Literature DB >> 19419756

Recombinant variant fibrinogens substituted at residues gamma326Cys and gamma339Cys demonstrated markedly impaired secretion of assembled fibrinogen.

Ayumi Haneishi1, Fumiko Terasawa, Noriko Fujihara, Kazuyoshi Yamauchi, Nobuo Okumura, Tsutomu Katsuyama.   

Abstract

BACKGROUND: To study the functions of residues gamma326Cys and gamma339Cys in the assembly and/or secretion of fibrinogen, recombinant fibrinogens were synthesized to replicate naturally occurring gamma326Tyr and gamma326Ser variants, along with gamma326Ala and gamma339Ala variants.
METHODS: A fibrinogen gamma-chain expression vector was altered and transfected into Chinese hamster ovary (CHO) cells. Cell lysates and culture media of the established cell lines were subjected to ELISA and immunoblotting analysis. In addition, pulse-chase analysis was performed.
RESULTS: The CHO cells synthesized mutant gamma-chains and assembled these into fibrinogen in the cells, although these variant fibrinogens were barely secreted into the culture media. Pulse-chase analysis indicated that the rates of both assembly and secretion of the variant fibrinogens were lower than that of normal fibrinogen.
CONCLUSIONS: The present study indicated that the 326-339 intrachain disulfide bond has a crucial role in maintaining the tertiary structure of the C-terminal domain of the gamma-module, which is necessary for fibrinogen assembly and specifically secretion. A combination of the present results and observations from naturally occurring heterozygous cases of gamma326Tyr and gamma326Ser suggest that heterozygous fibrinogen molecules containing variant gamma-chains might be secreted into plasma and show impaired fibrin polymerization, resulting in a phenotype of hypodysfibrinogenemia.

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Year:  2009        PMID: 19419756     DOI: 10.1016/j.thromres.2009.03.011

Source DB:  PubMed          Journal:  Thromb Res        ISSN: 0049-3848            Impact factor:   3.944


  4 in total

1.  The fibrous form of intracellular inclusion bodies in recombinant variant fibrinogen-producing cells is specific to the hepatic fibrinogen storage disease-inducible variant fibrinogen.

Authors:  Shinpei Arai; Naoko Ogiwara; Saki Mukai; Yuka Takezawa; Mitsutoshi Sugano; Takayuki Honda; Nobuo Okumura
Journal:  Int J Hematol       Date:  2017-02-04       Impact factor: 2.490

2.  Novel variant fibrinogen γp.C352R produced hypodysfibrinogenemia leading to a bleeding episode and failure of infertility treatment.

Authors:  Masahiro Yoda; Takahiro Kaido; Tomu Kamijo; Chiaki Taira; Yumiko Higuchi; Shinpei Arai; Nobuo Okumura
Journal:  Int J Hematol       Date:  2021-06-12       Impact factor: 2.490

3.  A novel fibrinogen γ-chain frameshift mutation, p. Cys365Phefs*41, causing hypofibrinogenemia with bleeding phenotype in a Chinese family.

Authors:  Weijie Zhou; Yan Huang; Jie Wei; Jun Li Wang; Boming Huang; Xiaoxuan Zhou; Jie Yan; Yangyang Wu; Faquan Lin; Wangrong Wen
Journal:  Ann Transl Med       Date:  2021-08

4.  Recombinant γY278H Fibrinogen Showed Normal Secretion from CHO Cells, but a Corresponding Heterozygous Patient Showed Hypofibrinogenemia.

Authors:  Tomu Kamijo; Takahiro Kaido; Masahiro Yoda; Shinpei Arai; Kazuyoshi Yamauchi; Nobuo Okumura
Journal:  Int J Mol Sci       Date:  2021-05-14       Impact factor: 5.923

  4 in total

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