Research Topics
Genomes and Genes
| Chen YanSummaryAffiliation: University of Rochester Country: USA Publications
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Detail Information
Publications
Vinpocetine suppresses pathological vascular remodeling by inhibiting vascular smooth muscle cell proliferation and migrationYujun Cai
Aab Cardiovascular Research Institute, Department of Medicine, University of Rochester School of Medicine and Dentistry, 601 Elmwood Ave, Box CVRI, Rochester, NY 14642, USA
J Pharmacol Exp Ther 343:479-88. 2012..Given the safety profile of vinpocetine, this study provides insight into the therapeutic potential of vinpocetine in proliferative vascular disorders...
Regulation of phosphodiesterase 3 and inducible cAMP early repressor in the heartChen Yan
Center for Cardiovascular Research, Aab Institute of Biomedical Science, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA
Circ Res 100:489-501. 2007..Hence, strategies that maintain PDE3A function may represent an attractive approach to circumvent myocyte apoptosis and cardiac dysfunction...- Activation of extracellular signal-regulated kinase 5 reduces cardiac apoptosis and dysfunction via inhibition of a phosphodiesterase 3A/inducible cAMP early repressor feedback loopChen Yan
Cardiovascular Research Institute, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA
Circ Res 100:510-9. 2007..These data suggest a new therapeutic paradigm for end stage of heart failure by inhibiting the PDE3A/ICER feedback loop via activating ERK5... - GIT1 is a scaffold for ERK1/2 activation in focal adhesionsGuoyong Yin
Center for Cardiovascular Research and Department of Medicine, University of Rochester, Rochester, New York 14642, USA
J Biol Chem 280:27705-12. 2005..In summary, the present study further supports a key role for GIT1 (a MEK1-binding protein) as a scaffold for signal transduction in focal adhesions... - Effects of MEK5/ERK5 association on small ubiquitin-related modification of ERK5: implications for diabetic ventricular dysfunction after myocardial infarctionTetsuro Shishido
Cardiovascular Research Institute, University of Rochester School of Medicine and Dentistry, West Henrietta, NY 14586, USA
Circ Res 102:1416-25. 2008..These results demonstrated that ERK5 transcriptional activity is subject to downregulation by diabetes-dependent SUMOylation, which resulted in a proapoptotic condition contributing to poor post-MI LV function... 
Extracellular signal-regulated kinase 5 SUMOylation antagonizes shear stress-induced antiinflammatory response and endothelial nitric oxide synthase expression in endothelial cellsChang Hoon Woo
Cardiovascular Research Institute, 601 Elmwood Ave, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA
Circ Res 102:538-45. 2008..These data clearly defined SUMOylation-dependent ERK5 transcriptional repression independent of kinase activity and suggested this process as among the molecular mechanisms of diabetes-mediated endothelial dysfunction...- GIT1 mediates Src-dependent activation of phospholipase Cgamma by angiotensin II and epidermal growth factorJudith Haendeler
Center for Cardiovascular Research and Department of Medicine, University of Rochester, Rochester, New York 14642, USA
J Biol Chem 278:49936-44. 2003..We propose that GIT1 is a novel regulator of PLCgamma function that mediates PLCgamma activation by c-Src and integrates signal transduction by GPCRs and TKRs... - GIT1 functions as a scaffold for MEK1-extracellular signal-regulated kinase 1 and 2 activation by angiotensin II and epidermal growth factorGuoyong Yin
Center for Cardiovascular Research and Department of Medicine, University of Rochester, 601 Elmwood Avenue, Rochester, NY 14642, USA
Mol Cell Biol 24:875-85. 2004..We propose that GIT1 serves as a scaffold protein to facilitate c-Src-dependent activation of MEK1-ERK1/2 in response to both GPCRs and TKRs... - Phosphorylation of G protein-coupled receptor kinase 2-interacting protein 1 tyrosine 392 is required for phospholipase C-gamma activation and podosome formation in vascular smooth muscle cellsJing Wang
