Woody eyes, be gone!

Research output: Contribution to journalComment/debate

Abstract

In this issue of Blood, Shapiro et al describe the first-in-class experience of infusing plasma-derived Glu-plasminogen to 14 patients with congenital deficiency of plasminogen as part of an ongoing, phase 2/3, open-label clinical trial, reporting encouraging results.1 Congenital plasminogen deficiency is caused by homozygous or compound-heterozygous mutations in the plasminogen (PLG) gene, located on chromosome 6q26. It is, in the words of the authors, “ultra-rare,” predicted to affect ∼1 to 2 per million people.2 Plasminogen is activated to plasmin and is critical for intravascular and extravascular fibrinolysis. Other functions include wound healing, cell migration, tissue remodeling, angiogenesis, and embryogenesis. Glu-plasminogen has a glutamic acid residue at its N-terminus, as opposed to Lys-plasminogen, which has a lysine. Glu-plasminogen is the predominant form found in circulation and has a half-life of 2 to 2.5 days, whereas the half-life of Lys-plasminogen is 0.8 days.3

Original languageEnglish (US)
Pages (from-to)1266-1267
Number of pages2
JournalBlood
Volume131
Issue number12
DOIs
StatePublished - Mar 22 2018

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Plasminogen
Half-Life
Fibrinolysin
Fibrinolysis
Wound Healing
Lysine
Embryonic Development
Cell Movement
Glutamic Acid
Chromosomes
Clinical Trials
Labels
Mutation
Blood
Genes
Tissue
Plasmas
Congenital Plasminogen Deficiency
lysyl-plasminogen

ASJC Scopus subject areas

  • Biochemistry
  • Immunology
  • Hematology
  • Cell Biology

Cite this

Woody eyes, be gone! / Wong, Trisha.

In: Blood, Vol. 131, No. 12, 22.03.2018, p. 1266-1267.

Research output: Contribution to journalComment/debate

Wong, Trisha. / Woody eyes, be gone!. In: Blood. 2018 ; Vol. 131, No. 12. pp. 1266-1267.
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abstract = "In this issue of Blood, Shapiro et al describe the first-in-class experience of infusing plasma-derived Glu-plasminogen to 14 patients with congenital deficiency of plasminogen as part of an ongoing, phase 2/3, open-label clinical trial, reporting encouraging results.1 Congenital plasminogen deficiency is caused by homozygous or compound-heterozygous mutations in the plasminogen (PLG) gene, located on chromosome 6q26. It is, in the words of the authors, “ultra-rare,” predicted to affect ∼1 to 2 per million people.2 Plasminogen is activated to plasmin and is critical for intravascular and extravascular fibrinolysis. Other functions include wound healing, cell migration, tissue remodeling, angiogenesis, and embryogenesis. Glu-plasminogen has a glutamic acid residue at its N-terminus, as opposed to Lys-plasminogen, which has a lysine. Glu-plasminogen is the predominant form found in circulation and has a half-life of 2 to 2.5 days, whereas the half-life of Lys-plasminogen is 0.8 days.3",
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