脳血管障害発症後の修復・再生機構の解明
キーワード：脳梗塞，神経機能再生,内皮細胞,ペリサイト，間葉系幹細胞,グリア, マクロファージ
2008.04.

レドックスによる心血管疾患発症および修復機構の解明
キーワード：レドックス，NADPHオキシダーゼ，抗酸化タンパク質，動脈硬化
2001.04.

脳卒中データベースの確立と脳卒中の病態解明に関する研究

キーワード：脳卒中データベース、多施設共同研究
2008.04.

脳血管障害の遺伝的要因・バイオマーカーの探索
キーワード：脳梗塞，バイオマーカー，遺伝子，タンパク質
2008.04.

食細胞NADPH oxidaseの活性化機構の解明　とくにp47phoxの立場から
キーワード：食細胞NADPH oxidase
1996.04～2002.03.

脳梗塞・修復機構の解明と再生治療の探索
2008.04, 代表者：吾郷哲朗.

Fukuoka Stroke Registry
2007.04, 代表者：北園孝成，　鴨打正浩, 九州大学大学院医学研究院病態機能内科学.

脳・心疾患におけるNox4の役割解明
2008.04, 代表者：Junichi Sadoshima, UMDNJ-New Jersey Medical School
心血管疾患におけるNox4の役割解明.

レドックスによる血管内皮細胞の機能および病態の制御
2009.04～2013.03, 代表者：吾郷哲朗.

レドックスナビ研究拠点　若手育成事業
2010.04～2017.03, 代表者：吾郷哲朗
脳梗塞におけるペリサイトの役割解明.

