About Dr. Abe
Dr. Jun-ichi Abe received his medical degree from the Yamagata University in 1987, and went on to pursue his Internal Medicine Residency, and continued his fellowship in cardiology at Mitsui Memorial Hospital in Tokyo, where he focused on interventional cardiology and echocardiography with Dr. Tetsu Yamaguchi. Following medical residency and cardiology fellowship, he was appointed Instructor of Medicine/Cardiology at the University of Tokyo in 1992 with Dr. Kiyoshi Kurokawa. In 1995 Dr. Abe decided to pursue his career in medical research and became senior fellow in cardiology and worked with Dr. Bradford C. Berk at University of Washington (UW), Seattle, WA. Dr. Abe received his Ph.D. degree in Medicine/Cardiology from the University of Tokyo in 1998 under the guidance of Drs. Kiyoshi Kurokawa and Yoh Takuwa. He was then recruited to the University of Rochester as an Assistant Professor in 1999, became Tenured Professor in 2011, and Dean’s professor in 2013. In 2014, Dr. Abe joined the faculty of the Department of Cardiology at the University of Texas MD Anderson Cancer Center. He also obtained adjunct professorship at Institute of Bioscience and Technology, Texas A&M in 2017.
Dr. Abe received grants from the National Institute of Health and American Heart Association. He was a Fellow of American Heart Association (FAHA), Dean’s Professor at University of Rochester, Established Investigator of the American Heart Association, and was elected to ATVB Special Recognition Award in Vascular Biology. He has written over 130 scientific papers and book chapters, and is a current member of the Editorial Board of the Journal of American College of Cardiology, Circulation Research, Arteriosclerosis, Thrombosis and Vascular Biology, Journal of Molecular and Cellular Cardiology, Journal of Cardiovascular Translational Research, Clinical Science, and Metabolism, and Specialty Chief Editor of Frontiers in Cardiovascular Medicine, Cardio-Oncology section.
Professor, Department of Cardiology - Research, Division of Internal Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX
Professor, Texas A&M Health Science Center Institute of Biosciences and Technology, Houston, TX
The long-term goal of our lab is to establish the Cardio-Oncology research within the next 7 years. Cardio-oncology is a medical subspecialty concerned with the diagnosis and treatment of cardiovascular disease (CVDs) and organ failure mediated by microcirculatory or macrocirculatory defects in cancer patients. Although identifying the cardiovascular side effects of emerging cancer therapies including radiation is critical, the key goal of cardio-oncology is to allow patients to receive maximum and uninterrupted treatment for cancer while protecting them from cardiovascular complications mediated by this treatment. We must understand not only the pathophysiology of CVDs but also the mechanisms through which each cancer treatment controls cancer growth and metastasis. Armed with this profound knowledge of the pathophysiological, clinical, and epidemiologic aspects of the cardiovascular complications of cancer therapies, we can establish strong, evidence-based strategies for managing both short-term and long-term cardiovascular complications after treatment.p90RSK-ERK5 module, scescent phenotype, and cardiovascular toxicities.
We are studying the role of p90RSK-ERK5 module after the exposure of cardiovascular (CV) toxic drugs including various cancer treatments and HIV drugs (combination of anti-retrovirus therpay; cART) in vitro, in vivo, and in human study. The incidence of cardiovascular disease is higher in HIV-positive (HIV + ) patients than it is in the average population, and combination antiretroviral therapy (cART) is a recognized risk factor for cardiovascular disease. However, the molecular mechanisms that link cART and cardiovascular disease are currently unknown. Our study explores the role of the activation of p90RSK, a reactive oxygen species-sensitive kinase, in engendering senescent phenotype in macrophages and accelerating atherogenesis in patients undergoing cART. We found that cART increased monocyte/macrophage sensitivity to reactive oxygen species- in HIV + individuals by suppressing NRF2-ARE activity via p90RSK-mediated ERK5 S496 phosphorylation, which coordinately elicited senescent phenotypes and proinflammatory responses. As such, our report underscores the importance of p90RSK regulation in monocytes/macrophages as a viable biomarker and therapeutic target for preventing cardiovascular disease, especially in HIV + patients treated with cART.Shear stress, radiation, and SUMOylation.