Aab Cardiovascular Research Institute and Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA
Arterioscler Thromb Vasc Biol 30:1976-82. 2010..In this study, we identified specific GIT1 tyrosines required for PLCγ activation and podosome formation in vascular smooth muscle cells (VSMC)... - ERK1/2 associates with the c-Met-binding domain of growth factor receptor-bound protein 2 (Grb2)-associated binder-1 (Gab1): role in ERK1/2 and early growth response factor-1 (Egr-1) nuclear accumulationMasaki Osawa
Center for Cardiovascular Research, University of Rochester, Rochester, New York 14642, USA
J Biol Chem 279:29691-9. 2004..These data suggest that Gab1-ERK1/2 binding and their nuclear translocation play a crucial role in Egr-1 nuclear accumulation... - The hinge-helix 1 region of peroxisome proliferator-activated receptor gamma1 (PPARgamma1) mediates interaction with extracellular signal-regulated kinase 5 and PPARgamma1 transcriptional activation: involvement in flow-induced PPARgamma activation in endMasashi Akaike
Center for Cardiovascular Research, 601 Elmwood Ave, Box 679, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA
Mol Cell Biol 24:8691-704. 2004..These data suggest that ERK5 mediates flow- and ligand-induced PPARgamma activation via the interaction of ERK5 with the hinge-helix 1 region of PPARgamma... - Cyclophilin A mediates vascular remodeling by promoting inflammation and vascular smooth muscle cell proliferationKimio Satoh
Aab Cardiovascular Research Institute, University of Rochester School of Medicine and Dentistry, 601 Elmwood Ave, Rochester, NY 14642, USA
Circulation 117:3088-98. 2008.... - Vinpocetine inhibits NF-kappaB-dependent inflammation via an IKK-dependent but PDE-independent mechanismKye Im Jeon
Aab Cardiovascular Research Institute and Department of Microbiology and Immunology, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA
Proc Natl Acad Sci U S A 107:9795-800. 2010..These studies thus identify vinpocetine as a unique antiinflammatory agent that may be repositioned for the treatment of many inflammatory diseases... - Cyclophilin A promotes cardiac hypertrophy in apolipoprotein E-deficient miceKimio Satoh
Aab Cardiovascular Research Institute, Department of Medicine, University of Rochester School of Medicine and Dentistry, Box CVRI, 601 Elmwood Ave, Rochester, NY 14642, USA
Arterioscler Thromb Vasc Biol 31:1116-23. 2011..In this study, we sought to evaluate the role of CyPA in Ang II-induced cardiac hypertrophy... - Inhibition of tumor necrosis factor-[alpha]-induced SHP-2 phosphatase activity by shear stress: a mechanism to reduce endothelial inflammationNicole Lerner-Marmarosh
Center for Cardiovascular Research, University of Rochester, NY 14642, USA
Arterioscler Thromb Vasc Biol 23:1775-81. 2003.... - p90RSK targets the ERK5-CHIP ubiquitin E3 ligase activity in diabetic hearts and promotes cardiac apoptosis and dysfunctionNhat Tu Le
University of Rochester School of Medicine and Dentistry, Aab Cardiovascular Research Institute, 601 Elmwood Avenue, Rochester, NY 14642, USA
Circ Res 110:536-50. 2012..The regulatory mechanism governing ERK5/CHIP interaction is unknown... - EVI1 acts as an inducible negative-feedback regulator of NF-κB by inhibiting p65 acetylationXiangbin Xu
Department of Microbiology and Immunology, University of Rochester Medical Center, Rochester, NY 14642, USA
J Immunol 188:6371-80. 2012..Thus, our study provides important insights into the novel role for EVI1 in negatively regulating NF-κB-dependent inflammation, and it may also shed light on the future development of novel anti-inflammatory strategies... - Tumor suppressor cylindromatosis acts as a negative regulator for Streptococcus pneumoniae-induced NFAT signalingTomoaki Koga
Department of Microbiology and Immunology and Cardiovascular Research Institute, University of Rochester Medical Center, Rochester, New York 14642, USA
