R01NS022576, R37NS022576)
- National Center for Research Resources (RR0118823, C06 RR-015455, C06 RR-018823)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Metabolism and Genetic Disorders
- Health Sciences › Medicine › Physiology › Lysosomal Storage Disorders Research
- Life Sciences › Neuroscience › Neurology › Neurological diseases and metabolism
- Keywords
- caffeic acid phenethyl ester, X-linked adrenoleukodystrophy, ABCD2, ABCD1, very long chain fatty acids, peroxisomal beta-oxidation, ELOVL1, peroxisomal disorders, neuroinflammation, astrocytes, oligodendrocytes, NF-κB, inducible nitric oxide synthase, cytokines, gene silencing, demyelination
- MeSH terms
- ATP Binding Cassette Transporter, Subfamily D, ATP Binding Cassette Transporter, Subfamily D, Member 1, Fatty Acid Elongases, Acetyltransferases, Adrenoleukodystrophy, Animals, Astrocytes, Caffeic Acids, Cells, Cultured, Child, Fibroblasts, Humans, Inflammation, Male, Mice, Inbred C57BL, Phenylethyl Alcohol, NF-kappa B, ATP-Binding Cassette Transporters, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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