Literature DB >> 7692927

Expression of GPIV and N(aka) antigen on monocytes in N(aka)-negative subjects whose platelets lack GPIV.

H Take1, H Kashiwagi, Y Tomiyama, S Honda, Y Honda, H Mizutani, T Furubayashi, T Karasuno, T Nishiura, Y Kanayama.   

Abstract

The platelet antigen N(aka) was once considered to be a platelet-specific alloantigen and is carried on platelet membrane glycoprotein (GP) IV. Recent studies suggest that N(aka)-negative subjects lack platelet GPIV. GPIV is an important adhesive receptor and expressed on the surface of monocytes as well as of platelets. In the present study, flow cytometry was used to detect GPIV and N(aka) antigen on the surface of monocytes. N(aka) antigen was expressed on monocytes as well as on platelets in N(aka)-positive subjects (n = 6) (P-GPIV-positive subjects). To our surprise, monocytes of N(aka)-negative subjects (n = 7) (P-GPIV-negative subjects) having no anti-N(aka) antibody in their serum expressed GPIV and N(aka) antigen to almost the same degree as did the monocytes of P-GPIV-positive subjects. Competitive experiments using OKM5 (a monoclonal antibody against GPIV) and anti-N(aka) antibody showed that the epitope of anti-N(aka) antibody on monocytes was very close to that of OKM5. In two P-GPIV-negative subjects having anti-N(aka) antibody in their serum, GPIV and N(aka) antigen were not expressed on the surface of either monocytes or platelets. These results indicate that the GPIV molecules and N(aka) antigen are expressed on the surface of monocytes in the majority of P-GPIV-negative subjects, but that in a very few P-GPIV-negative subjects neither GPIV nor N(aka) antigen is expressed on the surface of their monocytes. We hypothesize that P-GPIV-negative subjects who carry neither GPIV nor N(aka) antigen on their monocytes produce anti-N(aka) antibody as a result of transfusion or pregnancy.

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Year:  1993        PMID: 7692927     DOI: 10.1111/j.1365-2141.1993.tb03091.x

Source DB:  PubMed          Journal:  Br J Haematol        ISSN: 0007-1048            Impact factor:   6.998


  5 in total

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Authors:  Monika Ewa Rać; Krzysztof Safranow; Wojciech Poncyljusz
Journal:  Mol Med       Date:  2007 May-Jun       Impact factor: 6.354

2.  Reduced uptake of oxidized low density lipoproteins in monocyte-derived macrophages from CD36-deficient subjects.

Authors:  S Nozaki; H Kashiwagi; S Yamashita; T Nakagawa; B Kostner; Y Tomiyama; A Nakata; M Ishigami; J Miyagawa; K Kameda-Takemura
Journal:  J Clin Invest       Date:  1995-10       Impact factor: 14.808

3.  CD36 mediates long-chain fatty acid transport in human myocardium: complete myocardial accumulation defect of radiolabeled long-chain fatty acid analog in subjects with CD36 deficiency.

Authors:  S Nozaki; T Tanaka; S Yamashita; K Sohmiya; T Yoshizumi; F Okamoto; Y Kitaura; C Kotake; H Nishida; A Nakata; T Nakagawa; K Matsumoto; K Kameda-Takemura; S Tadokoro; Y Kurata; Y Tomiyama; K Kawamura; Y Matsuzawa
Journal:  Mol Cell Biochem       Date:  1999-02       Impact factor: 3.396

4.  Molecular basis of CD36 deficiency. Evidence that a 478C-->T substitution (proline90-->serine) in CD36 cDNA accounts for CD36 deficiency.

Authors:  H Kashiwagi; Y Tomiyama; S Honda; S Kosugi; M Shiraga; N Nagao; S Sekiguchi; Y Kanayama; Y Kurata; Y Matsuzawa
Journal:  J Clin Invest       Date:  1995-03       Impact factor: 14.808

5.  Functionalization of CD36 cardiovascular disease and expression associated variants by interdisciplinary high throughput analysis.

Authors:  Namrata Madan; Andrew R Ghazi; Xianguo Kong; Edward S Chen; Chad A Shaw; Leonard C Edelstein
Journal:  PLoS Genet       Date:  2019-07-25       Impact factor: 5.917

  5 in total

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