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Featured researches published by Daisuke Naito.


Proceedings of the National Academy of Sciences of the United States of America | 2014

MURC/Cavin-4 facilitates recruitment of ERK to caveolae and concentric cardiac hypertrophy induced by α1-adrenergic receptors

Takehiro Ogata; Daisuke Naito; Naohiko Nakanishi; Yukiko K. Hayashi; Takuya Taniguchi; Kotaro Miyagawa; Tetsuro Hamaoka; Naoki Maruyama; Satoaki Matoba; Koji Ikeda; Hiroyuki Yamada; Hidemasa Oh; Tomomi Ueyama

Significance Caveolae are recognized as a platform for preassembled complexes of receptors, signal components, and their targets, facilitating efficient and specific cellular responses at the plasma membrane. ERK is activated at the plasma membrane and an important molecule that has been well studied for its integral role in signal transduction events during physiological adaptation and pathological manifestation. Here we show that although muscle-restricted coiled-coil protein (MURC)/Cavin-4, a muscle-specific caveola component, is dispensable for caveolar formation in cardiomyocytes, MURC/Cavin-4 serves as an ERK-recruiting protein in the caveolae within cardiomyocytes. The recruiting function of MURC/Cavin-4 is necessary to elicit efficient signaling of the α1-adrenergic receptor–ERK cascade in concentric cardiac hypertrophy. Our findings provide unique insight into the molecular mechanisms underlying caveola-mediated signaling in cardiac hypertrophy. The actions of catecholamines on adrenergic receptors (ARs) induce sympathetic responses, and sustained activation of the sympathetic nervous system results in disrupted circulatory homeostasis. In cardiomyocytes, α1-ARs localize to flask-shaped membrane microdomains known as “caveolae.” Caveolae require both caveolin and cavin proteins for their biogenesis and function. However, the functional roles and molecular interactions of caveolar components in cardiomyocytes are poorly understood. Here, we showed that muscle-restricted coiled-coil protein (MURC)/Cavin-4 regulated α1-AR–induced cardiomyocyte hypertrophy through enhancement of ERK1/2 activation in caveolae. MURC/Cavin-4 was expressed in the caveolae and T tubules of cardiomyocytes. MURC/Cavin-4 overexpression distended the caveolae, whereas MURC/Cavin-4 was not essential for their formation. MURC/Cavin-4 deficiency attenuated cardiac hypertrophy induced by α1-AR stimulation in the presence of caveolae. Interestingly, MURC/Cavin-4 bound to α1A- and α1B-ARs as well as ERK1/2 in caveolae, and spatiotemporally modulated MEK/ERK signaling in response to α1-AR stimulation. Thus, MURC/Cavin-4 facilitates ERK1/2 recruitment to caveolae and efficient α1-AR signaling mediated by caveolae in cardiomyocytes, which provides a unique insight into the molecular mechanisms underlying caveola-mediated signaling in cardiac hypertrophy.


American Journal of Physiology-heart and Circulatory Physiology | 2015

The coiled-coil domain of MURC/cavin-4 is involved in membrane trafficking of caveolin-3 in cardiomyocytes

Daisuke Naito; Takehiro Ogata; Tetsuro Hamaoka; Naohiko Nakanishi; Kotaro Miyagawa; Naoki Maruyama; Takeru Kasahara; Takuya Taniguchi; Masahiro Nishi; Satoaki Matoba; Tomomi Ueyama

Muscle-restricted coiled-coil protein (MURC), also referred to as cavin-4, is a member of the cavin family that works cooperatively with caveolins in caveola formation and function. Cavins are cytoplasmic proteins with coiled-coil domains and form heteromeric complexes, which are recruited to caveolae in cells expressing caveolins. Among caveolins, caveolin-3 (Cav3) is exclusively expressed in muscle cells, similar to MURC/cavin-4. In the heart, Cav3 overexpression contributes to cardiac protection, and its deficiency leads to progressive cardiomyopathy. Mutations in the MURC/cavin-4 gene have been identified in patients with dilated cardiomyopathy. In the present study, we show the role of MURC/cavin-4 as a caveolar component in the heart. In H9c2 cells, MURC/cavin-4 was localized at the plasma membrane, whereas a MURC/cavin-4 mutant lacking the coiled-coil domain (ΔCC) was primarily localized to the cytoplasm. ΔCC bound to Cav3 and impaired membrane localization of Cav3 in cardiomyocytes. Additionally, although ΔCC did not alter Cav3 mRNA expression, ΔCC decreased the Cav3 protein level. MURC/cavin-4 and ΔCC similarly induced cardiomyocyte hypertrophy; however, ΔCC showed higher hypertrophy-related fetal gene expression than MURC/cavin-4. ΔCC induced ERK activation in cardiomyocytes. Transgenic mice expressing ΔCC in the heart (ΔCC-Tg mice) showed impaired cardiac function accompanied by cardiomyocyte hypertrophy and marked interstitial fibrosis. Hearts from ΔCC-Tg mice showed a reduction of the Cav3 protein level and activation of ERK. These results suggest that MURC/cavin-4 requires its coiled-coil domain to target the plasma membrane and to stabilize Cav3 at the plasma membrane of cardiomyocytes and that MURC/cavin-4 functions as a crucial caveolar component to regulate cardiac function.


