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Featured researches published by Atsuo Adachi.


American Journal of Physiology-heart and Circulatory Physiology | 2008

Downregulation of Dicer expression by serum withdrawal sensitizes human endothelial cells to apoptosis

Satoshi Asada; Tomosaburo Takahashi; Koji Isodono; Atsuo Adachi; Hiroko Imoto; Takehiro Ogata; Tomomi Ueyama; Hiroaki Matsubara; Hidemasa Oh

Although the modulated expression of Dicer is documented upon neoplastic transformation, little is known of the regulation of Dicer expression by environmental stimuli and its roles in the regulation of cellular functions in primary cells. In this study, we found that Dicer expression was downregulated upon serum withdrawal in human umbilical vein endothelial cells (HUVECs). Serum withdrawal induced a time-dependent repression of Dicer expression, which was specifically rescued by vascular endothelial cell growth factor or sphingosine-1-phosphate. When Dicer expression was silenced by short-hairpin RNA against Dicer, the cells were more prone to apoptosis under serum withdrawal, whereas the rate of apoptosis was comparable with control cells in the serum-containing condition. Real-time PCR-based gene expression profiling identified several genes, the expression of which was modulated by Dicer silencing, including adhesion and matrix-related molecules, caspase-3, and nitric oxide synthase 3 (NOS3). Dicer silencing markedly impaired migratory functions without affecting cell adhesion and repressed phosphorylation of focal adhesion kinase and proline-rich tyrosine kinase 2 in adherent HUVECs. Dicer knockdown upregulated caspase-3 and downregulated NOS3 expression, and serum withdrawal indeed increased caspase-3 and decreased NOS3 expression. Furthermore, the overexpression of Dicer in HUVECs resulted in a marked reduction in apoptosis upon serum withdrawal and a decreased caspase-3 and increased NOS3 expression. The inhibition of NOS activity by Nomega-nitro-L-arginine methyl ester abrogated the effect of Dicer overexpression to rescue the cells from serum withdrawal-induced apoptosis. These results indicated that serum withdrawal decreases Dicer expression, leading to an increased susceptibility to apoptosis through the regulation of caspase-3 and NOS3 expression.


PLOS ONE | 2010

PARM-1 Is an Endoplasmic Reticulum Molecule Involved in Endoplasmic Reticulum Stress-Induced Apoptosis in Rat Cardiac Myocytes

Koji Isodono; Tomosaburo Takahashi; Hiroko Imoto; Naohiko Nakanishi; Takehiro Ogata; Satoshi Asada; Atsuo Adachi; Tomomi Ueyama; Hidemasa Oh; Hiroaki Matsubara

To identify novel transmembrane and secretory molecules expressed in cardiac myocytes, signal sequence trap screening was performed in rat neonatal cardiac myocytes. One of the molecules identified was a transmembrane protein, prostatic androgen repressed message-1 (PARM-1). While PARM-1 has been identified as a gene induced in prostate in response to castration, its function is largely unknown. Our expression analysis revealed that PARM-1 was specifically expressed in hearts and skeletal muscles, and in the heart, cardiac myocytes, but not non-myocytes expressed PARM-1. Immunofluorescent staining showed that PARM-1 was predominantly localized in endoplasmic reticulum (ER). In Dahl salt-sensitive rats, high-salt diet resulted in hypertension, cardiac hypertrophy and subsequent heart failure, and significantly stimulated PARM-1 expression in the hearts, with a concomitant increase in ER stress markers such as GRP78 and CHOP. In cultured cardiac myocytes, PARM-1 expression was stimulated by proinflammatory cytokines, but not by hypertrophic stimuli. A marked increase in PARM-1 expression was observed in response to ER stress inducers such as thapsigargin and tunicamycin, which also induced apoptotic cell death. Silencing PARM-1 expression by siRNAs enhanced apoptotic response in cardiac myocytes to ER stresses. PARM-1 silencing also repressed expression of PERK and ATF6, and augmented expression of CHOP without affecting IRE-1 expression and JNK and Caspase-12 activation. Thus, PARM-1 expression is induced by ER stress, which plays a protective role in cardiac myocytes through regulating PERK, ATF6 and CHOP expression. These results suggested that PARM-1 is a novel ER transmembrane molecule involved in cardiac remodeling in hypertensive heart disease.


Biochemical and Biophysical Research Communications | 2013

Serglycin is a novel adipocytokine highly expressed in epicardial adipose tissue.

Hiroko Imoto-Tsubakimoto; Tomosaburo Takahashi; Tomomi Ueyama; Takehiro Ogata; Atsuo Adachi; Naohiko Nakanishi; Katsura Mizushima; Yuji Naito; Hiroaki Matsubara

Much recent work has highlighted the key role of adipose tissue as an endocrine organ that secretes a number of adipocytokines, linking adiposity, especially intra-abdominal visceral fat, and the pathogenesis of cardiovascular and metabolic diseases. However, the role of epicardial adipose tissue (EAT), another important visceral fat depot situated in close proximity to epicardial coronary arteries and myocardium, has been less well studied. In this study, we sought to characterize EAT by comparing gene expression profiles of EAT, omental adipose tissue (OAT), and subcutaneous adipose tissue (SCAT) in patients who underwent elective coronary artery bypass graft surgery for critical coronary artery disease (CAD) and identify molecules involved in inflammation. A total of 15,304 probes were detected in all depots, and 231 probes were differentially expressed. Significantly higher expression of pro-inflammatory genes such as interleukin-1β, -6, and -8, and chemokine receptor 2 was observed in EAT, even when compared with OAT. Among them, serglycin was one of the most abundantly expressed genes in EAT. Serglycin expression was induced during adipocytic differentiation of 3T3L1 cells. Serglycin was secreted from adipocytes, and tumor necrosis factor-α stimulated its expression and secretion in adipocytes. Serglycin was also present in human serum samples. These results suggest that human EAT has strong inflammatory properties in patients with CAD and provide novel evidence that serglycin is an adipocytokine highly expressed in EAT.


