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Assessment of Mitochondrial Functions and Cell Viability in Renal Cells Overexpressing Protein Kinase C Isozymes
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Myotonic dystrophy protein kinase (DMPK) prevents ROS-induced cell death by assembling a hexokinase II-Src complex on

B Pantic1, E Trevisan, A Citta

  • 11] CNR Institute of Neuroscience, University of Padova, Padova 35121, Italy [2] Department of Biomedical Sciences, University of Padova, Padova 35121, Italy.

Cell Death & Disease
|October 19, 2013
PubMed

Insights

Myotonic dystrophy protein kinase (DMPK) in mitochondria protects cells from oxidative stress by interacting with hexokinase II and Src. This complex enhances cell survival and is crucial for muscle fiber function.

Area of Science:

  • Mitochondrial biology
  • Cellular stress response
  • Biochemistry

Background:

  • The precise biological roles of myotonic dystrophy protein kinase (DMPK) are not fully elucidated.
  • Mutations in the DMPK gene are linked to myotonic dystrophy type 1 (DM1).
  • Longer DMPK isoforms localize to mitochondria, but their functions there are unknown.

Purpose of the Study:

  • To investigate the function of the mitochondrial-associated DMPK isoform A.
  • To determine the role of mitochondrial DMPK in cellular protection against oxidative stress.
  • To explore the interaction of DMPK with other proteins in the mitochondria.

Main Methods:

  • Studied the localization and kinase activity of DMPK isoform A in mitochondria.
  • Investigated the interaction of DMPK with hexokinase II (HK II) and Src kinase using biochemical assays.
  • Analyzed the effects of DMPK down-modulation and Src inhibition on cell survival and myogenesis under oxidative stress.

Main Results:

  • Mitochondrial DMPK protects cells from oxidative stress and mitochondrial permeability transition pore (PTP) opening.
  • DMPK enhances mitochondrial localization of HK II and forms a complex with HK II and active Src.
  • Oxidative stress increases DMPK-Src interaction and DMPK tyrosine phosphorylation; Src inhibition enhances cell death.
  • DMPK down-modulation impairs myogenesis, which is rescued by antioxidants.

Conclusions:

  • Mitochondrial DMPK, HK II, and Src form a pro-survival complex with antioxidant properties.
  • This complex plays a vital role in protecting cells against oxidative damage.
  • The DMPK-containing complex is potentially significant for muscle fiber function and differentiation.

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