Qing Lu

Summary

Affiliation: Brown University
Country: USA

Publications

  1. pmc Inhibition of ICMT induces endothelial cell apoptosis through GRP94
    Qing Lu
    Providence VA Medical Center, Pulmonary Critical Care Medicine Section, 830 Chalkstone Avenue, Providence, RI 02908, USA
    Am J Respir Cell Mol Biol 37:20-30. 2007
  2. pmc Pulmonary endothelial cell signaling and function
    Sharon Rounds
    Vascular Research Laboratory, Department of Medicine, Warren Alpert Medical School of Brown University, Providence VA Medical Center, Providence, Rhode Island 02903, USA
    Trans Am Clin Climatol Assoc 119:155-67; discussion 167-9. 2008
  3. doi request reprint Pyrimidine-based inhibitors of CaMKIIdelta
    Babu Mavunkel
    Scios, Inc, 6500 Paseo Padre Parkway, Fremont, CA 94555, USA
    Bioorg Med Chem Lett 18:2404-8. 2008
  4. pmc Sustained adenosine exposure causes lung endothelial apoptosis: a possible contributor to cigarette smoke-induced endothelial apoptosis and lung injury
    Qing Lu
    Vascular Research Laboratory, Providence Veterans Affairs Medical Center, Department of Medicine, Alpert Medical School of Brown University, Providence, RI 02908, USA
    Am J Physiol Lung Cell Mol Physiol 304:L361-70. 2013
  5. pmc Sustained adenosine exposure causes lung endothelial barrier dysfunction via nucleoside transporter-mediated signaling
    Qing Lu
    Alpert Medical School of Brown University, Providence VA Medical Center, Research Services, 830 Chalkstone Avenue, Providence, RI 02908, USA
    Am J Respir Cell Mol Biol 47:604-13. 2012
  6. pmc Transforming growth factor-beta1 protects against pulmonary artery endothelial cell apoptosis via ALK5
    Qing Lu
    Vascular Research Laboratory, Providence Veterans Affairs Medical Center, Providence, Rhode Island 02908, USA
    Am J Physiol Lung Cell Mol Physiol 295:L123-33. 2008
  7. pmc Cigarette smoke causes lung vascular barrier dysfunction via oxidative stress-mediated inhibition of RhoA and focal adhesion kinase
    Qing Lu
    Vascular Research Laboratory, Providence Veterans Affairs Medical Center, Department of Medicine, Alpert Medical School of Brown University, RI, USA
    Am J Physiol Lung Cell Mol Physiol 301:L847-57. 2011
  8. ncbi request reprint Transforming growth factor-beta1-induced endothelial barrier dysfunction involves Smad2-dependent p38 activation and subsequent RhoA activation
    Qing Lu
    Vascular Research Laboratory, Providence VA Medical Center, Research Services, 151, 830 Chalkstone Ave, Providence, RI 02908, USA
    J Appl Physiol (1985) 101:375-84. 2006
  9. pmc Transforming growth factor-beta1 causes pulmonary microvascular endothelial cell apoptosis via ALK5
    Qing Lu
    Providence VA Medical Center, Research Services, Providence, RI 02908, USA
    Am J Physiol Lung Cell Mol Physiol 296:L825-38. 2009
  10. pmc Adenosine protected against pulmonary edema through transporter- and receptor A2-mediated endothelial barrier enhancement
    Qing Lu
    Vascular Research Laboratory, Providence Veterans Affairs Medical Center, Department of Medicine, Alpert Medical School of Brown University, Providence, Rhode Island 02908, USA
    Am J Physiol Lung Cell Mol Physiol 298:L755-67. 2010

Collaborators

Detail Information

Publications37

  1. pmc Inhibition of ICMT induces endothelial cell apoptosis through GRP94
    Qing Lu
    Providence VA Medical Center, Pulmonary Critical Care Medicine Section, 830 Chalkstone Avenue, Providence, RI 02908, USA
    Am J Respir Cell Mol Biol 37:20-30. 2007
    ..We speculate that changes in the pI, subcellular localization, and protein level of GRP94 cause endothelial cell apoptosis, possibly through UPR dysfunction. These studies suggest a novel link between RhoA GTPases and the UPR...
