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Abstract-Although functional coupling between protein kinase C⑀ (PKC⑀) and mitochondria has been implicated in the genesis of cardioprotection, the signal transduction mechanisms that enable this link and the identities of the mitochondrial proteins modulated by PKC⑀ remain unknown. Based on recent evidence that the mitochondrial permeability transition pore may be involved in ischemia/reperfusion injury, we hypothesized that protein-protein interactions between PKC⑀ and mitochondrial pore components may serve as a signaling mechanism to modulate pore function and thus engender cardioprotection. Coimmunoprecipitation and GST-based affinity pull-down from mouse cardiac mitochondria revealed interaction of PKC⑀ with components of the pore, namely voltage-dependent anion channel (VDAC), adenine nucleotide translocase (ANT), and hexokinase II (HKII). VDAC1, ANT1, and HKII were present in the PKC⑀ complex at Ϸ2%, Ϸ0.2%, and Ϸ1% of their total expression, respectively. Moreover, in vitro studies demonstrated that PKC⑀ can directly bind and phosphorylate VDAC1. Incubation of isolated cardiac mitochondria with recombinant PKC⑀ resulted in a significant inhibition of Ca 2ϩ -induced mitochondrial swelling, an index of pore opening. Furthermore, cardiac-specific expression of active PKC⑀ in mice, which is cardioprotective, greatly increased interaction of PKC⑀ with the pore components and inhibited Ca 2ϩ -induced pore opening. In contrast, cardiac expression of kinase-inactive PKC⑀ did not affect pore opening. Finally, administration of the pore opener atractyloside significantly attenuated the infarct-sparing effect of PKC⑀ transgenesis. Collectively, these data demonstrate that PKC⑀ forms physical interactions with components of the cardiac mitochondrial pore. This in turn inhibits the pathological function of the pore and contributes to PKC⑀-induced cardioprotection.

Summary Porcine circovirus type 3 (PCV3) is a novel circovirus that was associated with porcine dermatitis and nephropathy syndrome, reproductive failure, and multisystemic inflammation. Recently, a PCV3 strain was identified from pyretic and pneumonic piglets in Guangdong province, China. This virus strain was sequenced and designated PCV3‐China/GD2016. The complete genome of PCV3‐China/GD2016 is 2,000 bp in length and shared 99.1% and 99.1% nucleotide identities with PCV3/29160 and PCV3/2164, respectively. [Corrections added after initial online publication on 13 March 2017: The numbers ‘98.5%’ and ‘97.4%’ has been changed to ‘99.1%’ and ‘99.1%’ in the previous sentence.] Phylogenetic analysis based on the complete genome showed that PCV3‐China/GD2016 clustered with the emerging PCV3 and separated with other virus in genus Circovirus. The results of this study suggest that PCV3 has existed within the pigs of China. It is urgent to investigate the pathogenicity and epidemiology of this novel circovirus China.

Abstract-An essential role for protein kinase C ⑀ (PKC⑀) has been shown in multiple forms of cardioprotection; however, there is a distinct paucity of information concerning the signaling architecture that is responsible for the manifestation of a protective phenotype. We and others have recently shown that signal transduction may proceed via the formation of signaling complexes (Circ Res. 2001;88:59 -62