主要著書

主要原著論文

1.	Shibahara T, Nakamura K, Wakisaka Y, Tachibana M, Makihara N, Kitazono T, Ago T, PDGFRβ-positive cell-mediated post-stroke remodeling of fibronectin and laminin α 2 for tissue repair and functional recovery., J Cereb Blood Flow Metab, 43, 4, 518-530, 2023.04.
2.	Yamanaka K, Nakamura K, Shibahara T, Takashima M, Takaki H, Hidaka M, Komori M, Yoshikawa Y, Wakisaka Y, Ago T, Kitazono T, Deletion of Nox4 enhances remyelination following cuprizone-induced demyelination by increasing phagocytic capacity of microglia and macrophages in mice, Glia, 2023.03.
3.	Kiyohara T, Matsuo R, Hata J, Nakamura K, Wakisaka Y, Kamouchi M, Kitazono T, Ago T, beta-Cell Function and Clinical Outcome in Nondiabetic Patients With Acute Ischemic Stroke, STROKE, 10.1161/STROKEAHA.120.031392, 52, 8, 2621-2628, 2021.08.
4.	Shibahara T, Ago T, et al. , Reciprocal Interaction Between Pericytes and Macrophage in Poststroke Tissue Repair and Functional Recovery, STROKE, 10.1161/STROKEAHA.120.029827, 51, 10, 3095-3106, 2020.10, BACKGROUND AND PURPOSE: Poststroke tissue repair, comprised of macrophage-mediated clearance of myelin debris and pericyte-mediated fibrotic response within the infarct area, is an important process for functional recovery. Herein, we investigated the reciprocal interaction between pericytes and macrophages during poststroke repair and functional recovery. METHODS: We performed a permanent middle cerebral artery occlusion in both wild-type and pericyte-deficient PDGFRbeta (platelet-derived growth factor receptor beta) heterozygous knockout (Pdgfrb(+/-)) mice and compared histological changes and neurological functions between the 2 groups. We also examined the effects of conditioned medium harvested from cultured pericytes, or bone marrow-derived macrophages, on the functions of other cell types. RESULTS: Localization of PDGFRbeta-positive pericytes and F4/80-positive macrophages was temporally and spatially very similar following permanent middle cerebral artery occlusion. Intrainfarct accumulation of macrophages was significantly attenuated in Pdgfrb(+/-) mice. Intrainfarct pericytes expressed CCL2 (C-C motif ligand 2) and CSF1 (colony stimulating factor 1), both of which were significantly lower in Pdgfrb(+/-) mice. Cultured pericytes expressed Ccl2 and Csf1, both of which were significantly increased by PDGF-BB and suppressed by a PDGFRbeta inhibitor. Pericyte conditioned medium significantly enhanced migration and proliferation of bone marrow-derived macrophages. Poststroke clearance of myelin debris was significantly attenuated in Pdgfrb(+/-) mice. Pericyte conditioned medium promoted phagocytic activity in bone marrow-derived macrophages, also enhancing both STAT3 (signal transducer and activator of transcription 3) phosphorylation and expression of scavenger receptors, Msr1 and Lrp1. Macrophages processing myelin debris produced trophic factors, enhancing PDGFRbeta signaling in pericytes leading to the production of ECM (extracellular matrix) proteins and oligodendrogenesis. Functional recovery was significantly attenuated in Pdgfrb(+/-) mice, parallel with the extent of tissue repair. CONCLUSIONS: A reciprocal interaction between pericytes and macrophages is important for poststroke tissue repair and functional recovery..
5.	Shibahara T, Ago T, et al., Pericyte-Mediated Tissue Repair through PDGFRbeta Promotes Peri-Infarct Astrogliosis, Oligodendrogenesis, and Functional Recovery after Acute Ischemic Stroke, eNeuro, 10.1523/ENEURO.0474-19.2020, 2020.03.
6.	Matsuo R, Ago T, et al. , Smoking Status and Functional Outcomes After Acute Ischemic Stroke, STROKE, 10.1161/STROKEAHA.119.027230, 51, 3, 846-852, 2020.03, Background and Purpose- Smoking is an established risk factor for stroke; however, it is uncertain whether prestroke smoking status affects clinical outcomes of acute ischemic stroke. This study aimed to elucidate the association between smoking status and functional outcomes after acute ischemic stroke. Methods- Using a multicenter hospital-based stroke registry in Japan, we investigated 10 825 patients with acute ischemic stroke hospitalized between July 2007 and December 2017 who had been independent before stroke onset. Smoking status was categorized into those who had never smoked (nonsmokers), former smokers, and current smokers. Clinical outcomes included poor functional outcome (modified Rankin Scale score >/=2) and functional dependence (modified Rankin Scale score 2-5) at 3 months. We adjusted for potential confounding factors using a