FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2107637196> ?p ?o ?g. }

• W2107637196 endingPage "533" @default.
• W2107637196 startingPage "532" @default.
• W2107637196 abstract "apolipoprotein E Primary localized cutaneous amyloidosis Apolipoprotein E (apoE) is a lipid transport protein, which is a component of lipoproteins, such as very low density lipoprotein, intermediate density lipoprotein, high density lipoprotein, and chylomicron. ApoE is also produced and secreted in the skin, and is implicated to play roles in epidermal differentiation and proliferation (1Barra R.M. Fenjves E.S. Taichman L.B. Secretion of apolipoprotein E by basal cells in cultures of epidermal keratinocytes.J Invest Dermatol. 1994; 102: 61-66Abstract Full Text PDF PubMed Google Scholar). We have reported that apoE was a component of amyloid deposits of primary localized cutaneous amyloidosis (PLCA) using immunohistochemistry, immunogold electron microscopy, and immunoblotting (Furumoto et al., 1998Furumoto H. Shimizu T. Asagami C. Muto M. Takahashi M. Hoshii Y. Ishihara T. Nakamura K. Apolipoprotein E is present in primary localized cutaneous amyloidosis.J Invest Dermatol. 1998; 111: 417-421Crossref PubMed Scopus (19) Google Scholar). PLCA, lichen amyloidosus, and macular amyloidosis are characterized by the finding that the amyloid deposits are limited to the papillary dermis (Kumakiri and Hashimoto, 1979Kumakiri M. Hashimoto K. Histogenesis of primary localized cutaneous amyloidosis: Sequential change of epidermal keratinocytes to amyloid via filamentous degeneration.J Invest Dermatol. 1979; 73: 150-162Crossref PubMed Scopus (140) Google Scholar). There is a hypothesis that the precursor protein of PLCA might be keratin protein from epidermal keratinocytes (Hashimoto et al., 1990Hashimoto K. Ito K. Taniguchi Y. Yang F. Youngberg G. Keratin in cutaneous amyloidoses.Clin Dermatol. 1990; 8: 55-65Abstract Full Text PDF PubMed Scopus (29) Google Scholar). The pathogenesis of PLCA, however, remains undetermined and the amyloid fibril protein has not been identified. There are three common alleles for apoE, e2, e3, and e4, and their gene products are apoE2, apoE3, and apoE4, respectively (Mahley, 1988Mahley R.W. Apolipoprotein E. Cholesterol transport protein with expanding role in cell biology.Science. 1988; 240: 622-630Crossref PubMed Scopus (3243) Google Scholar). In this study, we investigated whether the phenotypic variation of apoE is associated with PLCA. Fourteen Japanese patients (four females and 10 males) with PLCA were studied (mean age, 53 years; range, 26–82 years, Table I). The control group consisted of 100 healthy unrelated Japanese individuals randomly chosen from volunteers (mean age, 34.4 years; range, 21–83 years). Cutaneous amyloidosis was diagnosed clinically and histopathologically. Sera obtained from the peripheral venous blood samples were frozen at -80°C until use. Phenotypes of apoE were examined using analytical isoelectric focusing followed by immunoblotting with goat anti-apoE antibody and alkaline phosphatase-conjugated rabbit antigoat IgG (Furumoto et al., 1997Furumoto H. Nakamura K. Imamura T. Hamamoto Y. Shimizu T. Muto M. Asagami C. Association of apolipoprotein allele e2 with psoriasis vulgaris in Japanese population.Arch Dermatol Res. 1997; 289: 497-500Crossref PubMed Scopus (17) Google Scholar). Differences in apoE phenotype frequencies between the patients and control group were tested by the Chi-squared test with Yates' correction.Table IDetails of patients with primary localized cutaneous amyloidosis. Clinical data and phenotypes of apolipoprotein ENo.Type of amyloidosisaLA, lichen amyloidosis; MA, macular amyloidosis.SexAgebAge, age at onset.apoE phenotypes1LAMale45E3/32LAMale47E3/33LAMale54E3/34LAMale73E3/35LAMale82E3/36MAMale31E4/37MAMale36E4/38LAMale52E4/39LAMale64E4/310MAFemale26E4/311MAFemale62E4/312MAFemale65E4/313LAMale71E4/314LAMale44E4/4a LA, lichen amyloidosis; MA, macular amyloidosis.b Age, age at onset. Open table in a new tab There are six of the most common phenotypes of apoE, E4/4, E3/3, E2/2, E4/3, E4/2, and E3/2. As shown in Table I, nine of 