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Published on: September 28, 2016
Cryptogenic organizing pneumonia in Tomm5(-/-) mice.
1Department of Pathology, St Jude Children's Research Hospital, Memphis, TN 38105, USA. peter.vogel@stjude.org
Veterinary Pathology
|June 13, 2012
Summary
Mitochondrial protein import is crucial. Tomm5 knockout mice unexpectedly developed lung fibrosis, mimicking human cryptogenic organizing pneumonia, highlighting the role of TOMM5 in lung health.
Area of Science:
- Mitochondrial biology
- Genetics
- Pulmonology
Background:
- Mitochondrial proteins are synthesized in the cytosol and imported into mitochondria via the translocase of the outer mitochondrial membrane (TOMM) complex.
- TOMM40 is a central component of the TOMM complex, with TOMM5 being a small associated subunit.
Purpose of the Study:
- To investigate the in vivo function of TOMM5.
- To characterize the phenotype of Tomm5 knockout mice.
Main Methods:
- Generation and phenotyping of Tomm5 knockout mice.
- Histopathological analysis of lung tissue.
Main Results:
- Tomm5 knockout mice exhibited a lung-specific phenotype characterized by widespread intra-alveolar fibrosis.
- Histopathology revealed lesions consistent with human cryptogenic organizing pneumonia (COP)/bronchiolitis obliterans organizing pneumonia (BOOP).
- Lesions featured intraluminal fibrogenic buds and significant eosinophilic and macrophage infiltration.
Conclusions:
- The study reveals an unexpected role for TOMM5 in maintaining lung homeostasis.
- Tomm5 deficiency leads to lung fibrosis resembling human fibrotic lung diseases.
- Histopathology is a valuable tool in high-throughput phenotyping for identifying novel disease models.
