Ling Qi is an Assistant Professor of the Division of Nutritional Sciences at Cornell University since 2007. He graduated magna cum laude from Fudan University with a BS degree in Microbiology in 1997. He received a PhD degree in Immunology in Dr. Suzanne Ostrand-Rosenberg’s laboratory at UMBC in 2001 and performed his postdoctoral studies with Dr. Carol Greider at Johns Hopkins University (2001-2004) and with Dr. Marc Montminy at Salk Institute (2004-2007). He became a Leukemia and Lymphoma Society Postdoctoral Fellow in 2002 and Juvenile Diabetes Research Foundation Postdoctoral Fellow in 2005. In 2008, he was a recipient of the Junior Faculty Award from the American Diabetes Association and Young Investigator Award from the American Federation for Aging Research. In 2011, he received the Bio-Serv Award from the American Society for Nutrition. In 2012, he was awarded the Career Development Award by the American Diabetes Association. The Qi laboratory investigates the role of ER stress and inflammation in obesity, type-2 diabetes and inflammatory bowel diseases. Funding support for the laboratory are from American Diabetes Association (ADA), American Heart Association (AHA), American Federation for Aging Research (AFAR), Howard Hughes Medical Institute (HHMI), Juvenile Diabetes Research Foundation (JDRF), National Institute for Alcohol Abuse and Alcoholism (NIAAA) and National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). Work from his own laboratory has been published in Cell Metabolism, Developmental Cell, Diabetes, J Bio Chem, Biochem J and etc. Finally, Ling Qi teaches one 4-credit undergraduate course “Physiological and Biochemical Basis of Human Nutrition” - NS3310 with over 100 students every spring.
Teaching and Advising Statement:
I am indebted to the teachers who inspired me throughout my career. When I teach and train undergraduate students, my goal is to emulate my past teachers. Although undoubtedly teaching takes away my time from research, I have enjoyed teaching and interaction with undergraduate students as well as graduate students. At Cornell, I have taught up-level human nutrition class NS3310 entitled “Physiological and Biochemical Bases of Human Nutrition” and lectured in various graduate courses. I feel that not only my teaching has influenced and inspired a younger generation, but also my research have benefited from teaching, in part, because it drives me to be at the cutting-edge of many different but related topics in nutrition and metabolism.
Since taking over this required upper class level course in 2011, I have spent many many hours into planning, preparing, lecturing, evaluating, meeting with students in various outside-of-class settings and etc. I have been very excited to teach this course, to care for each student about their learning outcomes, and to inspire students to be interested in the subject of nutrition , nutrient metabolism and diseases. I conduct three surveys during the semester to gauge the learning outcome and progress. Students’ feedback has been very positive and are improving each year (see the table and charts on page 16). It was wonderful to read students’ feedbacks, just quoting a few here: “This course is awesome! I enjoyed a lot!”, “Dr. Qi should be recommended for every teaching award..., because this class has changed my life for the better.”, “This course is fantastic!” and “A perfect ending for my time at Cornell!”. They made everything worthwhile.
Current Professional Activities:
2007- Member, American Diabetes Association
2009- Member, American Society of Nutrition
2011- Member, American Society for Microbiology
2011- Member, American Society for Biochemistry and Molecular Biology
Current Research Activities:
Our laboratory explores the physiological role of (a) stress and (b) inflammatory responses in the context of metabolic disorders including obesity and diabetes. Our goal is to uncover new findings, to break new grounds, to delineate the etiology and pathogenesis of human diseases, and eventually to help develop therapeutic strategies. In the past 5 years, using genetic, biochemical, immunological and molecular biology approaches, we have published over 20 manuscripts, and made several important discoveries and produced new insights into the pathogenesis of these diseases. Below briefly details the research accomplishments from my own laboratory in two distinct areas of research:
ER stress: One of the fundamental questions in the ER stress-metabolism field is what is the function of UPR under physiological and pathological settings. In the first paper from the lab, we showed that XBP1s-mediated signaling pathways is critical for adipocyte differentiation. We recently developed a method to quantitate levels of ER stress in tissues under physiological and pathophysiological conditions. We now can quantitate the amount of ER stress based on the ratio of phosphorylated to total IRE1a protein levels. This study is significant as it has solved a huge challenge in the field. We are addressing many outstanding questions in vivo using this tools. Moreover, using proteomic screening, we recently identified a novel cytosolic regulator of UPR sensor activation, nonmuscle myosin IIB, suggesting for the first time that coordination between the ER and cytosol is required for ER stress response. Finally, we have collaborated with many other laboratories in their analysis of ER stress. Representative publications: Sha et al. Cell Metabolism 2009 and 2010; Chen et al. Biochem J. 2010; Yang et al. PLoS ONE 2010; Xue, et al. J Biol Chem. 2011; He et al. Dev. Cell. 2012.
