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Mitochondrial fission is necessary for vascular smooth muscle cell migration (761.1)
Author(s) -
Wang Li,
Yoon Yisang
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.761.1
Subject(s) - mitochondrial fission , microbiology and biotechnology , mitochondrion , mitochondrial fusion , cytosol , vascular smooth muscle , biology , chemistry , mitochondrial dna , biochemistry , endocrinology , smooth muscle , gene , enzyme
Intimal hyperplasia occurs in response to arterial injury and is also an important feature of atherosclerotic plaques. Vascular smooth muscle cell (VSMC) migration is one of the main processes contributing to intimal hyperplasia. Mitochondria are energy producing organelles that also generate reactive oxygen species as a byproduct of ATP synthesis. Mitochondria inside the cell redistribute frequently and undergo constant shape change mainly through fission and fusion, which is referred to as mitochondrial dynamics. Although the involvement of mitochondria in VSMC migration has been reported in the context of oxidative stress and mitochondrial dysfunction, the role of mitochondrial dynamics in VSMC migration has not been studied. In the present study, we found that platelet‐derived growth factor (PDGF), a strong migratory stimulant, induced mitochondrial shortening in VSMCs. This phenomenon was accompanied by the translocation of the fission protein Drp1/DLP1 from the cytosol to mitochondria, suggesting that PDGF activated mitochondrial fission to form short mitochondria. PDGF also increased the mitochondrial functional parameters including mitochondrial membrane potential, respiration, and ATP levels. Importantly, we found that inhibition of mitochondrial fission greatly decreased PDGF‐induced lamellipodia formation and VSMC migration. Fission inhibition blunted the PDGF‐induced ATP production, suggesting that reduced ATP production is an underlying mechanism for the diminished VSMC migration by fission inhibition. These data indicate that the PDGF‐induced activation of mitochondrial fission is required for augmenting ATP levels and VSMC migration, and suggest that mitochondrial dynamics is a controlling component regulating mitochondrial function.

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