J Biol Chem 283:12546-54. 2008..pneumoniae infections through the NFAT-dependent mechanism and further identify CYLD as a negative regulator for NFAT signaling, thereby opening up new therapeutic targets for these diseases... - Activation of big MAP kinase 1 (BMK1/ERK5) inhibits cardiac injury after myocardial ischemia and reperfusionScott J Cameron
Department of Pharmacology/Physiology, University of Rochester Medical Center, Rochester, NY 14642, USA
FEBS Lett 566:255-60. 2004..We propose a novel role for BMK1 in protecting the heart from ischemia/reperfusion-induced cardiac injury... - GIT1 mediates VEGF-induced podosome formation in endothelial cells: critical role for PLCgammaJing Wang
Aab Cardiovascular Research Institute, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA
Arterioscler Thromb Vasc Biol 29:202-8. 2009..Because GIT1 is a substrate of c-Src, and podosome formation is c-Src dependent, we hypothesized that GIT1 plays an important role in VEGF-induced EC podosome formation and cell migration... - Role of Ca2+/calmodulin-stimulated cyclic nucleotide phosphodiesterase 1 in mediating cardiomyocyte hypertrophyClint L Miller
Department of Pharmacology and Physiology, University of Rochester School of Medicine and Dentistry, NY 14642, USA
Circ Res 105:956-64. 2009..Ca(2+)/calmodulin (CaM)-activated cGMP-hydrolyzing PDE1 family may play a pivotal role in balancing intracellular Ca(2+)/CaM and cGMP signaling; however, its function in cardiomyocytes is unknown... - BMK1/ERK5 is a novel regulator of angiogenesis by destabilizing hypoxia inducible factor 1alphaXinchun Pi
Cardiovascular Research Institute, Department of Medicine, University of Rochester, NY, USA
Circ Res 96:1145-51. 2005..In summary, BMK1 is a novel negative regulator of HIF1alpha and angiogenesis by increasing HIF1alpha ubiquitination and inhibiting HIF1alpha activity in endothelial cells... - Cyclic nucleotide phosphodiesterase 1A: a key regulator of cardiac fibroblast activation and extracellular matrix remodeling in the heartClint L Miller
Department of Pharmacology and Physiology, Aab Cardiovascular Research Institute, University of Rochester School of Medicine and Dentistry, 601 Elmwood Ave, Box CVRI, Rochester, NY 14642, USA
Basic Res Cardiol 106:1023-39. 2011.... - Big mitogen-activated protein kinase (BMK1)/ERK5 protects endothelial cells from apoptosisXinchun Pi
Center for Cardiovascular Research and Department of Medicine, University of Rochester, Rochester, NY, USA
Circ Res 94:362-9. 2004..These results suggest that BMK1 activation by steady laminar flow is atheroprotective by inhibiting EC apoptosis via phosphorylation of Bad... - G-protein-coupled receptor kinase interacting protein-1 is required for pulmonary vascular developmentJinjiang Pang
Aab Cardiovascular Research Institute and the Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA
Circulation 119:1524-32. 2009..However, there have been no in vivo studies of GIT1 function to date... - Bcr kinase activation by angiotensin II inhibits peroxisome-proliferator-activated receptor gamma transcriptional activity in vascular smooth muscle cellsJeffrey D Alexis
Aab Cardiovascular Research Institute, Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA
Circ Res 104:69-78. 2009.... - GIT1 mediates HDAC5 activation by angiotensin II in vascular smooth muscle cellsJinjiang Pang
Aab Cardiovascular Research Institute and the Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, New York 14642, USA
Arterioscler Thromb Vasc Biol 28:892-8. 2008..Here we investigated the hypothesis that Ang II-mediated vascular smooth muscle cell (VSMC) gene transcription involves GIT1-CamK II-dependent phosphorylation of HDAC5... - A positive feedback loop of phosphodiesterase 3 (PDE3) and inducible cAMP early repressor (ICER) leads to cardiomyocyte apoptosisBo Ding
Cardiovascular Research Institute, Department of Pathology, University of Rochester, Rochester, NY 14642, USA