logistic regression analysis. Results- The mean age of patients was 70.2+/-12.2 years, and 37.0% were women. There were 4396 (42.7%) nonsmokers, 3328 (32.4%) former smokers, and 2561 (24.9%) current smokers. The odds ratio (95% CI) for poor functional outcome after adjusting for confounders increased in current smokers (1.29 [1.11-1.49] versus nonsmokers) but not in former smokers (1.05 [0.92-1.21] versus nonsmokers). However, among the former smokers, the odds ratio of poor functional outcome was higher in those who quit smoking within 2 years of stroke onset (1.75 [1.15-2.66] versus nonsmokers). The risk of poor functional outcome tended to increase as the number of daily cigarettes increased in current smokers (P for trend=0.002). All these associations were maintained for functional dependence. Conclusions- Current and recent smoking is associated with an increased risk of unfavorable functional outcomes at 3 months after acute ischemic stroke. Registration- URL: http://www.fukuoka-stroke.net/english/index.html. Unique identifier: 000000800..
7.	Kuniyuki Nakamura, Tomoko Ikeuchi, Kazuki Nara, Craig S. Rhodes, Peipei Zhang, Yuta Chiba, Saiko Kazuno, Yoshiki Miura, Tetsuro Ago, Eri Arikawa-Hirasawa, Yoh Suke Mukouyama, Yoshihiko Yamada, Perlecan regulates pericyte dynamics in the maintenance and repair of the blood-brain barrier, The Journal of cell biology, 10.1083/jcb.201807178, 218, 10, 3506-3525, 2019.10, [URL], Ischemic stroke causes blood-brain barrier (BBB) breakdown due to significant damage to the integrity of BBB components. Recent studies have highlighted the importance of pericytes in the repair process of BBB functions triggered by PDGFRβ up-regulation. Here, we show that perlecan, a major heparan sulfate proteoglycan of basement membranes, aids in BBB maintenance and repair through pericyte interactions. Using a transient middle cerebral artery occlusion model, we found larger infarct volumes and more BBB leakage in conditional perlecan (Hspg2)-deficient (Hspg2-/--TG) mice than in control mice. Control mice showed increased numbers of pericytes in the ischemic lesion, whereas Hspg2-/--TG mice did not. At the mechanistic level, pericytes attached to recombinant perlecan C-terminal domain V (perlecan DV, endorepellin). Perlecan DV enhanced the PDGF-BB-induced phosphorylation of PDGFRβ, SHP-2, and FAK partially through integrin α5β1 and promoted pericyte migration. Perlecan therefore appears to regulate pericyte recruitment through the cooperative functioning of PDGFRβ and integrin α5β1 to support BBB maintenance and repair following ischemic stroke..
8.	Yoji Yoshikawa, Tetsuro Ago, Junya Kuroda, Yoshinobu Wakisaka, Masaki Tachibana, Motohiro Komori, Tomoya Shibahara, Hideyuki Nakashima, Kinichi Nakashima, Takanari Kitazono, Nox4 Promotes Neural Stem/Precursor Cell Proliferation and Neurogenesis in the Hippocampus and Restores Memory Function Following Trimethyltin-Induced Injury, Neuroscience, 10.1016/j.neuroscience.2018.11.046, 398, 193-205, 2019.02, [URL], Reactive oxygen species (ROS) modulate the growth of neural stem/precursor cells (NS/PCs) and participate in hippocampus-associated learning and memory. However, the origin of these regulatory ROS in NS/PCs is not fully understood. In the present study, we found that Nox4, a ROS-producing NADPH oxidase family protein, is expressed in primary cultured NS/PCs and in those of the adult mouse brain. Nox inhibitors VAS 2870 and GKT137831 or Nox4 deletion attenuated bFGF-induced proliferation of cultured NS/PCs, while lentivirus-mediated Nox4 overexpression increased the production of H 2 O 2 , the phosphorylation of Akt, and the proliferation of cultured NS/PCs. Nox4 did not significantly affect the potential of cultured NS/PCs to differentiate into neurons or astrocytes. The histological and functional development of the hippocampus appeared normal in Nox4 − / − mice. Although pathological and functional damages in the hippocampus induced by the neurotoxin trimethyltin were not significantly different between wild-type and Nox4 − / − mice, the post-injury reactive proliferation of NS/PCs and neurogenesis in the subgranular zone (SGZ) of the dentate gyrus were significantly impaired in Nox4 − / − animals. Restoration from the trimethyltin-induced impairment in recognition and spatial working memory was also significantly attenuated in Nox4 − / − mice. Collectively, our findings suggest that Nox4 participates in NS/PC proliferation and neurogenesis in the hippocampus following injury, thereby helping to restore memory function..
