• Applied Biological Chemistry
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• 제16권3호
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• pp.112-117
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• 1973

The very low density apolipoproteins were separated by a newly developed method of isoelectric focusing in a narrow pH gradient. Four polypeptides were isolated that differed from the major proteins of the high density or low density lipoproteins. Three of these proteins had indistinguishable amino acid compositions, but different isoelectric points, COOH-terminal alanine, no isoleucine, cysteine or cystine. Two of these polypeptides had $NH_2-terminal$ serine. The polymorphism of apolipoprotein-Ala, so designated from the COOH-terminal residue, was related to sialic acid content; one form contained 2 moles of sialic acid per mole of protein, the second, 1 mole of protein, and the third, no sialic acid. The fourth polypeptide had an amino acid composition different from the first three polypeptides and from other polypetides obtained from very low density lipoprotein. This polypeptide had $NH_2-terminal$ threonine, COOH-terminal resistant to carboxypeptidase A, no histidine, cysteine, cystine or sialic acid. These four polypeptides constituted approx. 40% of the total protein in very low density lipoprotein.

• 한국동물번식학회:학술대회논문집
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• 한국동물번식학회 2002년도 춘계학술발표대회 발표논문초록집
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• pp.82-82
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• 2002

The Wnt signaling pathway plays pivotal roles in embryonic development and oncogenesis through various signaling molecules inculding Frizzled receptor, recently characterized LRP5/6 and Dickkopf protein. Although Wnt signaling has been characterized in both developmental and oncogenic processes, little is known about its function in the normal adult. The ability of LRP5 to bind apolipoprotein E(apoE) and the abundant expression of LRP5 transcripts in hepatocytes, raise the possibility that LRP5 plays a role in the hepatic clearance of ApoE-containing chylomicron remonants, a major plasma lipoprotein carrying diet-derived cholesterol. (omitted)

• 대한방사성의약품학회지
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• 제4권1호
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• pp.26-31
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• 2018

Macrophages play a key role in atherosclerotic plaque formation, but their participation has been discerned largely via ex vivo analyses of atherosclerotic lesions. Therefore, we aimed to identify atherosclerosis on noninvasive in vivo imaging using reporter gene system. This study demonstrated that recruitment of macrophages could be detected in atherosclerotic plaques of Apolipoprotein E knockout (ApoE-/-) mice with a sodium iodide symporter (NIS) gene imaging system using $^{99m}Tc-SPECT$. This novel approach to tracking macrophages to atherosclerotic plaques in vivo could have applications in studies of arteriosclerotic vascular disease.

• Journal of Microbiology and Biotechnology
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• 제22권5호
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• pp.654-658
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• 2012

Osteoarthritis (OA) is the most common rheumatic pathology. One of the major objectives of OA research is the development of early diagnostic strategies such as those using proteomic technology. Synovial fluid (SF) in OA patients is a potential source of biomarkers for OA. The efficient and reliable preparation of SF proteomes is a critical step towards biomarker discovery. In this study, we have optimized a pretreatment method for twodimensional gel electrophoresis (2DE) separation of the SF proteome, by enriching low-abundance proteins and simultaneously removing hyaluronic acid, albumin, and IgG. SF samples pretreated using this optimized method were then evaluated by 1DE and 2DE separation followed by immunodetection of cartilage oligomeric matrix protein (COMP), a known OA biomarker, and by the identification of 3 proteins (apolipoprotein, haptoglobin precursor, and fibrinogen D fragment) that are related to joint diseases.

