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Articles by Y Oshima
Total Records ( 3 ) for Y Oshima
  Y Oshima , N Ouchi , M Shimano , D. R Pimentel , K. N Papanicolaou , K. D Panse , K Tsuchida , E Lara Pezzi , S. J Lee and K. Walsh
 

Background— Transforming growth factor-β family cytokines have diverse actions in the maintenance of cardiac homeostasis. Activin A is a member of this family whose regulation and function in heart are not well understood at a molecular level. Follistatin-like 3 (Fstl3) is an extracellular regulator of activin A protein, and its function in the heart is also unknown.

Methods and Results— We analyzed the expression of various transforming growth factor-β superfamily cytokines and their binding partners in mouse heart. Activin βA and Fstl3 were upregulated in models of myocardial injury. Overexpression of activin A with an adenoviral vector (Ad-actβA) or treatment with recombinant activin A protein protected cultured myocytes from hypoxia/reoxygenation-induced apoptosis. Systemic overexpression of activin A in mice by intravenous injection of Ad-actβA protected hearts from ischemia/reperfusion injury. Activin A induced the expression of Bcl-2, and ablation of Bcl-2 by small interfering RNA abrogated its protective action in myocytes. The protective effect of activin A on cultured myocytes was abolished by treatment with Fstl3 or by a pharmacological activin receptor-like kinase inhibitor. Cardiac-specific Fstl3 knockout mice showed significantly smaller infarcts after ischemia/reperfusion injury that was accompanied by reduced apoptosis.

Conclusions— Activin A and Fstl3 are induced in heart by myocardial stress. Activin A protects myocytes from death, and this activity is antagonized by Fstl3. Thus, the relative expression levels of these factors after injury is a determinant of cell survival in the heart.

  K Kinouchi , A Ichihara , M Sano , G. H Sun Wada , Y Wada , A Kurauchi Mito , K Bokuda , T Narita , Y Oshima , M Sakoda , Y Tamai , H Sato , K Fukuda and H. Itoh
 

Rationale: The (pro)renin receptor [(P)RR], encoded in ATP6AP2, plays a key role in the activation of local renin-angiotensin system (RAS). A truncated form of (P)RR, termed M8.9, was also found to be associated with the vacuolar H+-ATPase (V-ATPase), implicating a non–RAS-related function of ATP6AP2.

Objective: We investigated the role of (P)RR/ATP6AP2 in murine cardiomyocytes.

Methods and Results: Cardiomyocyte-specific ablation of Atp6ap2 resulted in lethal heart failure; the cardiomyocytes contained RAB7- and lysosomal-associated membrane protein 2 (LAMP2)-positive multivesicular vacuoles, especially in the perinuclear regions. The myofibrils and mitochondria remained at the cell periphery. Cardiomyocyte death was accompanied by numerous autophagic vacuoles that contained undigested cellular constituents, as a result of impaired autophagic degradation. Notably, ablation of Atp6ap2 selectively suppressed expression of the VO subunits of V-ATPase, resulting in deacidification of the intracellular vesicles. Furthermore, the inhibition of intracellular acidification by treatment with bafilomycin A1 or chloroquine reproduced the phenotype observed for the (P)RR/ATP6AP2-deficient cardiomyocytes.

Conclusions: Genetic ablation of Atp6ap2 created a loss-of-function model for V-ATPase. The gene product of ATP6AP2 is considered to act as in 2 ways: (1) as (P)RR, exerting a RAS-related function; and (2) as the V-ATPase-associated protein, exerting a non–RAS-related function that is essential for cell survival.

  Y Oshima , H Sawada , F Hosokawa , E Okunishi , T Kaneyama , Y Kondo , S Niitaka , H Takagi , Y Tanishiro and K. Takayanagi
 

We visualized lithium atom columns in LiV2O4 crystals by combining scanning transmission electron microscopy with annular bright field (ABF) imaging using a spherical aberration-corrected electron microscope (R005) viewed from the [110] direction. The incident electron beam was coherent with a convergent angle of 30 mrad (semi-angle), and the detector collected scattered electrons over 20–30 mrad (semi-angle). The ABF image showed dark dots corresponding to lithium, vanadium and oxygen columns.

 
 
 
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