Although it has been reported that hormones or chemicals, which increse in intracellular cAMP, produced Mg2+ release from the heart, it is not well characterized whether a specific Mg2+ exchanger is involved in cAMP-induced Mg2+ efflux in themammalian hearts In this work, we studied the relationship between the increase in intracellular cAMP and ion transport system on Mg2+ regulation in the perfused rat heart and isolated myocytes. The Mg2+ content in the perfusate and supernatant were measured by atomic absorption spectrophotometer. The addition of membrane permeable cAMP analogue to the perfused hearts and myocytes. cAMP-induced Mg2+ efflux was ingibited by H7, benzamil or imipramine in the perfused hearts and myocytes, but not by EIPA. We confirmed that a significant Mg2+ efflux was induced by an increase in intracellular cAMP in the hearts and myocytes. The cAMP-induced increase of Mg2+ efflux in the hearts may be involved in ion transport system(Na+-Ca2+ and Na+-Mg2+ exchanger)

While the C-terminal cytoplasmic tail of anion exchanger 1 (AE1, band 3) has been reported to possess important physiological roles, including one for proper membrane trafficking, its precise characteristics remain unclear. To clarify the overall structural consequences of the conserved sequence EL(K/Q)(L/C)LD(A/G)DD, containing the core binding sequence LDADD for carbonic anhydrase II, in the C-terminal region, we analyzed the membrane expression and turnover of bovine AE1 with a series of truncation and substitution mutations in HEK293 cells. Immunofluorescence microscopy and cell-surface biotinylation demonstrated that truncation mutants missing 18 C-terminal residues targeted the plasma membrane, but the one lacking the conserved region, by truncation of 28 amino acid residues, was retained inside the cells. Substitutions of Ala for Glusup(901), Leusup(902), Leusup(905), and Aspsup(906) in the sequence E901L(K/Q)(L/C)LDADD909 of bovine AE1 or those in the corresponding murine sequence also caused intracellular retention, though these mutants had half-lives comparable to that for wild-type AE1. These data demonstrate that the conserved amino acid residues Glusup(1), Leusup(2), Leusup(5), and Aspsup(6) in the EL(K/Q)(L/C)LD(A/G)DD region have essential structural consequences in stable expression of AE1 at the plasma membrane regardless of the ability in binding to carbonic anhydrase II of this region.

In the course of studying porcine enterovirus infection in piglets, the vascular endothelial cells in the CNS of colostrum-deprived piglets with polioence-phalomyelitis were investigated by electron microscope. The experimental piglets were orally infected with the porcine enterovirus serogroup 3 isolated in Korea and necropsied at 7 days postinoculation. Crystalline arrays of viral particles were found in the vascular endothelial cells of the spinal cord and cerebellum. Aggregates of immature viral particles were occasionally observed in the vascular endothelial cells in the meninges. The rough ER was deprived of ribosomes, irregularly dilated and associated with viral crystals. There were abundant cytoplasmic filaments, dilatation of perivascular space, perivascular cuffing, and the partial disruptions of endothelial cell membrane and basal lamina