First, we are studying the role of SUMOylation in cancer treatments and flow-mediated vascular dysfunction. We discovered that disturbed flow (d-flow)-induced p90RSK activation is critical to regulate de-SUMOylation enzyme SENP2 nuclear export by phosphorylating SENP2 T369, and regulate both p53 and ERK5 SUMOylation, leading to endothelial activation and apoptosis. We also showed the critical role of p90RSK-SENP2 module in regulating atherosclerosis formation in vivo ( J Clin Invest, 2015 ). Next, we tried to establish the animal models, which can represent cardiovascular disease in cancer survivors. We demonstrate that ionizing radiation (IR) not only increases atherosclerotic events but also vulnerable plaque formation. These increases were a somewhat delayed effect of IR as they were observed in mice with Partial carotid ligation (PCL)surgery performed 26 days, but not 10 days, after IR exposure. We established the proper animal model to study how to minimize the cardiovascular toxicity due to cancer treatment ( Frontiers in Cardiovascular Medicine, Ko et al., 2018 ). We also showed the critical role of p90RSK-medaited ERK5 SUMOylation in regulating endothelial cell activation after IR exposure ( Frontiers in Cardiovascular Medicine, Vu et al.,2018).
We also investigated the role of tight and adherent junction molecule MAGI1, as one of the targets of p90RSK, in regulateing endothelial cell (EC) activation and apoptosis. In ECs exposed to disturbed flow (d-flow), p90 ribosomal S6 kinase (p90RSK) bound to MAGI1, causing MAGI1-S741 phosphorylation and sentrin/SUMO-specific protease 2 T368 phosphorylation-mediated MAGI1-K931 deSUMOylation. MAGI1-S741 phosphorylation upregulated EC activation via activating Rap1. MAGI1-K931 deSUMOylation induced both nuclear translocation of p90RSK-MAGI1 and ATF-6-MAGI1 complexes, which accelerated EC activation and apoptosis, respectively. Microarray screening revealed key roles for MAGI1 in the endoplasmic reticulum (ER) stress response. In this context, MAGI1 associated with activating transcription factor 6 (ATF-6). MAGI1 expression was upregulated in ECs and macrophages found in atherosclerotic-prone regions of mouse aortas as well as in the colonic epithelia and ECs of patients with inflammatory bowel disease. Further, reduced MAGI1 expression in Magi1-/+ mice inhibited d-flow-induced atherogenesis. In summary, EC activation and ER stress-mediated apoptosis are regulated in concert by two different types of MAGI1 posttranslational modifications, elucidating attractive drug targets for chronic inflammatory disease, particularly atherosclerosisShelterin complex, endothelial activation, and senescence.
Recently, we are working on the role of premature aging in cancer treatments-mediated cardiovascular disease. During the course of our study, we discover the unique and interesting role of telomeric repeat-binding factor 2-interacting protein (TERF2IP), a member of the shelterin complex at the telomere, in EC activation and apoptosis. We found that d-flow induced p90RSK and TERF2IP interaction in a p90RSK kinase activity-dependent manner. An in vitro kinase assay revealed that p90RSK directly phosphorylated TERF2IP at the serine 205 (S205) residue, and d-flow increased TERF2IP S205 phosphorylation as well as EC senescence, apoptosis, and activation by activating p90RSK. TERF2IP phosphorylation was crucial for nuclear export of the TERF2IP-TRF 2 complex, which led to EC activation by cytosolic TERF2IP-mediated NF-κB activation and also to senescence and apoptosis of ECs by depleting TRF2 from the nucleus. Lastly, using EC-specific TERF2IP-knockout (TERF2IP-KO) mice, we found that the depletion of TERF2IP inhibited d-flow-induced EC senescence, apoptosis, and activation, as well as atherosclerotic plaque formation. These findings demonstrate that TERF2IP is an important molecular switch that simultaneously accelerates EC senescence, apoptosis, and activation by S205 phosphorylation ( JCI Insight, Kotla et al., 2019 ). Furthermore, we investigated TERF2IP-dependent gene expression and its role in regulating d-flow-induced senescence-associated secretory phenotype (SASP). Our unbiased transcriptome analysis showed that TERF2IP caused alteration in the expression of a distinct set of genes, including rapamycin-insensitive companion of mTOR ( RICTOR ) and makorin-1 ( MKRN1 ) ubiquitin E3 ligase, under d-flow conditions. In particular, both depletion of TERF2IP and overexpression of the TERF2IP S205A phosphorylation site mutant in ECs increased the d-flow and p90RSK-induced MKRN1 expression and subsequently inhibited apoptosis, telomere shortening, and NF-B activation in ECs via suppression of p53, p21, and telomerase (TERT) induction. MKRN1 and RICTOR belong to a distinct reciprocal gene set that is both negatively and positively regulated by p90RSK. TERF2IP S205 phosphorylation, a downstream event of p90RSK activation, uniquely inhibits MKRN1 expression and contributes to EC activation and senescence, which are key events for atherogenesis ( Metabolism, Kotla et al., 2019 ).Onco-Cardiology and the role of premature aging in CVD.
