FXIIIA and TGF-β over-expression produces normal musculo-skeletal phenotype in TG2-/- mice

U. Tarantino, F. Oliva, G. Taurisano, A. Orlandi, V. Pietroni, E. Candi, G. Melino, N. Maffulli

Research output: Contribution to journalArticlepeer-review

Abstract

Transglutaminase (TGs) enzymes and proteins crosslinking have for long time been implicated in the formation of hard tissue development, matrix maturation and mineralization. Among the TGs family members, in the context of connective tissue formation, TG2 and Factor XIII are expressed in cartilage by hypertrophic chondrocytes. Here, we analyse the morphological consequences of TG2 deficiency, during the development of skeletal elements. When TG2 is absent, there are not gross abnormalities in the development of the skeletal system, probably from compensatory mechanisms resulting in increased expression of FXIIIA and TGF-ß 1. In vivo other TGs may be involved in promoting chondrocytes and osteoblast differentiation and matrix mineralisation

Original languageEnglish
Pages (from-to)679-684
Number of pages6
JournalAmino Acids
Volume36
Issue number4
DOIs
Publication statusPublished - Apr 2009

Keywords

  • Endochondral ossification
  • Transglutaminase

ASJC Scopus subject areas

  • Biochemistry
  • Clinical Biochemistry
  • Organic Chemistry

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