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Mitochondrial Rac1 GTPase Import and Electron Transfer from Cytochrome c Are Required for Pulmonary Fibrosis
Journal article   Open access   Peer reviewed

Mitochondrial Rac1 GTPase Import and Electron Transfer from Cytochrome c Are Required for Pulmonary Fibrosis

Heather L Osborn-Heaford, Alan J Ryan, Shubha Murthy, Ana-Monica Racila, Chao He, Jessica C Sieren, Douglas R Spitz and A. Brent Carter
The Journal of biological chemistry, Vol.287(5), pp.3301-3312
01/27/2012
DOI: 10.1074/jbc.M111.308387
PMCID: PMC3270985
PMID: 22157762
url
https://doi.org/10.1074/jbc.M111.308387View
Published (Version of record) Open Access

Abstract

Background: Rac1 activation is linked to H 2 O 2 generation in macrophages. Results: Two cysteine residues in Rac1 modulate mitochondrial H 2 O 2 generation via import and electron transfer from cytochrome c . Conclusion: Mitochondrial Rac1 activity in alveolar macrophages is associated with oxidative stress. Significance: Rac1 directly mediates mitochondrial H 2 O 2 production in alveolar macrophages, which is linked to pulmonary fibrosis. The generation of reactive oxygen species, particularly H 2 O 2 , from alveolar macrophages is causally related to the development of pulmonary fibrosis. Rac1, a small GTPase, is known to increase mitochondrial H 2 O 2 generation in macrophages; however, the mechanism by which this occurs is not known. This study shows that Rac1 is localized in the mitochondria of alveolar macrophages from asbestosis patients, and mitochondrial import requires the C-terminal cysteine of Rac1 (Cys-189), which is post-translationally modified by geranylgeranylation. Furthermore, H 2 O 2 generation mediated by mitochondrial Rac1 requires electron transfer from cytochrome c to a cysteine residue on Rac1 (Cys-178). Asbestos-exposed mice harboring a conditional deletion of Rac1 in macrophages demonstrated decreased oxidative stress and were significantly protected from developing pulmonary fibrosis. These observations demonstrate that mitochondrial import and direct electron transfer from cytochrome c to Rac1 modulates mitochondrial H 2 O 2 production in alveolar macrophages pulmonary fibrosis.
Cytochrome c Molecular Bases of Disease Mitochondria Rac1 Macrophages Fibrosis

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