• 한국컴퓨터정보학회논문지
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• 제21권12호
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• pp.139-145
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• 2016

In this paper, we propose to evaluate the effect of Resistin-like molecule alpha (Retnla) on the expression of transporters involved in modulating concentrations of peripheral cholesterol and plasma high-density lipoprotein (HDL) cholesterol. High levels of blood cholesterol are a well-recognized risk factor for atherosclerosis and are eliminated via the process of reverse cholesterol transport (RCT). We recently showed that Retnla ameliorates hypercholesterolemia and atherosclerosis by increasing biliary cholesterol secretion, the final step of the process, in low-density lipoprotein receptor-deficient mice. However, the role of Retnla in HDL-mediated cholesterol efflux, initial step of RCT pathway, is not yet clear. To identify cholesterol transport genes regulated by Retnla, we performed an extensive microarray-based gene expression screen using livers from Retnla-overexpressing (Tg) mice and control animals. The most significant change in Retnla-Tg mice was an upregulation of ATP-binding cassette sub-family G member 4 (Abcg4) transport and was validated using quantitative RT-PCR. The validated gene was also induced by treatment of purified Retnla protein in RAW 264.7 cells incubated with acetylated low-density lipoprotein and Hepa1c1c7 cells. Taken together, these results indicates that Retnla might also accelerate initial step of RCT pathway, suggesting therapeutic value of Retnla in the treatment of hypercholesterolemia and atherosclerosis.

• 한국컴퓨터정보학회논문지
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• 제23권10호
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• pp.135-141
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• 2018

In this paper, we propose to evaluate the effect of resistin-like molecule alpha ($Relm{\alpha}$) on the progression of anemia of inflammation. Anemia of inflammation is a common feature of inflammatory disorders, including chronic kidney disease, infections, and rheumatoid arthritis. $Relm{\alpha}$ is highly up-regulated in various inflammatory states, especially those involving asthma, intestinal inflammation, and parasitic diseases, and regulates the pathogenesis of those diseases. However, the role of $Relm{\alpha}$ in anemia of inflammation is unknown. To explore the roles of $Relm{\alpha}$ in anemia of inflammation in vivo, we generated mouse model of the disease by injecting 0.25 mg/kg lipopolysaccharides (LPS) intraperitoneally into $Relm{\alpha}-deficient$ and wild-type (WT) mice daily for 10 days. Research data was expressed as differences between LPS-treated $Relm{\alpha}-deficient$ and WT mice by a two-tailed non-parametric Mann-Whitney U-test using GraphPad Instat program. The results of the study are as follows: LPS-treated $Relm{\alpha}-deficient$ mice had significantly (p<0.05) lower hemoglobin contents, hematocrit levels and red blood cell indices including mean corpuscular volume, mean corpuscular hemoglobin than WT controls. This decrease was accompanied by significant (p<0.05) increase in total white blood cell and monocyte counts in the blood. However, there was no significant difference in mRNA levels of hepatic hepcidin and renal erythropoietin between the two animal groups. Taken together, these results indicates that $Relm{\alpha}$ deficiency exacerbates the anemia by increasing inflammation, suggesting therapeutic value of $Relm{\alpha}$ in the treatment of anemia of inflammation.