Proc Natl Acad Sci U S A 102:14771-6. 2005..Our findings may provide a therapeutic paradigm to prevent cardiomyocyte apoptosis and the progression of heart failure by inhibiting the PDE3A-ICER feedback loop... - Role of p90 ribosomal S6 kinase-mediated prorenin-converting enzyme in ischemic and diabetic myocardiumSeigo Itoh
Cardiovascular Research Institute, University of Rochester, Rochester, NY, USA
Circulation 113:1787-98. 2006.... - GPCR kinase 2 interacting protein 1 (GIT1) regulates osteoclast function and bone massPrashanthi Menon
Department of Medicine and Aab Cardiovascular Research Institute, University of Rochester School of Medicine and Dentistry, Rochester, New York 14642, USA
J Cell Physiol 225:777-85. 2010..These data show that GIT1 is a key regulator of bone mass in vivo by regulating osteoclast function and suggest GIT1 as a potential target for osteoporosis therapy... - Ca2+/calmodulin-stimulated PDE1 regulates the beta-catenin/TCF signaling through PP2A B56 gamma subunit in proliferating vascular smooth muscle cellsKye Im Jeon
Aab Cardiovascular Research Institute, University of Rochester Medical Center, Rochester, NY 14642, USA
FEBS J 277:5026-39. 2010..Taken together, these findings provide direct evidence for the first time that PP2A B56γ is a critical mediator for PDE1A in the regulation of β-catenin signaling in proliferating VSMCs... - Regulation of epidermal growth factor-induced connexin 43 gap junction communication by big mitogen-activated protein kinase1/ERK5 but not ERK1/2 kinase activationScott J Cameron
Department of Pharmacology Physiology, University of Rochester Medical Center, Rochester, New York 14642, USA
J Biol Chem 278:18682-8. 2003..These data indicate that BMK1 is more important than ERK1/2 in EGF-mediated Cx43 gap junction uncoupling by association and Cx43 Ser- 255 phosphorylation... - Reactive oxygen species-induced activation of p90 ribosomal S6 kinase prolongs cardiac repolarization through inhibiting outward K+ channel activityZhibo Lu
Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, NY 14642, USA
Circ Res 103:269-78. 2008..These findings indicate that p90RSK activation is critical for reactive oxygen species-mediated inhibition of voltage-gated K+ channel activity and leads to prolongation of cardiac repolarization... - Synergistic induction of nuclear factor-kappaB by transforming growth factor-beta and tumour necrosis factor-alpha is mediated by protein kinase A-dependent RelA acetylationHajime Ishinaga
Department of Microbiology and Immunology, University of Rochester Medical Center, Rochester, NY 14642, U S A
Biochem J 417:583-91. 2009..Thus the present study reveals a novel role for TGF-beta in inflammatory responses and provides new insight into the regulation of NF-kappaB by TGF-beta signalling... - Role of phosphodiesterase 3 in NO/cGMP-mediated antiinflammatory effects in vascular smooth muscle cellsToru Aizawa
University of Rochester, Center for Cardiovascular Research, 601 Elmwood Ave, Box 679, Rochester, NY 14642, USA
Circ Res 93:406-13. 2003..These results suggest that SNAP and CNP exert inhibitory effects on NF-kappaB-dependent transcription by activation of PKA via cGMP-dependent inhibition of PDE3 activity. Therefore, PDE3 is a novel mediator of inflammation in VSMCs... - Flow antagonizes TNF-alpha signaling in endothelial cells by inhibiting caspase-dependent PKC zeta processingGwenaele Garin
University of Rochester, Cardiovascular Research Institute, Box 679, 601 Elmwood Avenue, Rochester, NY 14642, USA
Circ Res 101:97-105. 2007..These results define a novel role for PKCzeta as a shared signaling mediator for flow and TNF-alpha, and important for flow-mediated inhibition of proinflammatory and apoptotic events in ECs... - 14-3-3beta binds to big mitogen-activated protein kinase 1 (BMK1/ERK5) and regulates BMK1 functionQinlei Zheng
Department of Medicine, University of Rochester School of Medicine and Dentistry, Aab Institute of Biomedical Sciences, Rochester, New York 14642, USA