Although cancer therapy causes both DNA damage and telomere shortening, only the phenotype of telomere shortening can be transmitted to daughter cells. Therefore, we expect that the late cardiovascular effects of cancer therapy can be explained by this telomere shortening and subsequent premature aging. In other words, by determining the role and regulatory mechanism of telomere shortening and consequent premature aging in cancer survivors, we can obtain crucial information on vascular aging induced by various proatherogenic stimuli observed in people without cancer ( Circ Res, Abe et al., 2016 ).
|1998||University of Tokyo, Tokyo, JPN, PHD, Medicine/Cardiology|
|1987||University of Yamagata, Yamagata, JPN, MD, Medicine|
|1995-1998||Research Fellowship, Cardiology, University of Washington, Seattle, WA|
|1992-1994||Instructor, Internal Medicine and Cardiology, First Department of Internal Medicine, University of Tokyo, Tokyo|
|1989-1992||Clinical Fellowship, Internal Medicine and Cardiology, Mitsui Memorial Hospital, Tokyo|
|1987-1989||Clinical Residency, Internal Medicine, Mitsui Memorial Hospital, Tokyo|
|1987||Medical License (Japan)|
Professor (with tenure), Division of Aab Cardiovascular Research Institute, University of Rochester, Rochester, NY, 2011 - 2014
Associate Professor (with tenure), Division of Aab Cardiovascular Research Institute, University of Rochester, Rochester, NY, 2008 - 2011
Associate Professor, Division of Center ofr Cardiovascular Research, University of Rochester, Rochester, NY, 2003 - 2008
Assistant Professor, Division of Center for Cardiovascular Research Institute, University of Rochester, Rochester, NY, 1999 - 2003
Member of Senior Faculties Meeting (Aab CVRI), University of Rochester, Rochester, NY, 2012 - 2014
Director, Virus Core, University of Rochester, Rochester, NY, 2008 - 2014
Institutional Committee Activities
Member, DoIM Research Committee, 2015 - Present
Dean's Professorship, University of Rochester, Rochester, NY, 2013 - 2014
Military or Other Governmental Service
Member, NHLBI AIDS Working Group: Refining Current Scientific Priorities & Identifying New Scientific Gaps in HIV-related Heart, Lung, and Blood (HLB) Research,, 2015 - 2015
|2016||UT MD Anderson President's Recognition of Faculty Excellence Award, MD Anderson|
|2016||Arteriosclerosis Thrombosis and Vascular Biology. Top 10 Reviewer Award, ATVB|
|2013||Dean's Professorship, University of Rochester|
|2013||Superior Editorial Consultant Award, Circulation Research|
|2013||Elite Reviewer, Journal of American College of Cardiology (JACC)|
|2010||ATVB Special Recognition Award in Vascular Biology, ATVB|
|2007||Established Investigator Award, American Heart Association|
|2007||Excellence in Research Award, University of Rochester|
- McBeath E, Parker-Thornburg J, Fujii Y, Aryal N, Smith C, Hofmann MC, Abe JI, Fujiwara K. Rapid Evaluation of CRISPR Guides and Donors for Engineering Mice. Genes (Basel) 11(6), 2020. e-Pub 2020. PMID: 32521708.
- Kinoshita D, Shishido T, Takahashi T, Yokoyama M, Sugai T, Watanabe K, Tamura H, Nishiyama S, Takahashi H, Arimoto T, Miyamoto T, Watanabe T, Kishida S, Kadomatsu K, Abe JI, Takeishi Y, Konta T, Kubota I, Watanabe M. Growth Factor Midkine Aggravates Pulmonary Arterial Hypertension via Surface Nucleolin. Sci Rep 10(1):10345, 2020. e-Pub 2020. PMID: 32587339.
- Quintana RA, Bui LP, Moudgil R, Palaskas N, Hassan S, Abe JI, Mouhayar E, Yusuf SW, Hernandez A, Banchs J. Speckle-Tracking Echocardiography in Cardio-Oncology and Beyond. Tex Heart Inst J 47(2):96-107, 2020. PMID: 32603473.