PLOS ONE | 2016

PTRF/Cavin-1 Deficiency Causes Cardiac Dysfunction Accompanied by Cardiomyocyte Hypertrophy and Cardiac Fibrosis

Takuya Taniguchi; Naoki Maruyama; Takehiro Ogata; Takeru Kasahara; Naohiko Nakanishi; Kotaro Miyagawa; Daisuke Naito; Tetsuro Hamaoka; Masahiro Nishi; Satoaki Matoba; Tomomi Ueyama

Mutations in the PTRF/Cavin-1 gene cause congenital generalized lipodystrophy type 4 (CGL4) associated with myopathy. Additionally, long-QT syndrome and fatal cardiac arrhythmia are observed in patients with CGL4 who have homozygous PTRF/Cavin-1 mutations. PTRF/Cavin-1 deficiency shows reductions of caveolae and caveolin-3 (Cav3) protein expression in skeletal muscle, and Cav3 deficiency in the heart causes cardiac hypertrophy with loss of caveolae. However, it remains unknown how loss of PTRF/Cavin-1 affects cardiac morphology and function. Here, we present a characterization of the hearts of PTRF/Cavin-1-null (PTRF−/−) mice. Electron microscopy revealed the reduction of caveolae in cardiomyocytes of PTRF−/− mice. PTRF−/− mice at 16 weeks of age developed a progressive cardiomyopathic phenotype with wall thickening of left ventricles and reduced fractional shortening evaluated by echocardiography. Electrocardiography revealed that PTRF−/− mice at 24 weeks of age had low voltages and wide QRS complexes in limb leads. Histological analysis showed cardiomyocyte hypertrophy accompanied by progressive interstitial/perivascular fibrosis. Hypertrophy-related fetal gene expression was also induced in PTRF−/− hearts. Western blotting analysis and quantitative RT-PCR revealed that Cav3 expression was suppressed in PTRF−/− hearts compared with that in wild-type (WT) ones. ERK1/2 was activated in PTRF−/− hearts compared with that in WT ones. These results suggest that loss of PTRF/Cavin-1 protein expression is sufficient to induce a molecular program leading to cardiomyocyte hypertrophy and cardiomyopathy, which is partly attributable to Cav3 reduction in the heart.


Nature Communications | 2016

MURC deficiency in smooth muscle attenuates pulmonary hypertension

Naohiko Nakanishi; Takehiro Ogata; Daisuke Naito; Kotaro Miyagawa; Takuya Taniguchi; Tetsuro Hamaoka; Naoki Maruyama; Takeru Kasahara; Masahiro Nishi; Satoaki Matoba; Tomomi Ueyama

Emerging evidence suggests that caveolin-1 (Cav1) is associated with pulmonary arterial hypertension. MURC (also called Cavin-4) is a member of the cavin family, which regulates caveolar formation and functions together with caveolins. Here, we show that hypoxia increased Murc mRNA expression in the mouse lung, and that Murc-null mice exhibited attenuation of hypoxia-induced pulmonary hypertension (PH) accompanied by reduced ROCK activity in the lung. Conditional knockout mice lacking Murc in smooth muscle also resist hypoxia-induced PH. MURC regulates the proliferation and migration of pulmonary artery smooth muscle cells (PASMCs) through Rho/ROCK signalling. Cav1 suppresses RhoA activity in PASMCs, which is reversed by MURC. MURC binds to Cav1 and inhibits the association of Cav1 with the active form of Gα13, resulting in the facilitated association of the active form of Gα13 with p115RhoGEF. These results reveal that MURC has a function in the development of PH through modulating Rho/ROCK signalling.


