MBI Publications

MBI Publications for J. Lechleiter (2)

  • C. Diekman, C. Fall, J. Lechleiter and D. Terman
    Modeling the neuroprotective role of enhancing astrocyte mitochondrial metabolism during stroke
    Biophysical Journal (2013) (In Press)

    Abstract

    A mathematical model that integrates the dynamics of cell membrane potential, ion homeostasis, cell volume, mitochondrial ATP production, mitochondrial and ER Ca2+ handling, IP3 production and GTP-binding protein coupled receptor (GPCR) signaling was developed. Simulations with this model support recent experimental data showing a protective effect of stimulating an astrocytic GPCR (P2Y1Rs) following cerebral ischemic stroke. The model was analyzed in order to better understand the mathematical behavior of the equations and to provide insights into the underlying biological data. This approach yielded explicit formulas determining how changes in IP3-mediated Ca2+ release, under varying conditions of oxygen and the energy substrate pyruvate, affected mitochondrial ATP production, and was utilized to predict rate-limiting v
  • C. Diekman, C. Fall, J. Lechleiter and D. Terman
    Modeling the neuroprotective role of enhanced astrocyte mitochondrial metabolism during stroke.
    Biophysical journalVol. 104 No. 8 (2013) pp. 1752-63

    Abstract

    A mathematical model that integrates the dynamics of cell membrane potential, ion homeostasis, cell volume, mitochondrial ATP production, mitochondrial and endoplasmic reticulum Ca(2+) handling, IP3 production, and GTP-binding protein-coupled receptor signaling was developed. Simulations with this model support recent experimental data showing a protective effect of stimulating an astrocytic GTP-binding protein-coupled receptor (P2Y1Rs) following cerebral ischemic stroke. The model was analyzed to better understand the mathematical behavior of the equations and to provide insights into the underlying biological data. This approach yielded explicit formulas determining how changes in IP3-mediated Ca(2+) release, under varying conditions of oxygen and the energy substrate pyruvate, affected mitochondrial ATP production, and was utilized to predict rate-limiting variables in P2Y1R-enhanced astrocyte protection after cerebral ischemic stroke.

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