Abstract
Our previous study with docosahexaenoic acid (DHA) supplementation to hypertriglyceridemic men showed that DHA reduced several risk factors for cardiovascular disease, including the plasma concentration of inflammatory markers. To determine the effect of DHA supplementation on the global gene expression pattern, we performed Affymetrix GeneChip microarray analysis of blood cells [treated with lipopolysaccharide (LPS) or vehicle] drawn before and after the supplementation of DHA from the hypertriglyceridemic men who participated in that study. Genes that were significantly differentially regulated by the LPS treatment and DHA supplementation were identified. Differential regulation of 18 genes was then verified by quantitative real-time polymerase chain reaction (qRT-PCR). Both microarray and qRT-PCR data showed that DHA supplementation significantly suppressed the expression of low-density lipoprotein (LDL) receptor and cathepsin L1, both of which were also up-regulated by LPS. DHA supplementation also suppressed oxidized LDL (lectin-like) receptor 1 (OLR1). However, LPS did not induce OLR1 mRNA expression. Enrichment with Gene Ontology categories demonstrated that the genes related to transcription factor activity, immunity, host defense and inflammatory responses were inversely regulated by LPS and DHA. These results provide supporting evidence for the anti-inflammatory effects of DHA supplementation, and reveal previously unrecognized genes that are regulated by DHA and are associated with risk factors of cardiovascular diseases.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 616-621 |
| Number of pages | 6 |
| Journal | Journal of Nutritional Biochemistry |
| Volume | 23 |
| Issue number | 6 |
| DOIs | |
| State | Published - Jun 2012 |
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Keywords
- Cardiovascular disease
- Cathepsin L1
- Docosahexaenoic acid
- Gene expression
- Inflammation
- LDL receptor
- Oxidized LDL receptor
ASJC Scopus subject areas
- Biochemistry
- Clinical Biochemistry
- Molecular Biology
- Endocrinology, Diabetes and Metabolism
- Nutrition and Dietetics
Cite this
Modulation of blood cell gene expression by DHA supplementation in hypertriglyceridemic men. / Dawson, Kevin; Zhao, Ling; Adkins, Yuriko; Vemuri, Madhuri; Rodriguez, Raymond L.; Gregg, Jeffrey; Kelley, Darshan S.; Hwang, Daniel H.
In: Journal of Nutritional Biochemistry, Vol. 23, No. 6, 06.2012, p. 616-621.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Modulation of blood cell gene expression by DHA supplementation in hypertriglyceridemic men
AU - Dawson, Kevin
AU - Zhao, Ling
AU - Adkins, Yuriko
AU - Vemuri, Madhuri
AU - Rodriguez, Raymond L.
AU - Gregg, Jeffrey
AU - Kelley, Darshan S.
AU - Hwang, Daniel H.
PY - 2012/6
Y1 - 2012/6
N2 - Our previous study with docosahexaenoic acid (DHA) supplementation to hypertriglyceridemic men showed that DHA reduced several risk factors for cardiovascular disease, including the plasma concentration of inflammatory markers. To determine the effect of DHA supplementation on the global gene expression pattern, we performed Affymetrix GeneChip microarray analysis of blood cells [treated with lipopolysaccharide (LPS) or vehicle] drawn before and after the supplementation of DHA from the hypertriglyceridemic men who participated in that study. Genes that were significantly differentially regulated by the LPS treatment and DHA supplementation were identified. Differential regulation of 18 genes was then verified by quantitative real-time polymerase chain reaction (qRT-PCR). Both microarray and qRT-PCR data showed that DHA supplementation significantly suppressed the expression of low-density lipoprotein (LDL) receptor and cathepsin L1, both of which were also up-regulated by LPS. DHA supplementation also suppressed oxidized LDL (lectin-like) receptor 1 (OLR1). However, LPS did not induce OLR1 mRNA expression. Enrichment with Gene Ontology categories demonstrated that the genes related to transcription factor activity, immunity, host defense and inflammatory responses were inversely regulated by LPS and DHA. These results provide supporting evidence for the anti-inflammatory effects of DHA supplementation, and reveal previously unrecognized genes that are regulated by DHA and are associated with risk factors of cardiovascular diseases.
AB - Our previous study with docosahexaenoic acid (DHA) supplementation to hypertriglyceridemic men showed that DHA reduced several risk factors for cardiovascular disease, including the plasma concentration of inflammatory markers. To determine the effect of DHA supplementation on the global gene expression pattern, we performed Affymetrix GeneChip microarray analysis of blood cells [treated with lipopolysaccharide (LPS) or vehicle] drawn before and after the supplementation of DHA from the hypertriglyceridemic men who participated in that study. Genes that were significantly differentially regulated by the LPS treatment and DHA supplementation were identified. Differential regulation of 18 genes was then verified by quantitative real-time polymerase chain reaction (qRT-PCR). Both microarray and qRT-PCR data showed that DHA supplementation significantly suppressed the expression of low-density lipoprotein (LDL) receptor and cathepsin L1, both of which were also up-regulated by LPS. DHA supplementation also suppressed oxidized LDL (lectin-like) receptor 1 (OLR1). However, LPS did not induce OLR1 mRNA expression. Enrichment with Gene Ontology categories demonstrated that the genes related to transcription factor activity, immunity, host defense and inflammatory responses were inversely regulated by LPS and DHA. These results provide supporting evidence for the anti-inflammatory effects of DHA supplementation, and reveal previously unrecognized genes that are regulated by DHA and are associated with risk factors of cardiovascular diseases.
KW - Cardiovascular disease
KW - Cathepsin L1
KW - Docosahexaenoic acid
KW - Gene expression
KW - Inflammation
KW - LDL receptor
KW - Oxidized LDL receptor
UR - http://www.scopus.com/inward/record.url?scp=84860889282&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84860889282&partnerID=8YFLogxK
U2 - 10.1016/j.jnutbio.2011.03.004
DO - 10.1016/j.jnutbio.2011.03.004
M3 - Article
C2 - 21775114
AN - SCOPUS:84860889282
VL - 23
SP - 616
EP - 621
JO - Journal of Nutritional Biochemistry
JF - Journal of Nutritional Biochemistry
SN - 0955-2863
IS - 6
ER -