• Tuberculosis and Respiratory Diseases
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• 제79권3호
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• pp.143-152
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• 2016

Background: Idiopathic pulmonary fibrosis (IPF) is a progressive and lethal lung disease characterized by the accumulation of excessive fibroblasts and myofibroblasts in the extracellular matrix. The transforming growth factor ${\beta}1$ (TGF-${\beta}1$)-induced epithelial-to-mesenchymal transition (EMT) is thought to be a possible source of fibroblasts/myofibroblasts in IPF lungs. We have previously reported that apolipoprotein A1 (ApoA1) has anti-fibrotic activity in experimental lung fibrosis. In this study, we determine whether ApoA1 modulates TGF-${\beta}1$-induced EMT in experimental lung fibrosis and clarify its mechanism of action. Methods: The A549 alveolar epithelial cell line was treated with TGF-${\beta}1$ with or without ApoA1. Morphological changes and expression of EMT-related markers, including E-cadherin, N-cadherin, and ${\alpha}$-smooth muscle actin were evaluated. Expressions of Smad and non-Smad mediators and TGF-${\beta}1$ receptor type 1 ($T{\beta}RI$) and type 2 ($T{\beta}RII$) were measured. The silica-induced lung fibrosis model was established using ApoA1 overexpressing transgenic mice. Results: TGF-${\beta}1$-treated A549 cells were changed to the mesenchymal morphology with less E-cadherin and more N-cadherin expression. The addition of ApoA1 inhibited the TGF-${\beta}1$-induced change of the EMT phenotype. ApoA1 inhibited the TGF-${\beta}1$-induced increase in the phosphorylation of Smad2 and 3 as well as that of ERK and p38 mitogen-activated protein kinase mediators. In addition, ApoA1 reduced the TGF-${\beta}1$-induced increase in $T{\beta}RI$ and $T{\beta}RII$ expression. In a mouse model of silica-induced lung fibrosis, ApoA1 overexpression reduced the silica-mediated effects, which were increased N-cadherin and decreased E-cadherin expression in the alveolar epithelium. Conclusion: Our data demonstrate that ApoA1 inhibits TGF-${\beta}1$-induced EMT in experimental lung fibrosis.

• Clinical and Experimental Pediatrics
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• 제48권12호
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• pp.1370-1377
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• 2005

목 적 : 가와사끼병에서의 지질대사의 변화는 특히 이 병이 관상동맥을 직접 침범하는 질환이므로 특히 중요하다고 하겠다. 성인에 있어서 TC의 증가 및 HDL-C의 감소, Lp(a)의 증가는 죽상경화증의 중요한 위험인자의 하나로 알려져 있다. 이에 가와사끼병에서의 혈중 지질성분 및 지단백, Lp(a)의 시기별 변화와 관상동맥 병변과의 상관관계를 알아보고자 하였다. 방 법 : 2002년 1월부터 2003년 12월까지 중앙대학교병원에서 가와사끼병으로 진단되어 고농도 감마글로불린으로 치료한 환아 51명을 대상으로 TL, PL, TG, HDL-C, LDL-C, TC, apo A1, apo B, Lp(a) 등을 급성발열기, 아급성기인 발열 2주, 회복기인 2개월, 1년 후 각각 측정하였고 초음파 검사 소견에 따라 비교 분석 하였다. 또한 대조군으로는 나이와 성별을 고려한 가와사끼병이 아닌 급성발열성 질환으로 입원한 25명을 대상으로 삼았다. 결 과 : 가와사끼병에서 급성 발열기에 대조군에 비하여 HDL-C($33.64{\pm}7.49mg/dL$ vs $50.43{\pm}14.41mg/dL$, P<0.01)과 apo A1($99.75{\pm}6.39mg/dL$ vs $113.34{\pm}11.35mg/dL$, P<0.05)이 통계적으로 의미있게 감소하였다. 그러나 관상동맥 확장이나 심염 등 심합병증 여부에는 큰 차이는 없었다. 아급성기에는 모든 지질성분이 통계적으로 의미있게 증가를 보였으며 발열 2개월째에는 모든 지질성분이 정상화되었고 발병 1년 후에 역시 정상범위였으며 어느 시기에서도 관상동맥 확장이 있었던 군과 정상인 군에서 지질성분의 통계적 차이는 없었다. 결 론 : 가와사끼병의 급성발열기에 HDL-C의 및 apo A1의 감소를 보였으며 발병 2주째에는 모든 지질성분이 일시적으로 통계적으로 의미있게 증가하였다. 그러나 이런 변화는 발열 2달째에는 모두 정상화되었으며 1년 경과 후에도 계속 정상소견을 보였다. 어느 시기에도 관상동맥병변이 있었던 군과 정상관상동맥을 보였던 군에서 지질성분의 의미있는 차이는 없어 이러한 급성기의 일시적인 HDL-C과 apo A1의 감소는 가와사끼병의 관상동맥 병변 여부나 장기적인 예후와는 직접적인 큰 상관은 없고 급성혈관염이라는 염증 반응의 하나의 현상으로 사료된다. 그러나 이들이 후에 성인이 되었을 때 동맥경화발현에 미치는 영향에 대해서는 더 많은 연구가 필요하리라 생각된다.

