The repair of skeletal muscle requires iron recycling through macrophage ferroportin

Gianfranca Corna, Imma Caserta, Antonella Monno, Pietro Apostoli, Angelo A. Manfredi, Clara Camaschella, Patrizia Rovere-Querini

Research output: Contribution to journalArticle

Abstract

Macrophages recruited at the site of sterile muscle damage play an essential role in the regeneration of the tissue. In this article, we report that the selective disruption of macrophage ferroportin (Fpn) results in iron accumulation within muscle-infiltrating macrophages and jeopardizes muscle healing, prompting fat accumulation. Macrophages isolated from the tissue at early time points after injury express ferritin H, CD163, and hemeoxygenase-1, indicating that they can uptake heme and store iron. At later time points they upregulate Fpn expression, thus acquiring the ability to release the metal. Transferrin-mediated iron uptake by regenerating myofibers occurs independently of systemic iron homeostasis. The inhibition of macrophage iron export via the silencing of Fpn results in regenerating muscles with smaller myofibers and fat accumulation. These results highlight the existence of a local pathway of iron recycling that plays a nonredundant role in the myogenic differentiation of muscle precursors, limiting the adipose degeneration of the tissue.

Original languageEnglish
Pages (from-to)1914-1925
Number of pages12
JournalJournal of Immunology
Volume197
Issue number5
DOIs
Publication statusPublished - Sep 1 2016

ASJC Scopus subject areas

  • Immunology
  • Medicine(all)

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