  2. pmc Pulmonary endothelial cell signaling and function
    Sharon Rounds
    Vascular Research Laboratory, Department of Medicine, Warren Alpert Medical School of Brown University, Providence VA Medical Center, Providence, Rhode Island 02903, USA
    Trans Am Clin Climatol Assoc 119:155-67; discussion 167-9. 2008
    ..Our data suggest that increasing intracellular adenosine is a useful therapeutic strategy against diseases characterized by increased vascular permeability...
  3. doi request reprint Pyrimidine-based inhibitors of CaMKIIdelta
    Babu Mavunkel
    Scios, Inc, 6500 Paseo Padre Parkway, Fremont, CA 94555, USA
    Bioorg Med Chem Lett 18:2404-8. 2008
    ..The results of the computational studies led to the design of ATP competitive inhibitors with optimized hinge interactions. Inhibitors of this class possessed improved enzyme and cellular activity compared to early leads...
  4. pmc Sustained adenosine exposure causes lung endothelial apoptosis: a possible contributor to cigarette smoke-induced endothelial apoptosis and lung injury
    Qing Lu
    Vascular Research Laboratory, Providence Veterans Affairs Medical Center, Department of Medicine, Alpert Medical School of Brown University, Providence, RI 02908, USA
    Am J Physiol Lung Cell Mol Physiol 304:L361-70. 2013
    ..Inhibition of adenosine uptake may become a new therapeutic target in treatment of CS-induced lung diseases...
  5. pmc Sustained adenosine exposure causes lung endothelial barrier dysfunction via nucleoside transporter-mediated signaling
    Qing Lu
    Alpert Medical School of Brown University, Providence VA Medical Center, Research Services, 830 Chalkstone Avenue, Providence, RI 02908, USA
    Am J Respir Cell Mol Biol 47:604-13. 2012
    ..Our data further suggest that sustained adenosine exposure may cause mitochondrial oxidative stress, leading to activation of p38, JNK, and RhoA in mitochondria and resulting in EC barrier dysfunction...
  6. pmc Transforming growth factor-beta1 protects against pulmonary artery endothelial cell apoptosis via ALK5
    Qing Lu
    Vascular Research Laboratory, Providence Veterans Affairs Medical Center, Providence, Rhode Island 02908, USA
    Am J Physiol Lung Cell Mol Physiol 295:L123-33. 2008
    ..Understanding the mechanism by which TGF-beta1 promotes endothelial cell survival may provide a better treatment for apoptosis-dependent vascular diseases, such as emphysema...
  7. pmc Cigarette smoke causes lung vascular barrier dysfunction via oxidative stress-mediated inhibition of RhoA and focal adhesion kinase
    Qing Lu
    Vascular Research Laboratory, Providence Veterans Affairs Medical Center, Department of Medicine, Alpert Medical School of Brown University, RI, USA
    Am J Physiol Lung Cell Mol Physiol 301:L847-57. 2011
    ..Our data indicate that CS causes endothelial barrier dysfunction via oxidative stress-mediated inhibition of RhoA and FAK...
  8. ncbi request reprint Transforming growth factor-beta1-induced endothelial barrier dysfunction involves Smad2-dependent p38 activation and subsequent RhoA activation
    Qing Lu
    Vascular Research Laboratory, Providence VA Medical Center, Research Services, 151, 830 Chalkstone Ave, Providence, RI 02908, USA
    J Appl Physiol (1985) 101:375-84. 2006
    ..Our data indicate that TGF-beta1 induces endothelial barrier dysfunction involving Smad2-dependent p38 activation, resulting in RhoA activation by possible transcriptional regulation...
  9. pmc Transforming growth factor-beta1 causes pulmonary microvascular endothelial cell apoptosis via ALK5
    Qing Lu
    Providence VA Medical Center, Research Services, Providence, RI 02908, USA
    Am J Physiol Lung Cell Mol Physiol 296:L825-38. 2009
    ..We speculate that imbalance of ALK1 and ALK5 may contribute to the development of pulmonary artery hypertension...
  10. pmc Adenosine protected against pulmonary edema through transporter- and receptor A2-mediated endothelial barrier enhancement
    Qing Lu
    Vascular Research Laboratory, Providence Veterans Affairs Medical Center, Department of Medicine, Alpert Medical School of Brown University, Providence, Rhode Island 02908, USA
    Am J Physiol Lung Cell Mol Physiol 298:L755-67. 2010
    ..The data suggest that adenosine deaminase inhibition may be useful in treatment of pulmonary edema in settings of ALI...
