Vascular endothelial cells, a monolayer lining the inner wall of blood vessels, play a crucial role in human health and disease. Pulmonary endothelium dysfunction and injury cause various devastating lung diseases. The focus of Dr. Lu's study is to understand the molecular mechanism(s) underlying pulmonary endothelium dysfunction and injury in response to biochemical stimulations. It is hope that her study will inform possible therapeutic strategies for lung diseases.

Biography

Qing Lu, PhD, is Assistant Professor of Medicine (Research) at Brown Medical School. Dr. Lu received PhD from Institute of Zoology at the Chinese Academy of Sciences in 1999. She completed 3 years of post-doctoral training in the area of Reproductive Biology and Molecular Biology at University of Michigan Medical School. Dr. Lu joined the Vascular Research Laboratory at Brown Medical School as a Research Associate in 2002 and was then appointed to the Brown faculty as Instructor of Medicine (Research) in 2003. She was subsequently appointed Assistant Professor of Medicine (Research) at Brown Medical School in 2004.

Institutions

VAMC

Research Description

Dr. Lu studies signaling in vascular endothelial cells. The focus of her research is to understand the molecular mechanism(s) underlying pulmonary endothelium dysfunction and injury in response to biochemical stimulations. Transforming growth factor (TGF)-beta1, a member of TGF-beta superfamily, is a multifunctional cytokine that regulates numerous cellular functions, such as proliferation, differentiation, extracellular matrix production, adhesion, migration, angiogenesis, apoptosis, and inflammatory responses. Abnormality of TGF-beta1 signaling has been implicated in several severe lung diseases, such as pulmonary edema, pulmonary emphysema, and pulmonary hypertension. The goal of her research is to elucidate the molecular mechanism(s) by which TGF-beta1 regulates endothelial monolayer permeability, endothelial cell proliferation, and endothelial cell apoptosis. The overall objective of her research is to understand the role of TGF-beta1 in the pathogenesis of these severe lung diseases and hopefully to obtain novel approaches for treatment and prevention these lung diseases.

Awards

BEST POSTER SUBMITTED BY A NEW INVESTIGATOR by the RI Science and Technology Advisory Council (STAC) and the statewide network of EPSCoR, INBRE, CTSA and COBRE investigators at the STAC meeting on June 3, 2008.
Research Award, ATS/Pulmonary Hypertension Association, 2008-2009
Fellow, Francis Family Foundation, 2004-2007
Research Award, American Lung Association, 2004-2006
Medical Research Award, Rhode Island Foundation, 2004
Weihua Science and Technology Award, The Chinese Academy of Sciences, 1999
Distinguished Graduate Student Achievement Award,The Chinese Academy of Sciences, 1998
Distinguished Graduate Student Achievement Award, Nanjing Agricultural University, China, 1995
Science and Technology Progress Award, Anhui Province, China, 1992
Science and Technology Progress Award, Hefei City, Anhui Province, China, 1992

Affiliations

4/2007, member, American Heart Association Northeast Consortium 1B peer review committee
4/2008, Member, American Heart Association REGION I Molecular Signaling 2 Study Group, peer review committee
Alternate Member, Research and Development Committee, Providence Veterans Affairs (VA) Medical Center, 2004
Member, Research and Development Committee, Providence VA Medical Center, 2005-2007
Member, Institutional Animal Care and Use Committee (IACUC), Providence VA Medical Center, 2005-present
Member, Zhi-Zhan Gu's Ph.D. Thesis Committee, 2005-2007

Funded Research

PI: Qing Lu
Agency: American Thoracic Society/Pulmonary Hypertension Association
"TGF-beta1 and Pulmonary Artery Hypertension"
Type: Research grant
Period: 1/1/08-12/31/09
Total direct costs: $100,000

PI: Qing Lu
Agency: Francis Family Foundation
"TGF-beta1 and endothelial monolayer permeability"
Type: Parker B. Francis Fellowship
Period: 7/1/04-6/30/07
Total direct costs: $126,000

PI: Qing Lu
Agency: American Lung Association
"The mechanism of TGF-beta1 regulation of endothelial monolayer permeability"
Type: Research Grant
Period: 7/1/04-6/30/06
Total direct costs: $70,000

PI: Qing Lu
Agency: Rhode Island Foundation
"TGF-beta1 and endothelial monolayer permeability"
Type: Medical Research Grant
Period: 1/1/04-12/31/04
Total direct costs: $10,000

PI: Sharon Rounds
Agency: National Heart, Lung, and Blood Institute (NHLBI)
"Small GTPases and Lung Endothelial Apoptosis"
Type: RO-1 HL 64936
Period: 4/1/06-3/31/11
Annual Direct Costs: $200,000
Role: co-investigator

