| 11. |
- Zhu, Zhechen, et al.
(författare)
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Association between the ABCC11 gene polymorphism and the expression of apolipoprotein D by the apocrine glands in axillary osmidrosis.
- 2015
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Ingår i: Molecular Medicine Reports. - : Spandidos Publications. - 1791-3004 .- 1791-2997. ; 11:6, s. 4463-4467
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Tidskriftsartikel (refereegranskat)abstract
- It has been suggested that the adenosine triphosphate‑binding cassette sub‑family C member 11 (ABCC11) gene polymorphism and apolipoprotein D (ApoD), an odor precursor carrier, may be important in the formation of axillary odor. To date, few studies have examined the potential correlation between these two factors. The present study aimed to investigate the association between a 538 G>A single‑nucleotide polymorphism (SNP) of the ABCC11 gene and the mRNA expression levels of ApoD in the apocrine gland of patients with osmidrosis. The 538 G>A polymorphism genotypes of 33 patients with a clinical diagnosis of osmidrosis were analyzed by polymerase chain reaction (PCR) and a base‑quenched probe method, and they were divided into two groups according to the results. The G allele functions as a dominant gene; therefore, patients with the GG or GA genotype were allocated to Group I (n=28) and patients with the AA genotype to Group II (n=5). The mRNA expression levels of ApoD in the apocrine glands were determined by reverse transcription‑PCR. The results indicated that the mRNA expression levels of ApoD were significantly higher in the apocrine glands of patients in Group I compared with those in Group II (P<0.01). In conclusion, the results indicated that the ABCC11 gene SNP of the 538 G>A allele was associated with a downregulation of the mRNA expression of ApoD in the apocrine glands, which may indicate a role for the ABCC11 gene in the mediation of osmidrosis by enhancing the transition of odor precursors via the ApoD pathway.
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| 12. |
- Wang, Min, et al.
(författare)
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Apolipoprotein M induces inhibition of inflammatory responses via the S1PR1 and DHCR24 pathways
- 2019
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Ingår i: Molecular Medicine Reports. - 1791-2997. ; 19:2, s. 1272-1283
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Tidskriftsartikel (refereegranskat)abstract
- © 2019 Spandidos Publications. All rights reserved. Apolipoprotein M (ApoM) is a type of apolipoprotein. It is well known that high-density lipoprotein (HDL) decreases inflammatory responses via the apoM-sphingosine-1-phosphate (S1P) pathway. The present study further investigated the importance of ApoM in the inhibitory effects of HDL on inflammation. Mice with an apoM gene deficiency (apoM-/-) were employed to investigate the effects of ApoM on the expression of interleukin-1β (IL-1β), monocyte chemotactic protein-1 (MCP-1), S1P receptor-1 (S1PR1) and 3β-hydroxysterol Δ-24-reductase (DHCR24), as compared with in wild-type mice (apoM+/+). Furthermore, cell culture experiments were performed using a permanent human hybrid endothelial cell line (EA.hy926). Cells were cultured in the presence of recombinant human apoM (rec-apoM) or were induced to overexpress apoM (apoMTg); subsequently, cells were treated with tumor necrosis factor-α (TNF-α), in order to investigate the effects of ApoM on IL-1β and MCP-1. The results demonstrated that the mRNA expression levels of IL-1β and MCP-1 were significantly higher in the liver following administration of lipopolysaccharide in apoM-/- mice compared with in apoM+/+ mice. In cell culture experiments, when cells were pre-cultured with rec-apoM or were engineered to overexpress apoM (apoMTg), they exhibited decreased expression levels of IL-1β and MCP-1 following TNF-α treatment compared with in normal apoM-expressing cells (apoMTgN). Furthermore, the mRNA expression levels of IL-1β and MCP-1 were significantly elevated following addition of the S1PR1 inhibitor W146, but not by the scavenger receptor class B type I inhibitor, block lipid transport-1 (BLT-1), in apoMTg cells prior to TNF-α treatment. Conversely, there were no differences in these inflammatory biomarkers under the same conditions in apoMTgN cells. The mRNA expression levels of DHCR24 were significantly reduced by the addition of BLT-1 prior to TNF-α treatment in apoMTg cells; however, there was no difference in the expression of this inflammatory biomarker in apoMTgN cells. In conclusion, ApoM displayed inhibitory effects against the inflammatory response in vivo and in vitro; these effects may be induced via the S1PR1 and DHCR24 pathways.
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