  11. ncbi request reprint Isoprenylcysteine carboxyl methyltransferase modulates endothelial monolayer permeability: involvement of RhoA carboxyl methylation
    Qing Lu
    Pulmonary Vascular Biology Laboratory, Providence VA Medical Center, Providence, R 02908, USA
    Circ Res 94:306-15. 2004
    ..Therefore, carboxyl methylation of RhoA may modulate endothelial barrier function...
  12. pmc Alterations in molecular chaperones and eIF2alpha during lung endothelial cell apoptosis
    Qing Lu
    Department of Medicine, Vascular Research Laboratory, Providence Veterans Affairs Medical Center, Alpert Medical School of Brown University, Providence, Rhode Island 02908, USA
    Am J Physiol Lung Cell Mol Physiol 298:L501-8. 2010
    ..We also speculate that increased eIF2alpha phosphorylation is a defensive response against endothelial cell apoptosis...
  13. ncbi request reprint PKCdelta regulates endothelial basal barrier function through modulation of RhoA GTPase activity
    Elizabeth O Harrington
    Pulmonary Vascular Research Laboratory, Providence VA Medical Center, Department of Medicine, Brown Medical School, 151 Research Services, 830 Chalkstone Avenue, Providence, RI 02908, USA
    Exp Cell Res 308:407-21. 2005
    ..Thus, PKCdelta may regulate basal endothelial barrier function by stabilizing microfilaments and focal contacts by regulating RhoA GTPase activity through upstream modulators, p190RhoGAP and p120RasGAP...
  14. pmc Isoprenylcysteine carboxyl methyltransferase activity modulates endothelial cell apoptosis
    Kristina Kramer
    Pulmonary Vascular Biology Laboratory, Providence Veterans Affairs Medical Center, Brown Medical School, Rhode Island 02908, USA
    Mol Biol Cell 14:848-57. 2003
    ..These findings suggest that inhibition of ICMT causes endothelial cell apoptosis by attenuation of Ras GTPase methylation and activation and its downstream antiapoptotic signaling pathway...
  15. pmc Focal adhesion kinase and endothelial cell apoptosis
    Qing Lu
    Vascular Research Laboratory, Providence Veterans Affairs Medical Center, Department of Medicine, Alpert Medical School of Brown University, Providence, RI 02908, USA
    Microvasc Res 83:56-63. 2012
    ..This review summarizes the signaling pathways of FAK in prevention of apoptosis and the role of FAK in mediating adenosine and homocysteine-induced endothelial cell apoptosis and in cardiovascular diseases...
  16. pmc Steroid receptor coactivator 3 is a coactivator for myocardin, the regulator of smooth muscle transcription and differentiation
    Hui Joyce Li
    Molecular Cardiology Research Institute, Department of Medicine, and Division of Cardiology, New England Medical Center Hospitals, Tufts University School of Medicine, Boston, MA 02111, USA
    Proc Natl Acad Sci U S A 104:4065-70. 2007
    ..The SRC3-myocardin interaction identifies a site of convergence for nuclear hormone receptor-mediated and VSMC-specific gene regulation and suggests a possible mechanism for the vascular protective effects of estrogen on vascular injury...
  17. ncbi request reprint Cigarette smoke-induced lung endothelial apoptosis and emphysema are associated with impairment of FAK and eIF2α
    Pavlo Sakhatskyy
    Vascular Research Laboratory, Providence Veterans Affairs Medical Center, Department of Medicine, Alpert Medical School of Brown University, Providence, RI 02908, USA
    Microvasc Res 94:80-9. 2014
    ..Taken together, our data suggest that inhibition of eIF2α and FAK signaling may play an important role in CS-induced lung EC apoptosis and emphysema. ..
  18. ncbi request reprint Apoptosis and lung injury
    Qing Lu
    Pulmonary Vascular Research Laboratory, Providence Veterans Affairs Medical Center, Department of Medicine Brown Medical School, Providence, RI 02908, USA
    Keio J Med 54:184-9. 2005
    ..We also review the current understanding of the role of lung cell apoptosis in acute lung injury, pulmonary fibrosis and emphysema...
