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Mitofusin-2 (Mfn-2) is a hyperplasia suppressor. Changes in Mfn-2 expression are thought to reflect mitochondrial remodeling during cell proliferation. However, it is unclear how the participation of Mfn-2 in mitochondrial remodeling prevents cellular proliferation. Here we show that arresting vascular smooth muscle cells (VSMCs) in the G0/G1 phase by serum starvation up-regulates Mfn-2 expression and causes mitochondria to assemble into a tubular network and to attach to the endoplasmic reticulum (ER). In the S phase, short rod-shaped mitochondrial structures that were dissociated from the ER were observed. Levels of glucose, ATP, l-amino acid, and NADP(+) did not vary throughout the cell cycle. However, NAD(+) level was lower and NADH level was higher in the G0/G1 phase than in the S phase. Mitochondrial membrane potential was lower in the S phase than in the G0/G1 phase. Infecting VSMCs with an adenovirus encoding full-length Mfn-2 increased NADH level and reduced NAD(+) level, while infecting the cells with an adenovirus that silences the p21(ras) signature motif produced opposite effects. These results suggest that Mfn-2 up-regulation causes mitochondrial fusion into tubular networks and attachment to the ER, which in turn halts proliferation of VSMCs. © The Author 2015. Published by ABBS Editorial Office in association with Oxford University Press on behalf of the Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences.


Dan Li, Xiaolan Li, Yang Guan, Xiaomei Guo. Mitofusin-2-mediated tethering of mitochondria and endoplasmic reticulum promotes cell cycle arrest of vascular smooth muscle cells in G0/G1 phase. Acta biochimica et biophysica Sinica. 2015 Jun;47(6):441-50

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PMID: 25926139

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