BMC Cardiovascular Disorders | 2017

“Pseudo aortoiliac bifurcation” leading to significant plaque shifting in the endovascular treatment of an aortoiliac bifurcation lesion: a case report

Yoshito Kadoya; Tsuneaki Kenzaka; Daisuke Naito; Kan Zen; Satoaki Matoba

BackgroundPlaque shifting is a serious complication of endovascular treatment (EVT) for aortoiliac bifurcation lesions. It is challenging to predict the occurrence of unfavorable plaque shifting correctly.Case presentationWe report the case of an 88-year-old Japanese woman who experienced constant pain at rest in her left leg. The ankle-brachial pressure index of her left leg was 0.57. Computed tomography (CT) angiography revealed severe stenosis of the left common iliac artery (CIA) and total occlusion of the left external iliac artery (EIA). We diagnosed the patient with acute exacerbation of a chronic limb ischemia and administered endovascular treatment (EVT) to treat the left CIA and EIA. The results of initial angiography agreed with those of CT angiography. After placing a self-expandable stent for the left CIA lesion, significant unfavorable plaque shifting occurred. From a comparison between pre- and post-stenting angiography, we realized that the plaque protrusion into the terminal aorta had formed a “pseudo aortoiliac bifurcation” that was situated more proximally compared to the true bifurcation. We had incorrectly assessed the height of the aortoiliac bifurcation and exact plaque position and had underestimated the risk of plaque shifting because of this misunderstanding. The patient ultimately developed fatal cholesterol embolization after EVT.ConclusionsPlaque protrusion into the terminal aorta can form a “pseudo aortoiliac bifurcation”, causing the wrong estimation of the height of the aortoiliac bifurcation; “angiographically”, the highest point is not always the true bifurcation. Careful assessment of initial angiography to detect the true aortoiliac bifurcation and exact plaque position is essential to avoid unfavorable plaque shifting.


SpringerPlus | 2016

Extensive ischemic ulcers due to limb occlusion after endovascular aneurysm repair: a case report.

Yoshito Kadoya; Tsuneaki Kenzaka; Daisuke Naito

IntroductionLimb occlusion after endovascular aneurysm repair (EVAR) is a well-known complication. However, extensive ischemic ulcers due to limb occlusion are extremely rare.Case descriptionWe report a rare case of extensive ischemic ulcers that developed seven months after EVAR in an 85-year-old Japanese man. He had been taking appropriate anticoagulant therapy because of paroxysmal atrial fibrillation. Angiography showed a left limb occlusion and superficial femoral artery (SFA) chronic total occlusion (CTO), and intravascular ultrasound showed limb kinking. Endovascular therapy (EVT) was performed, and stent placement was used to cover a large amount of thrombi and correct the limb kinking, leading to complete recovery of left limb blood flow. After additional EVT was performed for the SFA CTO, outflow improved and the ulcers healed completely.Discussion and evaluationIt seemed that the combination of poor inflow and poor outflow led to limb thrombosis.ConclusionsHere, we describe an extremely rare case of extensive ischemic ulcers due to limb occlusion after EVAR. Patients should undergo careful follow-up after EVAR to monitor blood flow to the lower extremities. Additionally, the early detection and correction of limb kinking and poor outflow are essential to prevent the development of ischemic ulcers.


Biochemical and Biophysical Research Communications | 2017

Loss of MURC/Cavin-4 induces JNK and MMP-9 activity enhancement in vascular smooth muscle cells and exacerbates abdominal aortic aneurysm

Kotaro Miyagawa; Takehiro Ogata; Tomomi Ueyama; Takeru Kasahara; Naohiko Nakanishi; Daisuke Naito; Takuya Taniguchi; Tetsuro Hamaoka; Naoki Maruyama; Masahiro Nishi; Taizo Kimura; Hiroyuki Yamada; Hiroki Aoki; Satoaki Matoba


Journal of the American College of Cardiology | 2015

TCTAP C-011 Stent Thrombosis That Long Inflation Using Perfusion Balloon Was Effective to Manage the Large Amount of Thrombus

Yoshito Kadoya; Daisuke Naito


Circulation | 2015

Abstract 15441: MURC/Cavin-4 Requires the Coiled-coil Domain for Membrane Trafficking of Caveolin-3 in Cardiomyocytes

Masahiro Nishi; Takehiro Ogata; Daisuke Naito; Tetsuro Hamaoka; Naohiko Nakanishi; Kotaro Miyagawa; Naoki Maruyama; Takeru Kasahara; Tomomi Ueyama


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

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Kotaro Miyagawa

Kyoto Prefectural University of Medicine

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Naohiko Nakanishi

Kyoto Prefectural University of Medicine

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Takehiro Ogata

Kyoto Prefectural University of Medicine

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Tomomi Ueyama

Kyoto Prefectural University of Medicine

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Takuya Taniguchi

Kyoto Prefectural University of Medicine

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Naoki Maruyama

Kyoto Prefectural University of Medicine

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Tetsuro Hamaoka

Kyoto Prefectural University of Medicine

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Satoaki Matoba

Kyoto Prefectural University of Medicine

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Takeru Kasahara

Kyoto Prefectural University of Medicine

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Masahiro Nishi

Kyoto Prefectural University of Medicine

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