14 patients (64.3%) with PLCA have apoE4/4 or E4/3 phenotype, whereas 18 of 100 (18%) of controls have apoE4/4 or E4/3 phenotype. The phenotype frequency of apoE4/3 in PLCA was significantly higher than in healthy controls (57% in PLCA vs. 17% in control, p <0.01), and this elevation was based on the increased frequency of e4 allele (0.357 in PLCA vs. 0.095 in control; Table II).Table IIApoE phenotypes and allele frequencies in PLCAPLCAControlsTotal (number/ females:males)144:1010050:50Phenotype (number/ females:males)E4/410:110:1E3/350:57639:37E2/200E4/38a4:4179:8E4/200E3/2062:4Allele frequency ε40.357a0.095ε30.6430.875ε20.00.030ap < 0.01 vs. control. Open table in a new tab ap < 0.01 vs. control. Our results indicate that the e4 allele is increased in frequency in PLCA. The e4 allele frequency in the Japanese population is 0.11, which is similar to that of Caucasians (Breslow, 1988Breslow J.L. ApoE.Physiol Rev. 1988; 68: 85-126Crossref PubMed Scopus (127) Google Scholar). ApoE4 is linked to the pathogenesis of Alzheimer's disease (AD), and the allele frequency in the AD population is significantly higher (3-fold) than that of controls (0.38 vs. 0.122) (Poirier et al., 1993Poirier J. Davignon J. Bouthillier D. Kogan S. Bertrand P. Gauthier S. Apolipoprotein E polymorphism and Alzheimer's disease.Lancet. 1993; 342: 697-699Abstract PubMed Scopus (1138) Google Scholar). ApoE is associated with amyloid plaque of the many amyloid- forming diseases (Namba et al., 1991Namba Y. Tomonaga M. Kawasaki H. Otomo E. Ikeda K. Apolipoprotein E immunoreactivity in cerebral amyloid deposits and neurofibrillary tangles in Alzheimer's disease and kuru plaque amyloid in Creutzfeldt-Jakob disease.Brain Res. 1991; 541: 163-166Crossref PubMed Scopus (973) Google Scholar;Wisniewski and Frangione, 1992Wisniewski T. Frangione B. Apolipoprotein E. a pathological chaperone protein in patients with cerebral and systemic amyloid.Neurosci Lett. 1992; 135: 235-238Crossref PubMed Scopus (709) Google Scholar;Strittmatter et al., 1993Strittmatter W.J. Saunders A.M. Schmechel D. Pericak-Vance M. Enghild J. Salvesen G.S. Roses A.D. Apolipoprotein E. High-avidity binding to β-amyloid and increased frequency of type 4 allele in late-onset familial Alzheimer disease.Proc Natl Acad Sci USA. 1993; 90: 1977-1981Crossref PubMed Scopus (3519) Google Scholar). Recently, it has been reported that carboxyl-terminal-truncated fragments of apoE4, especially apoE4 (272–299), which were generated inside cultured neurons and in AD brains resulted in large, filamentous intracellular inclusions resembling neurofibrillary tangles in AD brain (Huang et al., 2001Huang Y. Liu X.Q. Wyss-Coray T. Brecht W.J. Sanan D.A. Mahley R.W. Apolipoprotein E fragments present in Alzheimer's disease brains induce neurofibrillary tangle-like intracellular inclusions in neurons.Proc Natl Acad Sci USA. 2001; 98: 8838-8843Crossref PubMed Scopus (298) Google Scholar). The apoE4 fragments interact with phosphorylated tau and phosphorylated neurofilaments of high molecular weight. Therefore, it is suggested that apoE4 molecule plays an important role for the development and maintaining of amyloid deposit in AD brain. The function of apoE in epidermis is unknown, but it is naturally secreted by keratinocytes (Fenjves et al., 1989Fenjves E.S. Gordon D.A. Pershing L.K. Williams D.L. Taichman L.B. Systemic distribution of apolipoprotein E secreted by grafts of epidermal keratinocytes: Implications for epidermal function and gene therapy.Proc Natl Acad Sci USA. 1989; 86: 8803-8807Crossref PubMed Scopus (103) Google Scholar;Gordon et al., 1989Gordon D.A. Fenjves E.S. Williams D.L. Taichman L.B. Synthesis and secretion of apolipoprotein E by cultured human keratinocytes.J Invest Dermatol. 1989; 92: 96-99Crossref PubMed Scopus (37) Google Scholar). Our result indicates that apoE4 molecule synthesized by epidermal keratinocytes is strongly related to the pathogenesis of cutaneous amyloidosis, especially formation of amyloid fibrils. We thank Dr. Y. Hamamoto, Dr. K. Nagai, Dr. K. 1noue, and Prof. C. Asagami for their cooperation providing us the blood samples." @default.