J Biol Chem 279:8787-91. 2004..These data demonstrate an inhibitory function for 14-3-3beta binding to BMK1 and show that serine 486 phosphorylation represents a novel regulatory mechanism for BMK1... - Fluid shear stress inhibits TNF-mediated JNK activation via MEK5-BMK1 in endothelial cellsLingli Li
Aab Cardiovascular Research Institute and Department of Medicine, University of Rochester School of Medicine and Dentistry, Box 706, 601 Elmwood Avenue, Rochester, NY 14642, USA
Biochem Biophys Res Commun 370:159-63. 2008..These results support a key role for the MEK5-BMK1 signaling pathway in the atheroprotective effects of blood flow... - ERK5 activation inhibits inflammatory responses via peroxisome proliferator-activated receptor delta (PPARdelta) stimulationChang-Hoon Woo
Cardiovascular Research Institute, University of Rochester, 601 Elmwood Avenue, Rochester, NY 14642, USA
J Biol Chem 281:32164-74. 2006..Based on these data, we propose a new mechanism by which CO and HO-1 mediate anti-inflammatory effects via activating ERK5/PPARdelta, and ERK5 mediates CO and HO-1-induced PPARdelta activation via its interaction with PPARdelta... - Cyclic nucleotide phosphodiesterase 1 regulates lysosome-dependent type I collagen protein degradation in vascular smooth muscle cellsYujun Cai
Aab Cardiovascular Research Institute, University of Rochester, Rochester, NY 14642, USA
Arterioscler Thromb Vasc Biol 31:616-23. 2011..Herein, we investigate the role and underlying mechanism of cyclic nucleotide phosphodiesterase 1 (PDE1) in regulating collagen I in synthetic VSMCs... - Role of p90 ribosomal S6 kinase (p90RSK) in reactive oxygen species and protein kinase C beta (PKC-beta)-mediated cardiac troponin I phosphorylationSeigo Itoh
Cardiovascular Research Institute, University of Rochester, Rochester, New York 14642, USA
J Biol Chem 280:24135-42. 2005..LY333,531, a specific PKCbeta inhibitor, inhibited both p90RSK and cTnI (Ser(23/24)) phosphorylation by H2O2. Taken together, our data support a new redox-sensitive mechanism regulating cTnI phosphorylation in cardiomyocytes... - Glucocorticoids inhibit nontypeable Haemophilus influenzae-induced MUC5AC mucin expression via MAPK phosphatase-1-dependent inhibition of p38 MAPKKensei Komatsu
Department of Microbiology and Immunology, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, NY 14642, USA
Biochem Biophys Res Commun 377:763-8. 2008..These studies provide new insight into the molecular mechanism underlying glucocorticoid therapy and may lead to novel therapeutic intervention for inhibiting mucin overproduction in patients with NTHi infections... - Novel role of C terminus of Hsc70-interacting protein (CHIP) ubiquitin ligase on inhibiting cardiac apoptosis and dysfunction via regulating ERK5-mediated degradation of inducible cAMP early repressorChang Hoon Woo
Aab Cardiovascular Research Institute, University of Rochester, Rochester, New York 14642, USA
FASEB J 24:4917-28. 2010..We identified ICER as a novel CHIP substrate and that the ERK5-CHIP complex plays an obligatory role in inhibition of ICER expression, cardiomyocyte apoptosis, and cardiac dysfunction... - Fluid shear stress activates proline-rich tyrosine kinase via reactive oxygen species-dependent pathwayLung-Kuo Tai
Center for Cardiovascular Research, University of Rochester, Rochester, NY 14642, USA
Arterioscler Thromb Vasc Biol 22:1790-6. 2002..CONCLUSIONS: These results show a redox-sensitive pathway for flow-mediated activation of nonreceptor tyrosine kinase activity that requires ROS and intracellular calcium, but not Src kinase... - Role of nuclear Ca2+/calmodulin-stimulated phosphodiesterase 1A in vascular smooth muscle cell growth and survivalDavid J Nagel
Cardiovascular Research Institute, University of Rochester, New York, USA