• Asian-Australasian Journal of Animal Sciences
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• 제30권6호
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• pp.893-901
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• 2017

Objective: Hypocalcemia is an important metabolic disease of dairy cows during the transition period, although the effect of hypocalcemia on biological function in dairy cows remains unknown. Methods: In this study, proteomic, mass spectrum, bioinformatics and western blotting were employed to identify differentially expressed proteins related to serum Ca concentration. Serum samples from dairy cows were collected at three time points: 3rd days before calving (day -3), the day of calving (day 0), and 3rd days after calving (day +3). According to the Ca concentration on day 0, a total of 27 dairy cows were assigned to one of three groups (clinical, subclinical, and healthy). Samples collected on day -3 were used for discovery of differentially expressed proteins, which were separated and identified via proteomic analysis and mass spectrometry. Bioinformatics analysis was performed to determine the function of the identified proteins (gene ontology and pathway analysis). The differentially expressed proteins were verified by western blot analysis. Results: There were 57 differential spots separated and eight different proteins were identified. Vitamin D-binding protein precursor (group-specific component, GC), alpha-2-macroglobulin (A2M) protein, and apolipoprotein A-IV were related to hypocalcemia by bioinformatics analysis. Due to its specific expression (up-regulated in clinical hypocalcemia and down-regulated in subclinical hypocalcemia), A2M was selected for validation. The results were consistent with those of proteomic analysis. Conclusion: A2M was as an early detection index for distinguishing clinical and subclinical hypocalcemia. The possible pathogenesis of clinical hypocalcemia caused by GC and apolipoprotein A-IV was speculated. The down-regulated expression of GC was a probable cause of the decrease in calcium concentration.

• Journal of Nutrition and Health
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• 제32권6호
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• pp.628-636
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• 1999

There is a marked increase in geriatric disease, especially liver disease, due to the continuous increase in alcohol and fat consumption. Since the fatty liver, induced by alcohol or fat, is basically from abnormalities in the lipid metabolism, it is possible that fatty acid binding protein(FABP) which is related to the fatty acid metabolism may also be abnormal in these livers. FABP is a small molecular weight protein family present in cytosol in high concentration. It has been proposed as a fatty acid transfer protein and as a binding protein responsible for controlling intracellular free fatty acid concentration. In this research, we have examined the relationship between liver FABP and fatty liver induced by alcohol or high cholesterol diet. Rats were fed one of either semipurified liquid diets; control diet containing 65% carbohydrate, 20% protein, and 15% fat or high cholesterol diet containing 1%(w/w) cholesterol or alcohol diet containing 37% of alcohol instead of carbohydrate. After 5 weeks of feeding period, all rats received commercial chow diet for 5 weeks to examine recovery effect. Liver and blood samples were collected at 0, 1, 3, 5 and 10 weeks to analyze lipid compositions. FABP was purified from liver cytosol and injected to rabbit to obtain antiserum. Liver FABP amount was determined by SDS-PAGE and western blotting methods. Fatty acid binding capacity was determined by binding of 14Cpalmitate with the delipidated liver cytosol. Consumption of alcohol increased serum cholesterol, triglyceride concentration and decreased HDL-cholesterol concentration after 5 weeks. Serum apolipoprotein B concentration increased after 3 weeks and LDL-cholesterol and apolipoprotein A concentration changed after 1 week. Liver cholesterol and triglyceride concentration increased after 3 weeks. Consumption of high cholesterol diet changed liver and serum lipid composition after 3 weeks. Swiching to normal diet for 5 weeks did not normalize most of lipid composition in serum and liver except serum and liver except serum cholesterol, triglyceride and liver cholesterol. Liver cytosol FABP content and the fatty acid binding capacity decreased dramatically after 1 week with alcohol consumption. This results indicate that FABP content changes before the changes before the changes of blood or liver lipid composition, suggesting changes of FABP may cause development of the fatty liver induced by alcohol and can be used as an index of detecting a early development of fatty liver.