View My Full Publication List in pdf format

Selected Publications

• Lu Q (corresponding author). Transforming growth factor-beta1 protects against pulmonary artery endothelial cell apoptosis via ALK5. American Journal of Physiology: Lung Cellular and Molecular Physiology. 295, L123-L133, 2008.(2008)
• Harrington EO, Lu Q, and Rounds S. Endothelial Cell Apoptosis. In: Endothelial Biomedicine. Edited by W. C. Aird, Cambridge University Press, New York, NY, pp1081-1097, 2007.(2007)
• Lu Q, Harrington EO, Newton J, Jankowich M, and Rounds S. Inhibition of ICMT induces endothelial cell apoptosis through GRP94. American Journal of Respiratory Cell and Molecular Biology, 37: 20-30, 2007.(2007)
• Lu Q (corresponding author), Harrington EO, Jackson H, Shannon CJ, Morin N and Rounds S. Transforming growth factor-beta1-induced endothelial barrier dysfunction involves SMAD2-dependent p38 activation and subsequent RhoA activation. Journal of Applied Physiology, 101, 375-384, 2006.(2006)
• Lu Q, Harrington EO and Rounds S. Apoptosis and lung injury. Keio Journal of Medicine. 54 (4): 184-189, 2005.(2005)
• Harrington EO, Shannon CJ, Morin N, Rowlett H, Murphy C. and Lu Q. PKCdelta regulates endothelial basal barrier function through modulation of RhoA GTPase activity. Experimental Cell Research, 308: 407-421, 2005.(2005)
• Rounds S, Harrington EO, and Lu Q. Carboxyl methylation of small GTPases and endothelial cell function. In: J. Bhattacharya (Ed.), Cell Signaling in Vascular Inflammation, Humana Press, Totowa, NJ, pp 52-60, 2005.(2005)
• Lu Q, Harrington EO, Hai C-M, Newton J, Garber M, Hirase T and Rounds S. Isoprenylcysteine carboxyl methyltransferase modulates endothelial monolayer permeability: involvement of RhoA carboxyl methylation. Circulation Research, 94: 306-315, 2004(2004)
• Kramer K, Harrington EO, Lu Q, Bellas R, Newton J, Sheahan KL and Rounds S. Isoprenylcysteine carboxyl methytransferase activity modulates endothelial cell apoptosis. Molecular Biology of the Cell, 14: 848-857, 2003(2003)
• Lu Q, Hutchins AE, Doyle CM, Lundblad JR and Kwok RPS. Acetylation of CREB by CBP enhances CREB-dependent transcription. The Journal of Biological Chemistry, 278: 15727-15734, 2003(2003)
• Lu Q, Smith GD, Chen DY, Han ZM and Sun QY. Activation of protein kinase C induces mitogen-activated protein kinase dephosphorylation and pronucleus formation in rat oocytes. Biology of Reproduction, 67: 64-69, 2002(2002)
• Lu Q, Dunn RL, Angeles R and Smith GD. Regulation of spindle formation by active mitogen-activated protein kinase and protein phosphatase 2A during mouse oocyte meiosis. Biology of Reproduction, 66: 29-37, 2002(2002)
• Lu Q, Smith GD, Chen DY, Yang Z, Han ZM, Schatten H and Sun QY. Phosphorylation of mitogen-activated protein kinase is regulated by protein kinase C, cyclic 3, 5-adenosine monophosphate, and protein phosphatase modulators during meiosis resumption in rat oocytes. Biology of Reproduction, 64: 1444-1450, 2001(2001)
• Sun QY*, Lu Q*, Breitbart H and Chen DY. cAMP inhibits mitogen-activated protein (MAP) kinase activation and resumption of meiosis, but exerts no effects after spontaneous germinal vesicle breakdown (GVBD) in mouse oocytes. Reproduction, Fertility and Development, 11: 81-86, 1999.(1999)
• Lu Q, Sun QY, Breitbart H and Chen DY. Expression and phosphorylation of mitogen-activated protein kinase during spermatogenesis and epididymal sperm maturation in mice. Archives of Andrology, 43: 55-66, 1999(1999)
• * indicates equal contribution.
• Jankowich M, Lu Q, Newton J, Harrington EO, and Rounds S. Differential response of cell stress elements to apoptotic stimuli in endothelial cells: the role of ICMT in molecular chaperone expression. (In preparation).
• Harrington EO*, Lu Q*, Newton J, Casserly B, Warburton R, and Rounds S. Receptor characterization of adenosine-mediated protection against pulmonary edema. (Under review)
• Lu Q (corresponding author), Harrington EO, and Rounds S. Transforming growth factor-beta1 caused pulmonary microvascular endothelial cell apoptosis via ALK5. American Journal of Physiology: Lung Cellular and Molecular Physiology, under revision.
• Round S. and Lu Q. Pulmonary Endothelial Apoptosis/Necrosis. In: The Pulmonary Endothelium. Edited by Voelkel N.F. and Rounds S. John Wiley and Sons, Ltd. Chichester, UK. (In preparation)