- Moudgril R, Samra G, Ko KA, Vu HT, Thomas TN, Luo W, Chang J, Reddy AK, Fujiwara K, Abe JI. Topoisomerase 2B decrease results in diastolic dysfunction via p53 and Akt: A novel pathway. Front. Cardiovasc, 2020.
- Abe RJ, Savage H, Imanishi M, Banerjae P, Kotla S, Mayorga JP, Taunton J, Fugiwara K, Won JH, Yusuf SW, Palaskas NL, Banchs J, Lin SH, Schadler KL, Abe JI, Le NT. P90RSK-MAGI1 module controls endothelial permeability by post-translational modifications of MAGI1 and Hippo Pathway. Front. Cardiovasc, 2020.
- Mahadeo KM, Bajwa R, Abdel-Azim H, Lehmann LE, Duncan C, Zantek N, Vittorio J, Angelo J, McArthur J, Schadler K, Chan S, Tewari P, Khazal S, Auletta JJ, Choi SW, Shoberu B, Kalwak K, Harden A, Kebriaei P, Abe JI, Li S, Moffet JR, Abraham S, Tambaro FP, Kleinschmidt K, Richardson PG, Corbacioglu S, Pediatric Acute Lung Injury and Sepsis Investigators (PALISI) Network and the Pediatric Diseases Working Party of the European Society for Blood and Marrow Transplantation. Diagnosis, grading, and treatment recommendations for children, adolescents, and young adults with sinusoidal obstructive syndrome: an international expert position statement. Lancet Haematol 7(1):e61-e72, 2020. e-Pub 2019. PMID: 31818728.
- Luo W, Wang Y, Zhang L, Ren P, Zhang C, Li Y, Azares AR, Zhang M, Guo J, Ghaghada KB, Starosolski ZA, Rajapakshe K, Coarfa C, Li Y, Chen R, Fujiwara K, Abe JI, Coselli JS, Milewicz DM, LeMaire SA, Shen YH. Critical Role of Cytosolic DNA and Its Sensing Adaptor STING in Aortic Degeneration, Dissection, and Rupture. Circulation 141(1):42-66, 2020. e-Pub 2019. PMID: 31887080.
- Kotla S, Le NT, Vu HT, Ko KA, Gi YJ, Thomas TN, Giancursio C, Lusis AJ, Cooke JP, Fujiwara K, Abe JI. Endothelial senescence-associated secretory phenotype (SASP) is regulated by Makorin-1 ubiquitin E3 ligase. Metabolism 100:153962, 2019. e-Pub 2019. PMID: 31476350.
- Milgrom SA, Varghese B, Gladish GW, Choi AD, Dong W, Patel ZS, Chung CC, Rao A, Pinnix CC, Gunther JR, Dabaja BS, Lin SH, Hoffman KE, Huff JL, Slagowski J, Abe JI, Iliescu CA, Banchs J, Yusuf SW, Lopez-Mattei JC. Coronary Artery Dose-Volume Parameters Predict Risk of Calcification After Radiation Therapy. J Cardiovasc Imaging 27(4):268-279, 2019. PMID: 31614398.
- Lin L, Shi C, Sun Z, Le NT, Abe JI, Hu K. The Ser/Thr kinase p90RSK promotes kidney fibrosis by modulating fibroblast-epithelial crosstalk. J Biol Chem 294(25):9901-9910, 2019. e-Pub 2019. PMID: 31076505.
- Kotla S, Vu HT, Wang Y, Ko KA, Heo KS, Fujii Y, Thomas TN, Gi YJ, Mazhar H, Paez-Mayorga J, Shin JH,Tao Y, Giancursio CJ, Medina JLM, Taunton J, Lusis AJ, Cooke JP, Fujiwara K, Le NT, and Abe J. Phosphorylation of telomeric repeat binding factor 2-interacting protein (TERF2IP) promotes its nuclear export and induces endothelial cell activation and senescence. JCI Insight, 2019.
- Kotla S, Vu HT, Ko KA, Wang Y, Imanishi M, Heo KS, Fujii Y, Thomas TN, Gi YJ, Mazhar H, Paez-Mayorga J, Shin JH, Tao Y, Giancursio CJ, Medina JL, Taunton J, Lusis AJ, Cooke JP, Fujiwara K, Le NT, Abe JI. Endothelial senescence is induced by phosphorylation and nuclear export of telomeric repeat binding factor 2-interacting protein. JCI Insight 4(9), 2019. e-Pub 2019. PMID: 31045573.
