Cardioprotection requires flipping the ‘posttranslational modification’ switch

Plasma protein changes in horse after prolonged physical exercise: A proteomic study

“…Accordingly, proteins related to acute phase response, proteolytic activity, extracellular efflux, or modification of polypeptide clearance were highly affected. In some cases, quantitative changes concerned specific protein isoforms, which may be related to the occurrence of posttranslational modifications somehow related to physical exercise, as already reported for carbonylation [51] or phosphorylation [52,53]. Specific quantitative trends observed for HP, C4A and ALB fragments, differently to what is generally detected during acute phase, indicate a distinctive response to prolonged physical activity in horses.…”

Preconditioning with periodic acceleration (pGz) provides second window of cardioprotection

“…Further, we have not examined the potential contribution of oxidant/antioxidant pathways, or the phosphorylation of the signal transducer and activator of transcription 5 (STAT 5) which have been studied as cardioprotective signaling, or other post translational modification of proteins (Hamilton, 2003;Heusch et al, 2012;Marini et al, 2007;Penna et al, 2009;Porter et al, 2012). We have also not explored whether or not pGz can induce protection to other vital organs.…”

Mitochondrial targets for volatile anesthetics against cardiac ischemia-reperfusion injury

“…Mammalian mitochondria have three different VDAC isoforms: 1, 2, and 3 (Craigen and Graham, 2008) that perform different functions (Neumann et al, 2010). Recent reports also suggest a complex regulation of VDAC by mechanisms involving protein-protein interactions and post-translational modifications (PTMs) in normal and pathological conditions (Shimizu et al, 1999; Liu et al, 2009; Das et al, 2012; Porter et al, 2012; Yang et al, 2012). Effects of IR or other oxidative stresses can be exhibited by their ultimate actions on VDAC function.…”

“…Beneficial post-translational modifications (PTMs) of mitochondrial proteins have been proposed to modulate cardioprotection (Foster et al, 2009; Pagliaro et al, 2011; Porter et al, 2012). A modification of mitochondrial protein by O-glycosylation with O-linked-β-N-acetyl glucosamine (O-GlcNAc) was suggested to occur with IPC as assessed by improved cardiac myocyte survival due to attenuated ΔΨ m (Jones et al, 2008).…”