Circ Res 98:777-84. 2006..These suggest that nuclear PDE1A is important in VSMC growth and survival and may contribute to the neointima formation in atherosclerosis and restenosis... - Thioredoxin interacting protein promotes endothelial cell inflammation in response to disturbed flow by increasing leukocyte adhesion and repressing Kruppel-like factor 2Xiao Qun Wang
Aab Cardiovascular Research Institute, 601 Elmwood Avenue, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA
Circ Res 110:560-8. 2012..We previously showed that thioredoxin interacting protein (TXNIP) was required for tumor necrosis factor-mediated expression of vascular cell adhesion molecule-1... - Functional role of phosphodiesterase 3 in cardiomyocyte apoptosis: implication in heart failureBo Ding
Center for Cardiovascular Research, University of Rochester School of Medicine and Dentistry, Aab Institute of Biomedical Science, Rochester, NY 14642, USA
Circulation 111:2469-76. 2005..Although chronic treatment with PDE3 inhibitors increases mortality in patients with heart failure, the contribution of PDE3 expression/activity in heart failure is not well known... - Insulin-like growth factor-1 enhances inflammatory responses in endothelial cells: role of Gab1 and MEKK3 in TNF-alpha-induced c-Jun and NF-kappaB activation and adhesion molecule expressionWenyi Che
Center for Cardiovascular Research, University of Rochester, Rochester, NY, USA
Circ Res 90:1222-30. 2002..Furthermore, the IGF-1-mediated downregulation of Gab1 expression represents a novel mechanism to promote vascular inflammation and atherosclerosis... - NADPH oxidase is involved in angiotensin II-induced apoptosis in H9C2 cardiac muscle cells: effects of apocyninFuzhong Qin
Cardiology Unit, Department of Medicine, University of Rochester Medical Center, Rochester, NY 14642, USA
Free Radic Biol Med 40:236-46. 2006..These results suggest that angiotensin II-induced apoptosis is mediated via NADPH oxidase activation probably through p38 MAPK activation, a decrease in Bcl-2 protein, and caspase activation... - Tumor suppressor CYLD regulates acute lung injury in lethal Streptococcus pneumoniae infectionsJae Hyang Lim
Department of Microbiology and Immunology, University of Rochester Medical Center, Rochester, NY 14642, USA
Immunity 27:349-60. 2007..Thus, CYLD is detrimental for host survival, thereby indicating a mechanism underlying the high early mortality of pneumococcal pneumonia... - p90 ribosomal S6 kinase regulates activity of the renin-angiotensin system: a pathogenic mechanism for ischemia-reperfusion injuryXi Shi
Department of Pharmacology and Physiology, University of Rochester School of Medicine and Dentistry, Rochester, NY 14620, USA
J Mol Cell Cardiol 51:272-5. 2011..Thus, renin inhibition may provide an alternative therapeutic strategy under conditions of increased RAS... - Impaired spine formation and learning in GPCR kinase 2 interacting protein-1 (GIT1) knockout micePrashanthi Menon
Aab Cardiovascular Research Institute and Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA
Brain Res 1317:218-26. 2010..Thus, our data suggest that GIT1 plays an important role in brain in vivo by regulating spine density involved in synaptic plasticity that is required for processes involved in learning... - Cyclophilin A enhances vascular oxidative stress and the development of angiotensin II-induced aortic aneurysmsKimio Satoh
Department of Medicine, Aab Cardiovascular Research Institute, University of Rochester School of Medicine and Dentistry, Rochester, New York, USA
Nat Med 15:649-56. 2009..These data define a previously undescribed role for CypA in AAA formation and suggest CypA as a new target for treating cardiovascular disease... - Impaired vasorelaxation in inbred mice is associated with alterations in both nitric oxide and super oxide pathwaysChun Chen
Cardiovascular Research Institute, Department of Medicine, University of Rochester, Rochester, NY 14642, USA