9.	Motohiro Komori, Tetsuro Ago, Yoshinobu Wakisaka, Kuniyuki Nakamura, Masaki Tachibana, Yoji Yoshikawa, Tomoya Shibahara, Kei Yamanaka, Junya Kuroda, Takanari Kitazono, Early initiation of a factor Xa inhibitor can attenuate tissue repair and neurorestoration after middle cerebral artery occlusion, Brain Research, 10.1016/j.brainres.2019.05.020, 1718, 201-211, 2019.09, [URL], The timing of anti-coagulation therapy initiation after acute cardioembolic stroke remains controversial. We investigated the effects of post-stroke administration of a factor Xa inhibitor in mice, focusing on tissue repair and functional restoration outcomes. We initiated administration of rivaroxaban, a Xa inhibitor, immediately after permanent distal middle cerebral artery occlusion (pMCAO)in CB-17 mice harboring few leptomeningeal anastomoses at baseline. Rivaroxaban initiated immediately after pMCAO hindered the recovery of blood flow in ischemic areas by inhibiting leptomeningeal anastomosis development, and led to impaired restoration of neurologic functions with less extensive peri-infarct astrogliosis. Within infarct areas, angiogenesis and fibrotic responses were attenuated in rivaroxaban-fed mice. Furthermore, inflammatory responses, including the accumulation of neutrophils and monocytes/macrophages, local secretion of pro-inflammatory cytokines, and breakdown of the blood–brain barrier, were enhanced in infarct areas in mice treated immediately with rivaroxaban following pMCAO. The detrimental effects were not found when rivaroxaban was initiated after transient MCAO or on day 7 after pMCAO. Collectively, early post-stroke initiation of a factor Xa inhibitor may suppress leptomeningeal anastomosis development and blood flow recovery in ischemic areas, thereby resulting in attenuated tissue repair and functional restoration unless occluded large arteries are successfully recanalized..
10.	Tetsuro Ago, ペリサイトは脳機能にとってなぜ重要なのか？, Clinical Neurology, 10.5692/clinicalneurol.cn-001357, 59, 11, 707-715, 2019.01, [URL], Pericytes are mural cells embedded in the basal membrane surrounding endothelial cells in capillary and small vessels (from precapillary arterioles to postcapillary venules). They exist with a high coverage ratio to endothelial cells in the brain and play crucial roles in the formation and maintenance of the blood-brain barrier and the control of blood flow through a close interaction with endothelial cells. Thus, intactness of pericyte is absolutely needed for neuronal/ brain functions. Ageing, life-style diseases, hypoperfusion/ischemia, drugs, and genetic factors can primarily cause pericyte dysfunctions, thereby leading to the development or progression of various brain disorders, including cerebrovascular diseases. Because pericytes also play an important role in tissue repair after brain injuries, they have received much attention as a therapeutic target even from the standpoint of functional recovery..
11.	Ago T, Matsuo R, Hata J, Wakisaka Y, Kuroda J, Kitazono T, Kamouchi M. Insulin resistance and clinical outcomes after ischemic stroke., Insulin resistance and clinical outcomes after ischemic stroke., Neurology, 90, 17, 1470-1477, 2018.05, インスリン抵抗性と脳梗塞発症後機能転帰の関連について検討した．本検討では4,655名の急性期脳梗塞患者(平均年齢70.3歳，男性63,5%，入院前自立，発症7日以内，入院前-中にインスリン治療を受けていない患者)について解析している． 入院後，空腹時血糖およびインスリン値によって計算されたHOMA-IRをインスリン抵抗性の指標として用いた．入院後の神経増悪の有無，3ヶ月後の転帰不良(mRS 3以上)，及び 3ヶ月後再発・死亡との関連について解析した． HOMA-IRを値の低い方から５群(Q1-Q5)にわけ，Q1を基準とすると，Q5では入院中の神経症候改善率が低く(オッズ比 0.68 [95% confidence interval, 0.56–0.83]，転帰不良となるオッズ比が高値であった(2.02 [1.52–2.68])． ３ヶ月後の再発や死亡との関連は認められなかった．非糖尿病・非肥満の患者群でもこの関連は維持された．年齢，性，脳梗塞病型・重症度別に層別解析を行ったが異質性は認められなかった．.
12.	Rainer Malik, Ganesh Chauhan, Matthew Traylor, Muralidharan Sargurupremraj, Yukinori Okada, Aniket Mishra, Loes Rutten-Jacobs, Anne Katrin Giese, Sander W. Van Der Laan, Solveig Gretarsdottir, Christopher D. Anderson, Michael Chong, Hieab H.H. Adams, Tetsuro Ago, Peter Almgren, Philippe Amouyel, Hakan Ay, Traci M. Bartz, Oscar R. Benavente, Steve Bevan, Giorgio B. Boncoraglio, Robert D. Brown, Adam S. Butterworth, Caty Carrera, Cara L. Carty, Daniel I. Chasman, Wei Min Chen, John W. Cole, Adolfo Correa, Ioana Cotlarciuc, Carlos Cruchaga, John Danesh, Paul I.W. De Bakker, Anita L. Destefano, Marcel Den Hoed, Qing Duan, Stefan T. Engelter, Guido J. Falcone, Rebecca F. Gottesman, Raji P. Grewal, Vilmundur Gudnason, Stefan Gustafsson, Jeffrey Haessler, Tamara B. Harris, Ahamad Hassan, Aki S. Havulinna, Susan R. Heckbert, Elizabeth G. Holliday, George Howard, Fang