  19. pmc Striatin assembles a membrane signaling complex necessary for rapid, nongenomic activation of endothelial NO synthase by estrogen receptor alpha
    Qing Lu
    Molecular Cardiology Research Institute, Department of Medicine, Tufts New England Medical Center, Boston, MA 02111, USA
    Proc Natl Acad Sci U S A 101:17126-31. 2004
    ..Furthermore, by demonstrating independent regulation of nongenomic vs. genomic ER-dependent signaling, these findings provide conceptual support for the potential development of "pathway-specific" selective ER modulators...
  20. ncbi request reprint Acetylation of cAMP-responsive element-binding protein (CREB) by CREB-binding protein enhances CREB-dependent transcription
    Qing Lu
    Department of Obstetrics and Gynecology, University of Michigan, 6428 Medical Science Building 1, 1301 S Catherine Street, Ann Arbor, MI 48109, USA
    J Biol Chem 278:15727-34. 2003
    ..We propose that in addition to its functions as a bridging molecule and histone acetyltransferase, the ability of CBP to acetylate CREB may play a key role in modulating CREB-mediated gene expression...
  21. doi request reprint Aryl-indolyl maleimides as inhibitors of CaMKIIdelta. Part 3: Importance of the indole orientation
    Qing Lu
    Scios, Inc, 6500 Paseo Padre Parkway, Fremont, CA 94555, USA
    Bioorg Med Chem Lett 18:2399-403. 2008
    ..Key interactions with the kinase ATP site and hinge region, predicted by homology modeling, were confirmed...
  22. doi request reprint Aryl-indolyl maleimides as inhibitors of CaMKIIdelta. Part 2: SAR of the amine tether
    Daniel E Levy
    Scios, Inc, 6500 Paseo Padre Parkway, Fremont, CA 94555, USA
    Bioorg Med Chem Lett 18:2395-8. 2008
    ..Key interactions with the kinase ATP site and hinge region, predicted by homology modeling, were confirmed...
  23. doi request reprint Aryl-indolyl maleimides as inhibitors of CaMKIIdelta. Part 1: SAR of the aryl region
    Daniel E Levy
    Scios, Inc, 6500 Paseo Padre Parkway, Fremont, CA 94555, USA
    Bioorg Med Chem Lett 18:2390-4. 2008
    ..Key interactions with the kinase ATP site and hinge region were found to be consistent with homology modeling predictions...
  24. ncbi request reprint [Cloning of tight junction protein claudin-1 and construction of the mammalian expression vector]
    Lin Chen
    Institute for Digestive Diseases, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China
    Nan Fang Yi Ke Da Xue Xue Bao 27:349-51. 2007
    ..To construct a recombinant plasmid containing the coding region of tight junction protein claudin-1 gene to understand the functional role of claudin-1 in human colorectal carcinoma...
  25. ncbi request reprint Activation of protein kinase C induces mitogen-activated protein kinase dephosphorylation and pronucleus formation in rat oocytes
    Qing Lu
    State Key Laboratory of Reproductive Biology, Institute of Zoology, The Chinese Academy of Sciences, Beijing 100080, People s Republic of China
    Biol Reprod 67:64-9. 2002
    ..We also provide evidence supporting the involvement of such a process in fertilization...
  26. ncbi request reprint Regulation of estrogen receptor alpha-mediated transcription by a direct interaction with protein phosphatase 2A
    Qing Lu
    Department of Medicine and Molecular Cardiology Research Institute, New England Medical Center Hospitals, Inc, Tufts University School of Medicine, Boston, Massachusetts 02111, USA
    J Biol Chem 278:4639-45. 2003
    ....
  27. ncbi request reprint [p73 gene expression in apoptotic process of acute myeloid leukemia cell line U937 induced by methotrexate]
    Guang Fen Xiao
    Department of Hematology, The Second Affiliated Hospital of Nanhua University, Hengyang 421001, China
    Zhongguo Shi Yan Xue Ye Xue Za Zhi 10:104-7. 2002
    ..Sub-G(1) peak and S + G(2)/M arrest were also determined by FCM, but the quantity of p73 expression was generally constant. In conclusion, U937 cell apoptosis induced by MTX did not change p73 mRNA level...
  28. ncbi request reprint High-density lipoprotein increases the abundance of eNOS protein in human vascular endothelial cells by increasing its half-life
    Maria E Rämet
    Molecular Cardiology Research Institute and Department of Medicine, New England Medical Center Hospitals, Inc, Tufts University School of Medicine, Boston, Massachusetts 02111, USA
    J Am Coll Cardiol 41:2288-97. 2003
    ....