Biochemical and Biophysical Research Communications | 2012

PARM-1 promotes cardiomyogenic differentiation through regulating the BMP/Smad signaling pathway.

Naohiko Nakanishi; Tomosaburo Takahashi; Takehiro Ogata; Atsuo Adachi; Hiroko Imoto-Tsubakimoto; Tomomi Ueyama; Hiroaki Matsubara

PARM-1, prostatic androgen repressed message-1, is an endoplasmic reticulum (ER) molecule that is involved in ER stress-induced apoptosis in cardiomyocytes. In this study, we assessed whether PARM-1 plays a role in the differentiation of stem cells into cardiomyocytes. While PARM-1 was not expressed in undifferentiated P19CL6 embryonic carcinoma cells, PARM-1 expression was induced during cardiomyogenic differentiation. This expression followed expression of mesodermal markers, and preceded expression of cardiac transcription factors. PARM-1 overexpression did not alter the expression of undifferentiated markers and the proliferative property in undifferentiated P19CL6 cells. Expression of cardiac transcription factors during cardiomyogenesis was markedly enhanced by overexpression of PARM-1, while expression of mesodermal markers was not altered, suggesting that PARM-1 is involved in the differentiation from the mesodermal lineage to cardiomyocytes. Furthermore, overexpression of PARM-1 induced BMP2 mRNA expression in undifferentiated P19CL6 cells and enhanced both BMP2 and BMP4 mRNA expression in the early phase of cardiomyogenesis. PARM-1 overexpression also enhanced phosphorylation of Smads1/5/8. Thus, PARM-1 plays an important role in the cardiomyogenic differentiation of P19CL6 cells through regulating BMP/Smad signaling pathways, demonstrating a novel role of PARM-1 in the cardiomyogenic differentiation of stem cells.


Biochemical and Biophysical Research Communications | 2012

NFAT5 regulates the canonical Wnt pathway and is required for cardiomyogenic differentiation.

Atsuo Adachi; Tomosaburo Takahashi; Takehiro Ogata; Hiroko Imoto-Tsubakimoto; Naohiko Nakanishi; Tomomi Ueyama; Hiroaki Matsubara


The Journal of the Japanese Society of General Medicine | 2014

Careful Auscultation after Detection of Bacteremia Leading to a Diagnosis of Patent Ductus Arteriosus in Adult

Yoshito Kadoya; Mikio Wada; Atsushi Kawashima; Daisuke Naito; Atsuo Adachi; Takashi Sakamoto; Keizo Kagawa


Circulation | 2010

Abstract 16700: MURC, Muscle-Restricted Coiled-Coil Protein, Regulates Caveolae Morphology and Induces Hypertrophy in Cardiomyocytes

Takuya Taniguchi; Takehiro Ogata; Daisuke Naito; Naohiko Nakanishi; Kotaro Miyagawa; Katsuya Amano; Koji Isodono; Hiroko Imoto; Masashi Tagawa; Naofumi Takehara; Satoshi Asada; Atsuo Adachi; Tatsuya Morimoto; Tomosaburo Takahashi; Hidemasa Oh; Tomomi Ueyama; Hiroaki Matsubara


Japanese Circulation Journal-english Edition | 2009

OE-171 Downregulation of Dicer Expression by Serum Withdrawal Sensitizes Human Endothelial Cells to Apoptosis(OE29,Molecular Biology Myocardium (M),Oral Presentation (English),The 73rd Annual Scientific Meeting of The Japanese Circulation Society)

Satoshi Asada; Tomosaburo Takahashi; Koji Isodono; Hiroko Imoto; Atsuo Adachi; Takehiro Ogata; Tomomi Ueyama; Hiroaki Matsubara; Hidemasa Oh


Nihon Naika Gakkai zasshi. The Journal of the Japanese Society of Internal Medicine | 2008

Angiogenic therapy for critical limb ischemia

Yusuke Nakagawa; Atsuo Adachi; Satoaki Matoba; Koji Ikeda; Hiroaki Matsubara


Japanese Circulation Journal-english Edition | 2008

PE-088 Cellular functions of Dicer in human endothelial cells(Endothelium(02)(IHD),Poster Session(English),The 72nd Annual Scientific Meeting of the Japanese Circulation Society)

Satoshi Asada; Tomosaburo Takahashi; Koji Isodono; Hiroko Imoto; Atsuo Adachi; Tomomi Ueyama; Hiroaki Matsubara; Hidemasa Oh

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Hiroaki Matsubara

Kyoto Prefectural University of Medicine

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Tomomi Ueyama

Kyoto Prefectural University of Medicine

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Tomosaburo Takahashi

Kyoto Prefectural University of Medicine

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Takehiro Ogata

Kyoto Prefectural University of Medicine

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Koji Isodono

Kyoto Prefectural University of Medicine

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Naohiko Nakanishi

Kyoto Prefectural University of Medicine

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Satoshi Asada

Memorial Hospital of South Bend

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Hiroko Imoto-Tsubakimoto

Kyoto Prefectural University of Medicine

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