• Title/Summary/Keyword: apolipoprotein

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Different Functional and Structural Characteristics between ApoA-I and ApoA-4 in Lipid-Free and Reconstituted HDL State: ApoA-4 Showed Less Anti-Atherogenic Activity

  • Yoo, Jeong-Ah;Lee, Eun-Young;Park, Ji Yoon;Lee, Seung-Taek;Ham, Sihyun;Cho, Kyung-Hyun
    • Molecules and Cells
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    • v.38 no.6
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    • pp.573-579
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    • 2015
  • Apolipoprotein A-I and A-IV are protein constituents of high-density lipoproteins although their functional difference in lipoprotein metabolism is still unclear. To compare anti-atherogenic properties between apoA-I and apoA-4, we characterized both proteins in lipid-free and lipidbound state. In lipid-free state, apoA4 showed two distinct bands, around 78 and $67{\AA}$ on native gel electrophoresis, while apoA-I showed scattered band pattern less than $71{\AA}$. In reconstituted HDL (rHDL) state, apoA-4 showed three major bands around $101{\AA}$ and $113{\AA}$, while apoA-I-rHDL showed almost single band around $98{\AA}$ size. Lipid-free apoA-I showed 2.9-fold higher phospholipid binding ability than apoA-4. In lipid-free state, $BS_3$-crosslinking revealed that apoA-4 showed less multimerization tendency upto dimer, while apoA-I showed pentamerization. In rHDL state (95:1), apoA-4 was existed as dimer as like as apoA-I. With higher phospholipid content (255:1), five apoA-I and three apoA-4 were required to the bigger rHDL formation. Regardless of particle size, apoA-I-rHDL showed superior LCAT activation ability than apoA-4-rHDL. Uptake of acetylated LDL was inhibited by apoA-I in both lipid-free and lipid-bound state, while apoA-4 inhibited it only lipid-free state. ApoA-4 showed less anti-atherogenic activity with more sensitivity to glycation. In conclusion, apoA-4 showed inferior physiological functions in lipid-bound state, compared with those of apoA-I, to induce more pro-atherosclerotic properties.

Apolipoprotein E Expression in Experimentally Induced Intracranial Aneurysms of Rats

  • Choi, Young-Moon;Yi, Jin-Seok;Lee, Hyung-Jin;Yang, Ji-Ho;Lee, Il-Woo
    • Journal of Korean Neurosurgical Society
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    • v.39 no.1
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    • pp.46-51
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    • 2006
  • Objective : An Intracranial aneurysm is an important acquired cerebrovascular disease that can cause a catastrophic subarachnoid hemorrhage. Atherosclerosis is one of possible mechanism, but its contribution to aneurysm formation is unclear. Human apolipoprotein E[apoE] is best known for its arterial protection from atherosclerosis. In this study we observe apoE expression in experimental cerebral aneurysms of rats to elucidate the role of apoE in the process of cerebral aneurysm formation. Methods : Twenty-four male 7-week-old Sprague-Dawley strain rats received a cerebral aneurysm induction procedure. One month[12] and three months[12] after the operation, the rats were killed, their cerebral arteries were dissected, and the regions of the bifurcation of the right anterior cerebral artery-olfactory artery [ACA-OA] bifurcations were examined histologically and immunohistochemically. Results : In the 1 month group [n=12], the ACA-OA bifurcation showed no aneurysmal change in 7 rats and early aneurysmal change in 5 rats. In the 3 months group (n=12), the bifurcation showed no aneurysmal change in 2 rats and an advanced aneurysm in 10 rats. ApoE expression were in 3 specimen in early aneurysmal change, but not in advanced aneurysms. Conclusion : ApoE expression in early aneurysmal wall suggests a possible role for apoE in early events leading to aneurysm formation. Further studios are necessary to elucidate the exact role of apoE in the pathophysiology of cerebral aneurysm.

Study on pathology of Alzheimer's disease, trends and future strategy for research (치매의 병리(病理), 연구동향(硏究動向)과 향후(向後) 연구전략(硏究戰略)에 대(對)한 고찰(考察))

  • Oh, Young-Sun;Kim, Sung-Hoon
    • Journal of Haehwa Medicine
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    • v.8 no.1
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    • pp.793-825
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    • 1999
  • For the development of drugs for alzheimer,s disease, the study was done to review the oriental pathology, clinical data, recent trends for research and strategy for future study. The results were as follows: 1. The medical term Chi-dsi implying alzheimer,s disease was referred for the first time in a medical book, Hwatasheneubijeon written by Hwa-Ta and its differentiation and treatment were studied more in Ming or Ching dynasties. Chi-dai can be differentated as weak(虛) syndrome and Shi(實) syndrome. This can be caused by deficiencies of renal Yin, renal Yang, cardiac Yin and hepatic blood, while that by deficiencies of pathological fluid(痰飮) and clotted blood(瘀血). 2. Dementia can be roughly classified as alzheimer's disease and multi-infarct disease. Its causes were known to be cholinergic transmitter, C-peptide, amyloid-${\beta}$, apolipoprotein, APP(amyloid precursor protein), TGF, MMP-9 and free radical. 3. In Korea experimental studies were chiefly done for the elimataion of C-peptide, amyloid-${\beta}$, apolipoprotein, APP for alzheimer's disease, for the development of drug inhibiting degerative change following CVA and loss of memory and also administrative measure was done by support of government. 4. Drugs of dimentia developed so far were Chi-Dai dan, extracts from aloe, mushroom, green tea, Ganoderma and also folic acid, vitamin C, DHEA and silk amino acid were reported to be effective in dimenta. 5. Future strategic research had better be done on dementia-inducing factors such as acetylcholine, C-peptide, amyloid-${\beta}$, apolipoprotein, APP, TGF, MMP-9 and free radical, development of animal model for dimentia, clinical study, epidemiology, nursing and administrative studies and also consortium for dimentia research should be formed so that repeated investment be avoided.