J Vasc Res 44:504-12. 2007..In summary, relatively small alterations in redox (SOD-2) and NO pathways (eNOS and PKG) may contribute to significantly impaired vasorelaxation in SJL mice... - Vitamins C and E attenuate apoptosis, beta-adrenergic receptor desensitization, and sarcoplasmic reticular Ca2+ ATPase downregulation after myocardial infarctionFuzhong Qin
Cardiology Unit, Department of Medicine, University of Rochester Medical Center, Rochester, NY 14642, USA
Free Radic Biol Med 40:1827-42. 2006..The results suggest that antioxidant therapy may be beneficial in HF... - Opposing roles of PAK2 and PAK4 in synergistic induction of MUC5AC mucin by bacterium NTHi and EGFYuxian Huang
Department of Microbiology and Immunology, Box 672, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, NY 14642, USA
Biochem Biophys Res Commun 359:691-6. 2007..Our studies bring novel insights into our understanding of synergistic regulation of MUC5AC mucin by both pathological and physiological inducers... - Gas6 inhibits apoptosis in vascular smooth muscle: role of Axl kinase and AktMatthew G Melaragno
Center for Cardiovascular Research, Department of Medicine, Aab Institute for Biomedical Sciences, University of Rochester, Box MED, Rochester, NY 14642, USA
J Mol Cell Cardiol 37:881-7. 2004..These findings establish the Gas6-Axl-PI3K-Akt pathway as an anti-apoptotic mechanism for VSMC that may be important in the response to vascular injury... - TGF-beta induces p65 acetylation to enhance bacteria-induced NF-kappaB activationHajime Ishinaga
Department of Microbiology and Immunology, University of Rochester Medical Center, Rochester, NY 14642, USA
EMBO J 26:1150-62. 2007..These studies provide new insights into the novel regulation of NF-kappaB by TGF-beta signaling... - Targeting cyclic nucleotide phosphodiesterase in the heart: therapeutic implicationsClint L Miller
Aab Cardiovascular Research Institute, University of Rochester School of Medicine and Dentistry, 601 Elmwood Ave, Box CVRI, Rochester, NY 14642, USA
J Cardiovasc Transl Res 3:507-15. 2010..In particular, we will emphasize how these properties influence current and future development of PDE inhibitors for the treatment of pathological cardiac remodeling and dysfunction... - PDE1 isozymes, key regulators of pathological vascular remodelingStefan Chan
Department of Pharmacology and Physiology, Aab Cardiovascular Research Institute, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, United States
Curr Opin Pharmacol 11:720-4. 2011..This review summarizes the work done to characterize the role and therapeutic potential of PDE1 isozymes in pathological vascular remodeling... - Diminished arteriolar responses in nitrate tolerance involve ROS and angiotensin IIMary D Frame
Department of Anesthesiology, University of Rochester School of Medicine and Dentistry, Rochester, New York 14642, USA
Am J Physiol Heart Circ Physiol 282:H2377-85. 2002..In summary, terminal arterioles are affected by nitrates to a greater extent than the arcade arterioles that feed them, in a process dependent on angiotensin II and ROS... - Thioredoxin-interacting protein mediates nuclear-to-plasma membrane communication: role in vascular endothelial growth factor 2 signalingOded N Spindel
Department of Medicine, University of Rochester School of Medicine and Dentistry, Aab Cardiovascular Research Institute, Rochester, NY 14642, USA
Arterioscler Thromb Vasc Biol 32:1264-70. 2012..Because TXNIP is an α-arrestin that regulates VEGFR2 signaling, we hypothesized that PARP1 regulates TXNIP localization and function that might affect HUVEC stress-induced apoptosis... - Angiotensin II signaling pathways mediated by tyrosine kinasesGuoyong Yin
Cardiovascular Research Center, University of Rochester, 601 Elmwood Avenue, P.O. Box 679, Rochester, NY 14642, USA
Int J Biochem Cell Biol 35:780-3. 2003..These tyrosine kinases play critical roles in AngII-stimulated cell signal events... - Functional interplay between angiotensin II and nitric oxide: cyclic GMP as a key mediatorChen Yan
Center for Cardiovascular Research, University of Rochester, Rochester, NY, USA
