Zinc as a modulator of transglutaminase activity - Laboratory and pathophysiological aspects

Pål Stenberg; Bodil Roth; Bodil Ohlsson

doi:10.1016/j.jtauto.2021.100110

Zinc as a modulator of transglutaminase activity - Laboratory and pathophysiological aspects

J Transl Autoimmun. 2021 Jun 17:4:100110. doi: 10.1016/j.jtauto.2021.100110. eCollection 2021.

Authors

Pål Stenberg¹, Bodil Roth², Bodil Ohlsson²

Affiliations

¹ Lund University, Skåne University Hospital Malmö, Clinical Coagulation Research Unit, Malmö, Sweden.
² Lund University, Skåne University Hospital Malmö, Department of Internal Medicine, Malmö, Sweden.

Abstract

For a whole century, citrate has been used as an in vitro anticoagulant via chelation of calcium. Later, also EDTA was introduced as an anticoagulant. An often overlooked fact is that zinc is bound to citrate and EDTA with affinities much greater than that for calcium, imposing problems in biomedical research. In vivo, proteins of the S100 family are released from leukocytes and known to bind calcium. Some of them, e.g., calprotectin, also chelate zinc. Thus, at an inflamed site, the ratio between Ca²⁺ and Zn²⁺ is changed. This mechanism is of importance for the modulation of the activation of a fascinating family of post-translationally acting calcium-dependent thiol enzymes, the transglutaminases, which are inhibited by zinc. This presentation illustrates the complexity of in vitro studies with zinc. Moreover, it exemplifies the role of Zn²⁺ in pathophysiological situations such as celiac disease and neurodegeneration.

Keywords: Autoimmunity; Celiac disease; Citrate; Neurodegeneration; Transglutaminase; Zinc.

Publication types

Review