著者

KITAGAWA Hiroshi SATOH Hiroshi KOMATSUZAKI Chiyoko MORI Fumiaki KUDO Norio

出版者

北海道大学

雑誌

Japanese journal of veterinary research (ISSN:00471917)

巻号頁・発行日

vol.35, no.1, pp.21-39, 1987-01-30

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Morphological investagations were carried out on basophilic intranuclear and cytoplasmic inclusion bodies in epithelial cells of the hair bulbs of anagen hair follicles in wild foxes affected with an abnormal hair coat condition. The inclusions, which were DNA-positive, contained numerous minute virus-like particles ("FMVP"). The particles, having a diameter of approximately 13 nm, had an arrangement of capsomer-like subunits of approximately 2-3 nm in diameter and were nonenveloped. The striking resemblance to icosahedral virus was crystallographically and morphologically demonstrated.

著者

Nagasaka Shiro Katoh Hideki Niu Chim Feng Matsui Saori Urushida Tsuyoshi Satoh Hiroshi Watanabe Yasuhide Hayashi Hideharu

出版者

社団法人日本循環器学会

雑誌

Circulation journal : official journal of the Japanese Circulation Society (ISSN:13469843)

巻号頁・発行日

vol.71, no.3, pp.429-436, 2007-02-20

被引用文献数

2 23

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Background The identification of protein kinase A(PKA) anchoring proteins on mitochondria implies a direct effect of PKA on mitochondrial function. However, little is known about the relationship between PKA and mitochondrial metabolism. Methods and Results The effects of PKA on the mitochondrial redox state(flavin adenine dinucleotide(FAD)), mitochondrial membrane potential(ΔΨ_m) and reactive oxygen species(ROS) production were investigated in saponin-permeabilized rat cardiomyocytes. The PKA catalytic subunit(PKA_<cat>; 50 unit/ml) increased FAD intensities by 56.6±7.9%(p<0.01), 2'7'-dichlorofluorescin diacetate(DCF) intensities by 10.5±3.3 fold(p<0.01) and depolarized ΔΨ_m to 48.1±9.5% of the control(p<0.01). Trolox(a ROS scavenger; 100μmol/L) inhibited PKA_<cat>-induced ΔΨ_m, FAD and DCF alteration. PKA_<cat>-induced ΔΨ_m depolarization was inhibited by an inhibitor of the inner membrane anion channel(IMAC), 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid(DIDS: 1μmol/L) but not by an inhibitor of mitochondrial permeability transition pore(mPTP), cyclosporine A(lOOnmol/L). Conclusions PKA_<cat> alters FAD and ΔΨ_m via mitochodrial ROS generation, and PKAcat-induced ΔΨ_m depolarization was not caused by mPTP but rather by DIDS-sensitive mechanisms, which could be caused by opening of the IMAC. The effects of PKA on mitochondrial function could be related to myocardial function under the condition of extensive β-adrenergic stimulation.