  29. ncbi request reprint [Cytokine and inflammatory mediators in acute respiratory distress syndrome]
    Zhong ji Sun
    Emergency Department, Affiliated Hospital of Chinese People s Armed Police Forces College, Tianjin 300162, China
    Zhongguo Wei Zhong Bing Ji Jiu Yi Xue 15:186-9. 2003
  30. ncbi request reprint Micro- and macrocirculatory effects of apheresis in patients with familial hyperlipidemia
    Qing Lu
    Department of Medicine, Huddinge University Hospital, Karolinska Institutet, Stockholm, Sweden
    Ther Apher Dial 7:115-8. 2003
    ..We have found no previous report with parallel assessments at the microcirculatory and macrocirculatory levels...
  31. ncbi request reprint The relationship between aromatase in primary breast tumors and response to treatment with aromatase inhibitors in advanced disease
    Paul Chr de Jong
    St Antonius Hospital, P O Box 2500, 3430 EM Nieuwegein, The Netherlands
    J Steroid Biochem Mol Biol 87:149-55. 2003
    ....
  32. ncbi request reprint [Effect of percutaneous intervention on adrenomedullin and tumor necrosis factor in the coronary circulation]
    Hai chao Liu
    Department of Cardiology, Zhujiang Hospital, First Military Medical University, Guangzhou 510282, China
    Di Yi Jun Yi Da Xue Xue Bao 24:636-8, 645. 2004
    ..To evaluate the effect of percutaneous intervention (PCI) on coronary circulation levels of adrenomedullin (ADM) and tumor necrosis factor alpha (TNF-alpha) in patients with coronary heart disease (CHD)...
  33. ncbi request reprint Modulator recognition factor 1, an AT-rich interaction domain family member, is a novel corepressor for estrogen receptor alpha
    Serban P Georgescu
    Molecular Cardiology Research Institute, New England Medical Center and Department of Medicine, Tufts University School of Medicine, Boston, Massachusetts 02111, USA
    Mol Endocrinol 19:2491-501. 2005
    ..These data identify MRF1 as a repressor of ERalpha-mediated transcriptional activation and support a role for MRF1 in regulating ER-dependent gene expression in cardiovascular and other cells...
  34. ncbi request reprint 4-Aryl-1,2,3-triazole: a novel template for a reversible methionine aminopeptidase 2 inhibitor, optimized to inhibit angiogenesis in vivo
    Lara S Kallander
    GlaxoSmithKline Pharmaceuticals, King of Prussia, Pennsylvania 19406, USA
    J Med Chem 48:5644-7. 2005
    ..Compound 24, a potent inhibitor of cobalt-activated hMetAP2, also inhibits human and mouse endothelial cell growth. Using a mouse matrigel model, this reversible hMetAP2 inhibitor was also shown to inhibit angiogenesis in vivo...
  35. ncbi request reprint [Effects of D-limonene on leukemia cells HL-60 and K562 in vitro]
    Xiao ming Guo
    Department of Pediatrics, The Second Affiliated Hospital of Dalian Medical University, Dalian 116027, China
    Zhongguo Shi Yan Xue Ye Xue Za Zhi 14:692-5. 2006
    ..It is concluded that D-L can inhibit proliferation and induce apoptosis of HL-60 and K562 cells. The bcl-2, mutant type of p53 and bax may be involved in the gene regulation of D-L-induced apoptosis...
  36. ncbi request reprint Echocardiographic diagnosis of anomalous origin of the left coronary artery from the pulmonary artery
    Ya li Yang
    Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People s Republic of China
    Echocardiography 24:405-11. 2007
    ..Based on the apprehension of ultrasonic features and the enhancement of diagnostic alertness, the echocardiography can evaluate ALCAPA accurately and give more information than angiography. It may be the first diagnostic choice...
  37. ncbi request reprint MAP kinase mediates growth factor-induced nuclear translocation of estrogen receptor alpha
    Qing Lu
    Molecular Cardiology Research Institute, Department of Medicine, and Division of Cardiology, New England Medical Center Hospitals, Tufts University School of Medicine, 750 Washington Street, P O Box 80, 02111, Boston, MA, USA
    FEBS Lett 516:1-8. 2002
    ....