Tissue transglutaminase (TG2) - a wound response enzyme

Dilek Telci, Martin Griffin

Research output: Contribution to journalArticle

Abstract

Repair of tissue after injury depends on a series of concerted but overlapping events including, inflammation, re-epithelialization, neovascularization and synthesis and stabilization of a fibrous extracellular matrix (ECM) that is remodeled to emulate normal tissue over time. Particular members of the transglutaminase (TG) family are upregulated during wound healing and act as a novel class of wound-healing mediators during the repair process. This group of enzymes which crosslink proteins via epsilon(gamma-glutamyl) lysine bridges are involved in wound healing through their ability to stabilize proteins and also by regulating the behavior of a wide variety of cell types that are recruited to the damaged area in order to carry out tissue repair. In this article we discuss the function of the most widely expressed member of the TG family "tissue transglutaminase" (TG2) in wound repair. Using both early and recent evidence from the literature we demonstrate how the multifunctional TG2 affects the stability of the ECM, cell-ECM interactions and as a consequence cell behavior within the different phases of wound healing, and highlight how TG2 itself might be exploited for therapeutic use.
Original languageEnglish
Pages (from-to)867-882
Number of pages16
JournalFrontiers in Bioscience
Volume11
Issue number1
DOIs
Publication statusPublished - 1 Jan 2006

Fingerprint

Wound Healing
Repair
Extracellular Matrix
Transglutaminases
Wounds and Injuries
Enzymes
Tissue
Re-Epithelialization
Aptitude
Therapeutic Uses
Proteins
Stabilization
Inflammation
transglutaminase 2

Keywords

  • enzyme
  • tissue transglutaminase
  • wound healing
  • extracellular matrix
  • review

Cite this

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Tissue transglutaminase (TG2) - a wound response enzyme. / Telci, Dilek; Griffin, Martin.

In: Frontiers in Bioscience, Vol. 11, No. 1, 01.01.2006, p. 867-882.

Research output: Contribution to journalArticle

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