- Abe JI, Ko KA, Kotla S, Wang Y, Paez-Mayorga J, Shin IJ, Imanishi M, Vu HT, Tao Y, Leiva-Juarez MM, Thomas TN, Medina JL, Won JH, Fujii Y, Giancursio CJ, McBeath E, Shin JH, Guzman L, Abe RJ, Taunton J, Mochizuki N, Faubion W, Cooke JP, Fujiwara K, Evans SE, Le NT. MAGI1 as a link between endothelial activation and ER stress drives atherosclerosis. JCI Insight 4(7), 2019. e-Pub 2019. PMID: 30944250.
- Takahashi T, Shishido T, Kinoshita D, Watanabe K, Toshima T, Sugai T, Narumi T, Otaki Y, Tamura H, Nishiyama S, Arimoto T, Takahashi H, Miyamoto T, Watanabe T, Woo CH, Abe JI, Takeishi Y, Kubota I, Watanabe M. Cardiac Nuclear High-Mobility Group Box 1 Ameliorates Pathological Cardiac Hypertrophy by Inhibiting DNA Damage Response. JACC Basic Transl Sci 4(2):234-247, 2019. e-Pub 2019. PMID: 31061925.
- Singh MV, Kotla S, Le NT, Ae Ko K, Heo KS, Wang Y, Fujii Y, Thi Vu H, McBeath E, Thomas TN, Jin Gi Y, Tao Y, Medina JL, Taunton J, Carson N, Dogra V, Doyley MM, Tyrell A, Lu W, Qiu X, Stirpe NE, Gates KJ, Hurley C, Fujiwara K, Maggirwar SB, Schifitto G, Abe JI. Senescent Phenotype Induced by p90RSK-NRF2 Signaling Sensitizes Monocytes and Macrophages to Oxidative Stress in HIV-Positive Individuals. Circulation 139(9):1199-1216, 2019. PMID: 30586719.
- Venkatesulu BP, Mahadevan LS, Aliru ML, Yang X, Bodd MH, Singh PK, Yusuf SW, Abe JI, Krishnan S. Radiation-Induced Endothelial Vascular Injury: A Review of Possible Mechanisms. JACC Basic Transl Sci 3(4):563-572, 2018. e-Pub 2018. PMID: 30175280.
- Vu HT, Kotla S, Ko KA, Fujii Y, Tao Y, Medina J, Thomas T, Hada M, Sood AK, Singh PK, Milgrom SA, Krishnan S, Fujiwara K, Le NT, Abe JI. Ionizing Radiation Induces Endothelial Inflammation and Apoptosis via p90RSK-Mediated ERK5 S496 Phosphorylation. Front Cardiovasc Med 5:23, 2018. e-Pub 2018. PMID: 29594152.
- Sylvester CB, Abe JI, Patel ZS, Grande-Allen KJ. Radiation-Induced Cardiovascular Disease: Mechanisms and Importance of Linear Energy Transfer. Front Cardiovasc Med 5:5, 2018. e-Pub 2018. PMID: 29445728.
- Ko KA, Wang Y, Kotla S, Fujii Y, Vu HT, Venkatesulu BP, Thomas TN, Medina JL, Gi YJ, Hada M, Grande-Allen J, Patel ZS, Milgrom SA, Krishnan S, Fujiwara K, Abe JI. Developing a Reliable Mouse Model for Cancer Therapy-Induced Cardiovascular Toxicity in Cancer Patients and Survivors. Front Cardiovasc Med 5:26, 2018. e-Pub 2018. PMID: 29675417.
- Le NT, Martin JF, Fujiwara K, Abe JI. Sub-cellular localization specific SUMOylation in the heart. Biochim Biophys Acta 1863(8):2041-2055, 2017. e-Pub 2017. PMID: 28130202.
- Lin SC, Lee YC, Yu G, Cheng CJ, Zhou X, Chu K, Murshed M, Le NT, Baseler L, Abe JI, Fujiwara K, deCrombrugghe B, Logothetis CJ, Gallick GE, Yu-Lee LY, Maity SN, Lin SH. Endothelial-to-Osteoblast Conversion Generates Osteoblastic Metastasis of Prostate Cancer. Dev Cell 41(5):467-480.e3, 2017. PMID: 28586644.