Arterioscler Thromb Vasc Biol 23:26-36. 2003..In this review, we focus on the diverse ways in which Ang II and NO interact and the importance of the balance between the signaling pathways activated by these mediators... - Differential expression of genes from nitrate-tolerant rat aortaXinchun Pi
Center for Cardiovascular Research, Medical Center, University of Rochester, NY 14642, USA
J Vasc Res 39:304-10. 2002..These identified genes may play important roles in the development of nitrate tolerance and represent promising candidates to understand the mechanisms of nitrate tolerance and endothelial dysfunction in the vasculature... - The novel role of the C-terminal region of SHP-2. Involvement of Gab1 and SHP-2 phosphatase activity in Elk-1 activationQunhua Huang
Center for Cardiovascular Research, University of Rochester, Rochester, New York 14642, USA
J Biol Chem 277:29330-41. 2002..Furthermore, we identified a novel sequence for SHP-2/Gab1 interactions in the C-terminal region of SHP-2... - NAD(P)H oxidase-derived reactive oxygen species regulate angiotensin-II induced adventitial fibroblast phenotypic differentiationWei-Li Shen
Joint laboratory of Vascular Biology of Health Science Center and Shanghai Institute of Hypertension, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, 225 Chong Qing South Road, Shanghai 200025, China
Biochem Biophys Res Commun 339:337-43. 2006..These findings demonstrate that angiotensin II induces adventitial fibroblast differentiation to myofibroblast via a pathway that involves NADPH oxidase generation of ROS and activation of p38MAPK and JNK pathways... - Differential regulation of endothelial cell permeability by cGMP via phosphodiesterases 2 and 3James Surapisitchat
University of Washington, Department of Pharmacology, 1959 NE Pacific St, Seattle, WA 98195 7280, USA
Circ Res 101:811-8. 2007..These findings suggest that the effect of increasing concentrations of cGMP on endothelial permeability is biphasic, which, in large part, is attributable to the relative amounts of PDE2A and PDE3A in endothelial cells... - Expression and function of vascular endothelial growth factor receptors (Flt-1 and Flk-1) in vascular adventitial fibroblastsXin Jin
Laboratory of Vascular Biology, Institute of Health Science Center, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China
J Mol Cell Cardiol 43:292-300. 2007..We concluded that functional expression of Flt-1 in adventitial fibroblasts might be an important mediator in the pathogenesis of vascular remodeling after arterial injury... - Cyclic GMP phosphodiesterases and regulation of smooth muscle functionSergei D Rybalkin
Department of Pharmacology, University of Washington, Seattle, Wash 98195, USA
Circ Res 93:280-91. 2003..In humans, this decrease is caused in large part by induction of another Ca2+/calmodulin-dependent PDE (PDE1C) that allows the brake to be released and proliferation to start... - Angiotensin II increases phosphodiesterase 5A expression in vascular smooth muscle cells: a mechanism by which angiotensin II antagonizes cGMP signalingDongsoo Kim
Departement of cardiology, Yong Dong Severance Hospital, Yonsei University, Seoul, South Korea
J Mol Cell Cardiol 38:175-84. 2005..These observations establish a new mechanism by which Ang II antagonizes cGMP signaling and stimulates VSMC growth...
Research Grants
- Regulation and Function of Phosphodiesterase in the HeartChen Yan; Fiscal Year: 2009..Significance: The findings will provide novel insights into the molecular mechanisms underlying the development of heart failure, and may lead to the identification of novel therapeutic targets for treating heart failure. ..
- Regulation and Function of Phosphodiesterase in the HeartChen Yan; Fiscal Year: 2010..Significance: The findings will provide novel insights into the molecular mechanisms underlying the development of heart failure, and may lead to the identification of novel therapeutic targets for treating heart failure. ..