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The mitochondrial inhibitor oligomycin induces an inflammatory response in the rat knee joint

Overview of attention for article published in BMC Musculoskeletal Disorders, June 2017
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Title
The mitochondrial inhibitor oligomycin induces an inflammatory response in the rat knee joint
Published in
BMC Musculoskeletal Disorders, June 2017
DOI 10.1186/s12891-017-1621-2
Pubmed ID
Authors

Carlos Vaamonde-García, Jesús Loureiro, Marta N. Valcárcel-Ares, Romina R. Riveiro-Naveira, Olalla Ramil-Gómez, Laura Hermida-Carballo, Alberto Centeno, Rosa Meijide-Failde, Francisco J. Blanco, María J. López-Armada

Abstract

Recent findings support a connection between mitochondrial dysfunction and activation of inflammatory pathways in articular cells. This study investigates in vivo in an acute model whether intra-articular administration of oligomycin, an inhibitor of mitochondrial function, induces an oxidative and inflammatory response in rat knee joints. Oligomycin was injected into the rat left knee joint on days 0, 2, and 5 before joint tissues were obtained on day 6. The right knee joint served as control. Results were evaluated by macroscopy and histopathology and by measuring cellular and mitochondrial reactive oxygen species (ROS), 4-hydroxy-2-nonenal (4-HNE, a marker of lipid peroxidation), nuclear factor erythroid 2-related factor 2 (Nrf2), and CD68 (macrophages) and chemokine levels. The marker of mitochondrial mass COX-IV was also evaluated. The macroscopic findings showed significantly greater swelling in oligomycin-injected knees than in control knees. Likewise, the histological score of synovial damage was also increased significantly. Immunohistochemical studies showed high expression of IL-8, coinciding with a marked infiltration of polymorphonuclears and CD68+ cells in the synovium. Mitochondrial mass was increased in the synovium of oligomycin-injected joints, as well as cellular and mitochondrial ROS production, and 4-HNE. Relatedly, expression of the oxidative stress-related transcription factor Nrf2 was also increased. As expected, no histological differences were observed in the cartilage; however, cytokine-induced neutrophil chemoattractant-1 mRNA and protein expression were up-regulated in this tissue. Mitochondrial failure in the joint is able to reproduce the oxidative and inflammatory status observed in arthritic joints.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 54 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 54 100%

Demographic breakdown

Readers by professional status Count As %
Student > Master 9 17%
Student > Ph. D. Student 8 15%
Student > Bachelor 8 15%
Other 5 9%
Student > Doctoral Student 4 7%
Other 9 17%
Unknown 11 20%
Readers by discipline Count As %
Medicine and Dentistry 12 22%
Biochemistry, Genetics and Molecular Biology 8 15%
Immunology and Microbiology 5 9%
Nursing and Health Professions 2 4%
Agricultural and Biological Sciences 2 4%
Other 10 19%
Unknown 15 28%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 14 June 2017.
All research outputs
#20,428,633
of 22,981,247 outputs
Outputs from BMC Musculoskeletal Disorders
#3,665
of 4,088 outputs
Outputs of similar age
#276,107
of 317,411 outputs
Outputs of similar age from BMC Musculoskeletal Disorders
#72
of 82 outputs
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