• Reproductive and Developmental Biology
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• 제29권3호
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• pp.187-191
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• 2005

본 연구는 한우 난포란이 체외성숙된 환경의 변화를 단백질 측면으로부터 검토하기 위하여 체외성숙 배지와 세포질내 단백질 변화와 종류를 검토하였다. 그 결과 배지 내의 단백질 발현량은 배양 4.5시간째까지 감소하였고, 배양 13.5시간째까지는 변화가 없었다. 그러나 배양 $13.5\~18$시간 사이에 증가한 후 배양 18시간 이후에 다시 감소하는 경향이었다. 세포질내의 단백질 발현량은 배양 4.5시간째까지 증가하였고 배양 9시간째까지 급격히 감소하였다. 배양 9시간째부터 18시간째 까지는 단백질 발현량이 유사한 경향이었으나 배양 18시간째부터 24시간째까지 다시 증가하였다. 한편 체외성숙한 배지와 세포질을 2차원 전기영동하여 각각 298개 및 35개의 단백질 spot을 확인하였고, 그 중 배지에서는 28개, 세포질에서는 5개의 spot이 유의적인 변화를 확인하였다. 이들 spot 대한MALDI-TOP분석으로 배지와 세포질에서 각각 8개 및 1개의 단백질을 동정하였다. 그 종류는 aldose reductase, alpha enolase, apolipoprotein A-1 precursor, 43M1a collectin precursor, heat shock 27kDa protein, plasminogen activator inhibitor-1 precursor, thrombospondin 1 transitional endoplasmic reticulum ATPase 및 $\beta$-tubulin이었다.

• Nutrition Research and Practice
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• 제9권4호
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• pp.379-384
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• 2015

BACKGROUND/OBJECTIVE: Apolipoprotein A5 gene promoter region T-1131C polymorphism (APOA5 T-1131C) is known to be associated with elevated plasma TG levels, although little is known of the influence of the interaction between APOA5 T-1131C and lifestyle modification on TG levels. To investigate this matter, we studied APOA5 T-1131C and plasma TG levels of subjects participating in a three-month lifestyle modification program. SUBJECTS/METHODS: A three-month lifestyle modification program was conducted with 297 participants (Age: $57{\pm}8years$) in Izumo City, Japan, from 2001-2007. Changes in energy balance (the difference between energy intake and energy expenditure) and BMI were used to evaluate the participants' responses to the lifestyle modification. RESULTS: Even after adjusting for confounding factors, plasma TG levels were significantly different at baseline among three genotype subgroups: TT, $126{\pm}68mg/dl$; TC, $134{\pm}74mg/dl$; and CC, $172{\pm}101mg/dl$. Lifestyle modification resulted in significant reductions in plasma TG levels in the TT, TC, and CC genotype subgroups: $-21.9{\pm}61.0mg/dl$, $-20.9{\pm}51.0mg/dl$, and $-42.6{\pm}78.5mg/dl$, respectively, with no significant differences between them. In a stepwise regression analysis, age, APOA5 T-1131C, body mass index (BMI), homeostasis model assessment-insulin resistance (HOMA-IR), and the 18:1/18:0 ratio showed independent association with plasma TG levels at baseline. In a general linear model analysis, APOA5 T-1131C C-allele carriers showed significantly greater TG reduction with decreased energy balance than wild type carriers after adjustment for age, gender, and baseline plasma TG levels. CONCLUSIONS: The genetic effects of APOA5 T-1131C independently affected plasma TG levels. However, lifestyle modification was effective in significantly reducing plasma TG levels despite the APOA5 T-1131C genotype background.