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Apolipoprotein E in Synaptic Plasticity and Alzheimer's Disease: Potential Cellular and Molecular Mechanisms

  • Kim, Jaekwang;Yoon, Hyejin;Basak, Jacob;Kim, Jungsu
    • Molecules and Cells
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    • v.37 no.11
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    • pp.767-776
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    • 2014
  • Alzheimer's disease (AD) is clinically characterized with progressive memory loss and cognitive decline. Synaptic dysfunction is an early pathological feature that occurs prior to neurodegeneration and memory dysfunction. Mounting evidence suggests that aggregation of amyloid-${\alpha}$ ($A{\alpha}$) and hyperphosphorylated tau leads to synaptic deficits and neurodegeneration, thereby to memory loss. Among the established genetic risk factors for AD, the ${\varepsilon}4$ allele of apolipoprotein E (APOE) is the strongest genetic risk factor. We and others previously demonstrated that apoE regulates $A{\alpha}$ aggregation and clearance in an isoform-dependent manner. While the effect of apoE on $A{\alpha}$ may explain how apoE isoforms differentially affect AD pathogenesis, there are also other underexplored pathogenic mechanisms. They include differential effects of apoE on cerebral energy metabolism, neuroinflammation, neurovascular function, neurogenesis, and synaptic plasticity. ApoE is a major carrier of cholesterols that are required for neuronal activity and injury repair in the brain. Although there are a few conflicting findings and the underlying mechanism is still unclear, several lines of studies demonstrated that apoE4 leads to synaptic deficits and impairment in long-term potentiation, memory and cognition. In this review, we summarize current understanding of apoE function in the brain, with a particular emphasis on its role in synaptic plasticity and the underlying cellular and molecular mechanisms, involving low-density lipoprotein receptor-related protein 1 (LRP1), syndecan, and LRP8/ApoER2.

Quantitation of Plasma Apolipoprotein A-I with a Sandwich Type Enzyme-Linked Immunosorbent Assay Using Monoclonal Antibodies

  • Lee, Min-Gyu;Kang, Jae-Seon;Jeong, Jae-Yeon;Jue, Dae-Myung;Kim, Hack-Joo
    • BMB Reports
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    • v.30 no.6
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    • pp.390-396
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    • 1997
  • A sandwich-type enzyme-linked immunosorbent assay (ELISA) for the quantification of human apolipoprotein A-I (apoA-I) was developed using monoclonal antibodies. For this assay, we used three monoclonal antibodies to trap and detect apo A-I. HDAI16 and HDA15 monoclonal antibodies were used for trapping apoA-I and HDAI8 monoclonal antibody was for detecting apoA-I. These three monoclonal antibodies were produced by immunizing mice with high density lipoprotein (HDL) isolated from human plasma. By immunoblot analysis, these three monoclonal antibodies were specific to apoA-I and showed no cross-reactivities with other plasma proteins. The results of competition assays for epitope cross-reactivity test also verified that these monoclonal antibodies identified separate and distinct epitopes on HDL and apoA-I. Affinity constants of monoclonal antibodies were measured by ELISA. Their association constants ranged from $10^7$ to $10^8$ $M^{-1}$. For this assay, pure apoA-I was isolated by affinity chromatography using monoclonal antibodies. In this sandwich assay, the amount of HRP-labeled HDAI8 bound to apoA-I trapped by HDAI16 and HDAI5 was proportional to apoA-I concentration in the range of 0 to 500ng/ml. ApoA-I concentration in plasma was calculated from the linear regression equation of standard curve. The precision and reliability of the assays are reflected in the low intra-and interassay coefficients of variation that averaged 3.25% and 4.30%, respectively. This assay is sensitive, simple, reproducible, convenient in incubation interval, and does not use radioisotope: thus it can be widely applied in clinical laboratories.

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Study on Relationship between Iris Constitution and Apolipoprotein E Gene Polymorphism

  • Kang, Sung-Do;Hwang, Woo-Jun;Kim, Kyung-A;Kim, Kyung-Sik;Lee, Ho-Sub;Kim, Jong-Uk;Choi, Sung-Yong;Jin, Kyong-Son
    • The Journal of Korean Medicine
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    • v.24 no.4
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    • pp.25-33
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    • 2003
  • lridology, a form of complementary and alternative medicine (CAM), is the diagnosis of medical conditions through noting irregularities of the pigmentation in the iris. lridological constitution has a strong familial aggregation and is implicated in heredity. Apolipoprotein E (apoE) gene polymorphism is one of the most well studied genetic markers of vascular disease. I investigated the relationship between iridological constitution and apoE polymorphism. I classified 87 hypertensive patients with family history of cerebral infarction and 79 controls according to iris constitution, and determined apoE genotype. Neurogenic type in hypertensives was 32.2% compared with 16.5% in controls (P<0.001). No differences in the apoE genotypes frequencies were observed in patients compared with those in controls ($x^2=0.726$, df-=2, P=0.696). However, in a population with ${\varepsilon}3/{\varepsilon}4$ genotype, the frequency of neurogenic constitution was significantly higher in hypertensives than in controls (60% vs. 0%) ($x^2=5.265$, df=l, P=0.022). These results could imply that apoE ${\varepsilon}3/{\varepsilon}4$ genotype and neurogenic iris constitution are risk factors for hypertension.

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