- Le NT, Sandhu UG, Quintana-Quezada RA, Hoang NM, Fujiwara K, Abe JI. Flow signaling and atherosclerosis. Cell Mol Life Sci 74(10):1835-1858, 2017. e-Pub 2016. PMID: 28039525.
- Mao Y, Luo W, Zhang L, Wu W, Yuan L, Xu H, Song J, Fujiwara K, Abe JI, LeMaire SA, Wang XL, Shen YH. STING-IRF3 Triggers Endothelial Inflammation in Response to Free Fatty Acid-Induced Mitochondrial Damage in Diet-Induced Obesity. Arterioscler Thromb Vasc Biol 37(5):920-929, 2017. e-Pub 2017. PMID: 28302626.
- Ko KA, Fujiwara K, Krishnan S, Abe JI. En Face Preparation of Mouse Blood Vessels. J Vis Exp(123), 2017. e-Pub 2017. PMID: 28570508.
- Abe JI, Sandhu UG, Hoang NM, Thangam M, Quintana-Quezada RA, Fujiwara K, Le NT. Coordination of Cellular Localization-Dependent Effects of Sumoylation in Regulating Cardiovascular and Neurological Diseases. Adv Exp Med Biol 963:337-358, 2017. PMID: 28197922.
- Heo KS, Berk BC, Abe J. Disturbed Flow-Induced Endothelial Proatherogenic Signaling Via Regulating Post-Translational Modifications and Epigenetic Events. Antioxid Redox Signal 25(7):435-50, 2016. e-Pub 2016. PMID: 26714841.
- Abe J. Multiple Functions of Protein Inhibitor of Activated STAT1 in Regulating Endothelial Cell Proliferation and Inflammation. Arterioscler Thromb Vasc Biol 36(9):1717-9, 2016. PMID: 27559144.
- Abe J, Martin JF, Yeh ET. The Future of Onco-Cardiology: We Are Not Just "Side Effect Hunters". Circ Res 119(8):896-9, 2016. PMID: 27688305.
- Chang E, Abe J. Kinase-SUMO networks in diabetes-mediated cardiovascular disease. Metabolism 65(5):623-33, 2016. e-Pub 2016. PMID: 27085771.
- Abe J, Morrell C. Pyroptosis as a Regulated Form of Necrosis: PI+/Annexin V-/High Caspase 1/Low Caspase 9 Activity in Cells = Pyroptosis?. Circ Res 118(10):1457-60, 2016. PMID: 27174943.
- Batchu SN, Xia J, Ko KA, Doyley MM, Abe J, Morrell CN, Korshunov VA. Axl modulates immune activation of smooth muscle cells in vein graft remodeling. Am J Physiol Heart Circ Physiol 309(6):H1048-58, 2015. e-Pub 2015. PMID: 26276821.
- Cameron SJ, Ture SK, Mickelsen D, Chakrabarti E, Modjeski KL, McNitt S, Seaberry M, Field DJ, Le NT, Abe J, Morrell CN. Platelet Extracellular Regulated Protein Kinase 5 Is a Redox Switch and Triggers Maladaptive Platelet Responses and Myocardial Infarct Expansion. Circulation 132(1):47-58, 2015. e-Pub 2015. PMID: 25934838.
- Narumi T, Shishido T, Otaki Y, Kadowaki S, Honda Y, Funayama A, Honda S, Hasegawa H, Kinoshita D, Yokoyama M, Nishiyama S, Takahashi H, Arimoto T, Miyamoto T, Watanabe T, Tanaka A, Woo CH, Abe J, Takeishi Y, Kubota I. High-mobility group box 1-mediated heat shock protein beta 1 expression attenuates mitochondrial dysfunction and apoptosis. J Mol Cell Cardiol 82:1-12, 2015. e-Pub 2015. PMID: 25736854.
- Heo KS, Le NT, Cushman HJ, Giancursio CJ, Chang E, Woo CH, Sullivan MA, Taunton J, Yeh ETH, Fujiwara K, Abe J. Disturbed flow-activated p90RSK-SENP2 module accelerates atherosclerosis. J Clin Invest 125:1299-1230, 2015.