Chi Hsu, Multiancestry genome-wide association study of 520,000 subjects identifies 32 loci associated with stroke and stroke subtypes, Nature genetics, 10.1038/s41588-018-0058-3, 50, 4, 524-537, 2018.04, [URL], Stroke has multiple etiologies, but the underlying genes and pathways are largely unknown. We conducted a multiancestry genome-wide-association meta-analysis in 521,612 individuals (67,162 cases and 454,450 controls) and discovered 22 new stroke risk loci, bringing the total to 32. We further found shared genetic variation with related vascular traits, including blood pressure, cardiac traits, and venous thromboembolism, at individual loci (n = 18), and using genetic risk scores and linkage-disequilibrium-score regression. Several loci exhibited distinct association and pleiotropy patterns for etiological stroke subtypes. Eleven new susceptibility loci indicate mechanisms not previously implicated in stroke pathophysiology, with prioritization of risk variants and genes accomplished through bioinformatics analyses using extensive functional datasets. Stroke risk loci were significantly enriched in drug targets for antithrombotic therapy..
13.	Tachibana M, Ago T, Wakisaka Y, Kuroda J, Kitazono T, Early reperfusion after brain ischemia has beneficial effects beyond rescuing neurons, Stroke, 2017.08.
14.	Nishimura A, Ago T, Kuroda J, et al., Detrimental role of pericyte Nox4 in the acute phase of brain ischemia., J Cereb Blood Flow Metab, 36, 6, 1143-1154, 2016.06.
15.	Nakamura K, Arimura K, Ago T, et al., Possible involvement of basic FGF in the upregulation of PDGFR beta in pericytes after ischemic stroke, BRAIN RESEARCH, 10.1016/j.brainres.2015.11.003, 1630, 98-108, 2016.01.
16.	Makihara N, Ago T, et al., Involvement of platelet-derived growth factor receptor β in fibrosis through extracellular matrix protein production after ischemic stroke, Exp Neurol, 2015.02.
17.	Ago T, Kitazono T, Brain pericyte in health and cerebrovascular diseases., 福岡医学雑誌, 2014.06.
18.	Ishitsuka K, Ago T(Corresponding author), Arimura K, Nakamura K, Tokami H, Makihara N, Kuroda J, Kamouchi M, Kitazono T., Neurotrophin production in brain pericytes during hypoxia: a role of pericytes for neuroprotection, Microvascular Research, 83, 3, 352-9, 2012.05.
19.	Arimura K, Ago T(Corresponding author), Kamouchi M, Nakamura K, Ishitsuka K, Kuroda J, Sugimori H, Ooboshi H, Sasaki T, Kitazono T., PDGF receptor β signaling in pericytes following ischemic brain injury, Current Neurovascular Research, 9, 1, 1-9, 2012.02.
20.	Kuroda J, Ago T, Matsushima S, Zhai P, Schneider MD, Sadoshima J, NADPH oxidase 4 (Nox4) is a major source of oxidative stress in the failing heart., PNAS, 107, 35, 15565-70, 2010.08.
21.	Ago T, Kuroda J, Pain J, Fu C, Li H, Sadoshima J., Upregulation of Nox4 by Hypertrophic Stimuli Promotes Apoptosis and Mitochondrial Dysfunction in Cardiac Myocytes., Circulation Research, 2010.04.
22.	Ago T, Liu T, Zhai P, Chen W, Li H, Molkentin JD, Vatner SF, Sadoshima J., A redox-dependent pathway for regulating class II HDACs and cardiac hypertrophy., Cell, 133 (6), 978-993, 2008.06.
23.	Ago T, Kitazono T, Kuroda J, Kumai Y, Kamouchi M, Ooboshi H, Wakisaka M, Kawahara T, Rokutan K, Ibayashi S, Iida M, NAD(P)H oxidases in rat basilar arterial endothelial cells, Stroke, 10.1161/01.STR.0000163111.05825.0b, 36, 5, 1040-1046, 36(5): 1040-1046 , 2005.05.
24.	Ago T, Kitazono T, Ooboshi H, Iyama T, Han YH, Takada J, Wakisaka M, Ibayashi S, Utsumi H, Iida M. , Nox4 as the major catalytic component of an endothelial NAD(P)H oxidase., Circulation, 10.1161/01.CIR.0000105680.92873.70, 109, 2, 227-233, 109(2): 227-233., 2004.01.
25.	Ago T, Kuribayashi F, Hiroaki H, Takeya R, Ito T, Kohda D, Sumimoto H. , Phosphorylation of p47phox directs PX domain from SH3 domain towards phosphoinositides, leading to phagocyte NADPH oxidase activation. , PNAS, 10.1073/pnas.0735712100, 100, 8, 4474-4479, 100(8): 4474-9., 2003.04.
26.	Hiroaki H, Ago T, Ito T, Sumimoto H, Kohda D. , Solution structure of the PX domain, a target of the SH3 domain. , Nature Structural Biology, 10.1038/88591, 8, 6, 526-530, 8, 526-30 , 2001.08.
27.	Ago T, Nunoi H, Ito T, Sumimoto H., Mechanism for phosphorylation-induced activation of the phagocyte NADPH oxidase protein p47phox. Triple replacement of serines 303, 304, and 328 with aspartates disrupts the SH3 domain-mediated intramolecular interaction in p47phox, thereby activating the oxidase. , J Biol Chem , 10.1074/jbc.274.47.33644, 274, 47, 33644-33653, 274(47): 33644-33653., 1999.11.

