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Thymosin β4-sulfoxide attenuates inflammatory cell infiltration and promotes cardiac wound healing.

Abstract：

:The downstream consequences of inflammation in the adult mammalian heart are formation of a non-functional scar, pathological remodelling and heart failure. In zebrafish, hydrogen peroxide released from a wound is the initial instructive chemotactic cue for the infiltration of inflammatory cells, however, the identity of a subsequent resolution signal(s), to attenuate chronic inflammation, remains unknown. Here we reveal that thymosin β4-sulfoxide lies downstream of hydrogen peroxide in the wounded fish and triggers depletion of inflammatory macrophages at the injury site. This function is conserved in the mouse and observed after cardiac injury, where it promotes wound healing and reduced scarring. In human T-cell/CD14+ monocyte co-cultures, thymosin β4-sulfoxide inhibits interferon-γ, and increases monocyte dispersal and cell death, likely by stimulating superoxide production. Thus, thymosin β4-sulfoxide is a putative target for therapeutic modulation of the immune response, resolution of fibrosis and cardiac repair.

journal_name

Nat Commun

journal_title

Nature communications

authors

Evans MA,Smart N,Dubé KN,Bollini S,Clark JE,Evans HG,Taams LS,Richardson R,Lévesque M,Martin P,Mills K,Riegler J,Price AN,Lythgoe MF,Riley PR

doi

10.1038/ncomms3081

subject

Has Abstract

pub_date

2013-01-01 00:00:00

pages

2081

issn

2041-1723

pii

ncomms3081

journal_volume

4

pub_type

杂志文章

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