- Narumi T, Shishido T, Otaki Y, Kadowaki S, Honda Y, Funayama A,Honda S, Hasegawa H, Kinoshita D, Yokoyama M, Nishiyama S,Takahashi H, Arimoto T, Miyamoto T, Watanabe T, Tanaka A, Woo CH, Abe J, Takeishi Y, Kubota I. High-mobility group box 1-mediated heat shock protein beta 1 expression attenuates mitochondrial dysfunction and apoptosis. J Mol Cell Cardiol 82:1-12, 2015.
- Quintana RA, Bui LP, Palaskas N, Mougdil R, Yusuf SW, Hernandez A, Abe J, Hassan S, Banchs J.. Clinical Utility of Speckle-Tracking Echocardiography in Cancer Care and beyond. Texas Heart Institute Journal,2019.
- Milgrom S, Varghese B, Gladish G, Choi A, Dong W, Patel Z, Chung C, Rao A, Pinnix C, Gunther J, Dabaja B, Lin S, Hoffman K, Huff J, Slagowski J, Abe J, Iliescu C, Banchs J, Yusuf SW. Coronary Artery Dose-Volume Parameters Predict the Risk of Calcification After Radiation Therapy. Journal of Cardiovascular Computed Tomography.
- Cornwell A, Palli R, Singh MV, Benoodt L, Tyrell A, Abe JI, Schifitto G, Maggirwar SB, Thakar J.. Molecular characterization of atherosclerosis in HIV positive persons. Sci Rep.
- Wang X, Palaskas NL, Yusuf SW, Abe JI, Lopez-Mattei J, Banchs J, Gladish GW, Lee P, Liao Z, Deswal A, Lin SH. Incidence and Onset of Severe Cardiac Events After Radiotherapy for Esophageal Cancer. J Thorac Oncol. e-Pub 2020. PMID: 32599073.
- Le NT, Martin JF, Fujiwara K, Abe J,. Sub-cellular localization specific SUMOylation in the heart. Biochim Biophys Acta 1863(2041-2055), 2017.
- . Le NT, Sandhu UG, Quintana-Quezada RA, Martin JF, Fujiwara K, and Abe J. Flow signaling and atherosclerosis. Cell Mol Life Sci 74:1835-1858, 2017.
- Chang E and Abe J. Kinase-SUMO Networks in Diabetes-mediated Cardiovascular Disease. Metabolism 65(623-33), 2016.
- Le NT, Abe J, Hoang NH, Fujiwara K. MEK5/ERK5. Encyclopidia of Signaling Molecule 2nd Edition, 2016.
- Abe J, Le NT, Heo KS. Role for SUMOylation in disturbed flow-induced atherosclerotic plaque formation. Biomed Eng Lett 5:162-171, 2015.
- Heo KS, Berk BC, and Abe J. Disturbed flow-induced endothelial pro-atherogenic signaling via regulating post-translational modifications and epigenic events. Antioxid Redox Signal, 2015.
- Dominic A, Banerjee P, Hamilton DJ, Le NT, Abe JI. Time-dependent replicative senescence vs. disturbed flow-induced pre-mature aging in atherosclerosis. Redox Biol:101614. e-Pub 2020. PMID: 32863187.
- Shen YH, Abe JI. Enigma of Inflammasome Activation by Kinases. Arterioscler Thromb Vasc Biol 39(8):1501-1503, 2019. PMID: 31339780.
- Abe JI, Sood AK, Martin JF. Editorial: Cardio-Oncology: From Bench to Bedside. Front Cardiovasc Med 6:37, 2019. PMID: 31024931.
- Le NT, Abe JI. MicroRNA 199a and the eNOS (Endothelial NO Synthase)/NO Pathway. Arterioscler Thromb Vasc Biol 38(10):2278-2280, 2018. PMID: 30354226.
- Le NT, and Abe J. Regulation of Kir2.1 Function Under Shear Stress and Cholesterol Loading. J Am Heart Assoc, 2018.
- Abe J,. Multiple Functions of Protein Inhibitor of Activated STAT1 in Regulating Endothelial Cell Proliferation and Inflammation. Arterioscler Thromb Vasc Biol 36:1717-1719, 2016.
- Abe J, Martin JF, and Yeh ETH.. The future of onco-cardiology medicine: We are not just “side effect hunters”. Circ Res 30(119):896-9, 2016.
- Abe J, Morrell C. Pyroptosis as a regulated form of necrosis. PI+/Annexin V-/high caspase 1/low caspase 9 activity in cells = pyroptosis?. Circ Res, 2016.