主要総説, 論評, 解説, 書評, 報告書等

1.	吾郷哲朗, 「発展する脳卒中診療の最前線」Neurovascular unit - 脳梗塞発症から機能回復まで., 医学のあゆみ, 2022.03.
2.	吾郷哲朗, 脳血管障害のリスクコントロール, 診断と治療, 2021.05.
3.	吾郷哲朗, ペリサイトは脳機能にとってなぜ重要なのか？, 臨床神経, 2019.11.
4.	吾郷哲朗, ペリサイトを標的とした脳血管障害治療の可能性．, 日本臨床, 2019.06.
5.	吾郷 哲朗, The neurovascular unit in health and ischemic stroke, 日本臨床, 2016.04.
6.	吾郷 哲朗, なぜ周皮細胞か？—脳梗塞病対における周皮細胞の挙動とその重要性—, 脳循環代謝, 2016.02.
7.	吾郷 哲朗, 虚血性脳卒中治療の基礎的研究の進歩, 動脈硬化予防, 2016.01.
8.	吾郷 哲朗, 脳梗塞のバイオマーカー, Heart View, 2015.12.
9.	吾郷 哲朗, 血液脳関門/Neurovascular unitの 形成・維持における脳ペリサイトの重要性, 2013.09.
10.	Kamouchi M, Ago T, Kuroda J, Kitazono T. , The possible roles of brain pericytes in brain ischemia and stroke, Cell Mol Neurobiol, 2012.03.
11.	Ago T, Kuroda J, Kamouchi M, Sadoshima J, Kitazono T. , Pathophysiological Roles of NADPH Oxidase/Nox Family Proteins in the Vascular System – Review and Perspective – , Circulation Journal , 2011.07.
12.	Kamouchi M, Ago T, Kitazono T., Brain pericytes: emerging concepts and functional roles in brain homeostasis., Cell Mol Neurobiol. , 2011.03.
13.	Ago T, Matsushima S, Kuroda J, Zablocki D, Kitazono T, Sadoshima J., The NADPH oxidase Nox4 and aging in the heart, Aging, 2010.12.
14.	Ago T, Sadoshima J. , Thioredoxin1 as a negative regulator of cardiac hypertrophy. , 2007.06.
15.	立花 正輝, 吾郷 哲朗, 脳梗塞と血液検査, 日本臨床.
16.	中村 晋之, 吾郷 哲朗, 脳微小循環とneurovascular unit. 内皮細胞・周皮細胞の立場から, 日本臨床.

主要学会発表等

1.	Tetsuro Ago, Roles of Pericyte in brain health and cerebrovascular diseases (Pericytes -Functional diversity and commonality in health and disease), 第100回日本生理学会大会, 2023.03.
2.	吾郷哲朗, 意外と知らない脳梗塞の基本病態〜基礎研究から学ぶ. , 第5回 日本神経学会特別教育研修会：脳卒中コース, 2022.07.
3.	Ago T, Reciprocal interaction between pericytes and macrophage in post-stroke tissue repair and functional recovery. “High Impact Articles in Post-stroke Outcomes 2020, International Stroke Conference 2021, 2021.03.
4.	吾郷 哲朗, 脳虚血病態におけるペリサイトの役割, 第56回日本神経学会学術大会, 2015.05.
5.	吾郷 哲朗, 活性酸素種産生酵素Nox4による内皮・周皮細胞の分子制御とその意義, 脳心血管抗加齢研究会, 2014.12.
6.	Ago T, Role of pericytes in neuroprotection during brain ischemia, BRI International Symposium 2012, 2012.03.
7.	Arimura K, Ago T, et al., Neuroprotective Roles of Brain Pericytes through PDGFRβ-Akt Signaling in Ischemic Stroke , International Stroke Conference 2012, 2012.02.
8.	Arimura K, Ago T, Role of NADPH oxidase 4 in Brain Endothelial Cells after Ischemic Stroke , International Stroke Conference 2012, 2012.02.
9.	Arimura K, Ago T, et al, Roles of PDGF–PDGF-Rβ Signaling in Brain Pericytes in Ischemic Stroke, International Stroke Conference 2011, 2011.02.
10.	Ago T, Nox4 is a major source of ROS in the failing heart, Gordon Research Conference on Nox family NADPH oxidases 2010, 2010.06, [URL].
11.	Ago T, Liu T, Li H, Molkentin J, Sadoshima J, Redox-mediated regulation of HDAC4, a class II HDAC, by Thioredoxin1 through interaction with DnaJb5, a Heat Shock Protein 40., AHA Scientific Session 2007, 2007.11, [URL].

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