• W2107637196 created "2016-06-24" @default.
• W2107637196 creator A5000876079 @default.
• W2107637196 creator A5037488751 @default.
• W2107637196 creator A5043094265 @default.
• W2107637196 creator A5047199720 @default.
• W2107637196 creator A5086183940 @default.
• W2107637196 date "2002-08-01" @default.
• W2107637196 modified "2023-10-13" @default.
• W2107637196 title "Apolipoprotein E4 is Associated with Primary Localized Cutaneous Amyloidosis" @default.
• W2107637196 cites W1965496447 @default.
• W2107637196 cites W1973116444 @default.
• W2107637196 cites W1973193861 @default.
• W2107637196 cites W1981541187 @default.
• W2107637196 cites W2021181758 @default.
• W2107637196 cites W2031220281 @default.
• W2107637196 cites W2034968148 @default.
• W2107637196 cites W2040952083 @default.
• W2107637196 cites W2048436366 @default.
• W2107637196 cites W2051953116 @default.
• W2107637196 cites W2063505049 @default.
• W2107637196 cites W2072682191 @default.
• W2107637196 cites W2280187329 @default.
• W2107637196 cites W4233622592 @default.
• W2107637196 doi "https://doi.org/10.1046/j.1523-1747.2002.18581.x" @default.
• W2107637196 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/12190881" @default.
• W2107637196 hasPublicationYear "2002" @default.
• W2107637196 type Work @default.
• W2107637196 sameAs 2107637196 @default.
• W2107637196 citedByCount "9" @default.
• W2107637196 countsByYear W21076371962012 @default.
• W2107637196 countsByYear W21076371962016 @default.
• W2107637196 countsByYear W21076371962017 @default.
• W2107637196 countsByYear W21076371962018 @default.
• W2107637196 countsByYear W21076371962020 @default.
• W2107637196 crossrefType "journal-article" @default.
• W2107637196 hasAuthorship W2107637196A5000876079 @default.
• W2107637196 hasAuthorship W2107637196A5037488751 @default.
• W2107637196 hasAuthorship W2107637196A5043094265 @default.
• W2107637196 hasAuthorship W2107637196A5047199720 @default.
• W2107637196 hasAuthorship W2107637196A5086183940 @default.
• W2107637196 hasBestOaLocation W21076371961 @default.
• W2107637196 hasConcept C121332964 @default.
• W2107637196 hasConcept C126322002 @default.
• W2107637196 hasConcept C1276947 @default.
• W2107637196 hasConcept C142724271 @default.
• W2107637196 hasConcept C16005928 @default.
• W2107637196 hasConcept C2777977315 @default.
• W2107637196 hasConcept C2778163477 @default.
• W2107637196 hasConcept C2779951007 @default.
• W2107637196 hasConcept C62746215 @default.
• W2107637196 hasConcept C71924100 @default.
• W2107637196 hasConceptScore W2107637196C121332964 @default.
• W2107637196 hasConceptScore W2107637196C126322002 @default.
• W2107637196 hasConceptScore W2107637196C1276947 @default.
• W2107637196 hasConceptScore W2107637196C142724271 @default.
• W2107637196 hasConceptScore W2107637196C16005928 @default.
• W2107637196 hasConceptScore W2107637196C2777977315 @default.
• W2107637196 hasConceptScore W2107637196C2778163477 @default.
• W2107637196 hasConceptScore W2107637196C2779951007 @default.
• W2107637196 hasConceptScore W2107637196C62746215 @default.
• W2107637196 hasConceptScore W2107637196C71924100 @default.
• W2107637196 hasIssue "2" @default.
• W2107637196 hasLocation W21076371961 @default.
• W2107637196 hasLocation W21076371962 @default.
• W2107637196 hasOpenAccess W2107637196 @default.
• W2107637196 hasPrimaryLocation W21076371961 @default.
• W2107637196 hasRelatedWork W1901818852 @default.
• W2107637196 hasRelatedWork W1983513655 @default.
• W2107637196 hasRelatedWork W1985064032 @default.
• W2107637196 hasRelatedWork W2022470945 @default.
• W2107637196 hasRelatedWork W2032588993 @default.
• W2107637196 hasRelatedWork W2061971339 @default.
• W2107637196 hasRelatedWork W2187075330 @default.
• W2107637196 hasRelatedWork W221467299 @default.
• W2107637196 hasRelatedWork W2614940532 @default.
• W2107637196 hasRelatedWork W2949989742 @default.
• W2107637196 hasVolume "119" @default.
• W2107637196 isParatext "false" @default.
• W2107637196 isRetracted "false" @default.
• W2107637196 magId "2107637196" @default.
• W2107637196 workType "article" @default.