- Kotla S, Zhang A, Ko KA, Imanishi M, Fujiwara K, Yoon Y, Brooks PS, Hamilton D, and Abe JI.. Poly (ADP-ribose) polymerase (PARP) activation and mitochondrial hibernation induced by p90RSK-mediated ERK5 S496 phosphorylation promote mitochondrial ROS production in macrophage. IVBM, 2020.
- Kotla S, Zhang A, Ko KA, Imanishi M, Fujiwara K, Yoon Y, Brookes PS, Hamilton D, and Abe JI. Poly (ADP-ribose) polymerase (PARP) activation and mitochondrial hibernation induced by p90RSK-mediated ERK5 S496 phosphorylation promote mitochondrial ROS production in macrophage. ATVB, 2020.
- Kotla S, Ko KA, Imanishi M, Banchs J, Palaskas NL, Yusuf SW, Fujiwara K, Le NT, Anita Deswal A, Chung C, Lin SH, and Abe JI.. p90RSK-mediated ERK5 S496 phosphorylation and Poly (ADP-ribose) polymerase (PARP) activation promote monocyte/macrophage priming in mouse and cancer patients after radiation therapy (RT). ATVB, 2020.
- Imanishi M, Ko KA, Kotla S, Thomas TN, Gi YJ, Wang Y, Fujiwara K, Savage H, Velatooru LR, Schadler KL, Shen YH, Le NT, Burks JK, and Abe JI.. Novel simultaneous multiplexed imaging with subcellular resolution by mass cytometry (Imaging mass cytometry: IMC) in atherosclerosis plaque (AS). ATVB, 2020.
- Kotla S, Singh MV, Le NT, Ko KA, Heo KS, Fujii Y, Vu HT, McBeath E, Thomas TN, Tao Y, Medina J, Stirpe NE, Lu W, Tyrell A, Gates KJ, Qui X, Fujiwara K, Maggirwar SJ, Schifitto G, and Abe J.. Senescent phenotype induced by p90RSK-NRF2 signaling sensitizes monocytes and macrophages to oxidative stress in HIV+ individuals: implications for atherogenesis. NAVBO, Boston, MA, 2018.
- Ko KA, Kotla S, Wang Y, Fujii Y, Vu HT, Venkatesulu BP, Thomas TN, Medina J, Gi YJ1, Hada M, Grande-Allen J, Patel ZS, Milgrom SA, Kirshnan S, Fujiwara K,, and Abe J.. Radiation induced atherosclerosis on mice. ATVB, San Francisco, CA, 2018.
- Abe J, Sandhu UG, Hoang NM, Thangam M, Quintana-Quezada RA, Fujiwara K, Le NT.. Coordination of cellular localization-dependent effects of SUMOylation in regulating cardiovascular and neurological diseases. In: SUMO Regulation of Cellular Processes, Second edition. Springer, 2017.
- Le NT, Hoang NM, Abe J, and Fujiwara K. 7. MEK5/ERK5. In: . Encyclopedia of Signaling Molecules, 2nd Edition: Springer, 2016.
|Title:||P90RSK: A Flow Responsive Mediator of Inflammation|
|Title:||Ubiquitin-like Protein Modification in Diabetic Cardiomyopathy|
|Title:||Fluid Shear Stress Signal Transduction in Endothelium|
|Title:||P90RSK-ERK Module, Efferocytosis, and Vulnerable Plaque Formation|
|Title:||Oxidative Stress and Vascular Smooth Muscle Cell Growth|
|Title:||Nuclear beta-catenin Signaling in the Heart|
|Title:||Function and Regulation of Phosphodiesterase in the Heart|
|Title:||Regulation of Lung Autophagy and Inflammation|
|Title:||cART accelerates vascular aging in HIV infected subjects|
|Title:||Pathological flow-induced endothelial damage and plaque erosion|
|Title:||Disturbed flow-induced TERF2IP post-translational modifications and atherosclerosis|
|Title:||Role of S1PR1 in exercise-induced tumor vascular remodeling|
|Funding Source:||Cancer Prevention & Research Institute of Texas (CPRIT)|
|Title:||A Novel Role of MAGI1 in regulating non-canonical LATS signaling and atherosclerotic plaque formation|
|Title:||Inducible epithelial resistance: a program investigating mechanisms to protect against acute and chronic complications of pneumonia|
|Title:||Novel genetic insight into molecular pathogenesis of atherosclerosis|