Inflammation: One of the fundamental questions in the immunometabolism field is how inflammation is initiated. We reported the role of immature myeloid cells and extracellular ATP in this process. We recently identified unique immune cell populations in adipose tissue that link HFD feeding to inflammation. We established a novel paradigm “HFD → NKT → inflammation → metabolic regulation” (shown in the box). We showed that upon acute and long-term HFD, natural killer T (NKT) cells are activated and promote macrophage polarization in adipose tissue and improve glucose homeostasis via the IL-4/STAT6 signaling axis. Importantly, our data reveal unexpectedly pronounced immunological events in adipose tissue within days following acute HFD feeding. Representative publications: Xia et al. J Biol Chem 2011; Sun et al. Diabetes 2012; Ji et al. J Biol Chem 2012a and 2012b.
In summary, in the last several years, we have demonstrated our productivity and innovation with 21 publications. It is worth to mention that we started everything from scratch 5 year ago. What is especially exciting for me is the unique niche and tools that have been developed, the research directions we are now taking, and the dedication and motivation of the students/fellows.
B.S., Fudan University, Shanghai, China (1993-1997)
Ph.D., University of Maryland (1997-2001)
Postdoctoral training, Johns Hopkins University (2001-2004) and Salk Institute (2004-2007)
Taught NS3310 (100%): Physiological and Biochemical Bases of Human Nutrition (with 100 students)
Guest lecture in NS6320 Regulation of Macronutrient Metabolism (four lectures) - 12 students
Guest lecture in VETMI7050: Advanced Immunology (two lectures) - 10 students
Sha, H.B., He, Y., Chen H., Wang, C., Zenno, A., Shi, H., Yang, X., Zhang, X., and Qi, L.* 2009. The IRE1α-XBP1 pathway of the unfolded protein response is required for adipogenesis. Cell Metabolism. 9, 556-564. PMID:19490910 (* Corresponding author) Highlighted in Faculty 1000
Chen, H., and Qi, L.* 2010. SUMO modification regulates transcriptional activity of XBP1. Biochem. J. 429, 95-102. PMID: 20408817 (* Corresponding author)
Yang, L., Xue, Z., He, Y., Sun, S., Chen, H., and Qi, L.* 2010. A Phos-tag-based approach reveals the extent of physiological endoplasmic reticulum stress. PLoS ONE. 5: e11621. PMID: 20408817 (* Corresponding author)
Francisco, A.B., Singh, R., Li, S., Vani, A.K., Yang, L., Munroe, R.J., Diaferia, G., Cardano, M., Biunno, I., Qi, L., Schimenti, J.C., and Long, Q. 2010. Deficiency of SEL1L in mice leads to systemic ER stress and embryonic lethality. J. Biol. Chem. 285: 13694-13703. PMID: 20197277
Zeng, L., Liu, Y. P., Sha, H., Chen, H., Qi, L., and Smith, J.A. 2010. XBP1 couples ER stress to augmented IFN-β induction via a cis-acting enhancer in macrophages. J. Immunol. 185: 2324-30. PMID: 20660350
Zmuda, E. J., Qi, L., Zhu, M., Mirmira, R., Montminy, M. and Hai, T. 2010. The role of ATF3, an adaptive-responsive gene, in high fat diet induced diabetes and pancreatic beta cell dysfunction. Mol. Endo. 24: 1423-33. PMID: 20519332
Liew, C.W., Bochenski, J., Kawamori, D., Hu, J., Leech, C.A., Wanic, K., Malecki, M., Warram, J., Qi, L., Krolewski, A.S., and Kulkarni, R.N. 2010. The tribbles protein interacts with ATF4 to regulate insulin exocytosis in human and mouse beta-cells. J. Clin. Invest. 120: 2876-88. PMID: 20592469
Lichtenstein, L., Mattijssen, F., de Wit, N. J., Georgiadi, A., Hooiveld, G. J., van der Meer, R., He, Y., Qi, L. Koster, A., Tamsma, J.T., Tan, N. S., Muller, M., and Kersten, S. 2010. Angptl4 protects against severe pro-inflammatory effects of dietary saturated fat by inhibiting lipoprotein lipase-dependent uptake of fatty acids in mesenteric lymph node macrophages. Cell Metabolism. 12: 580-92. PMID: 21109191
He, Y., Sun, S., Sha, H., Liu, Z., Yang, L., Xue, Z., Chen, H. and Qi, L.* (2010) Emerging Roles of XBP1, a sUPeR transcription factor. Gene Expression. 15: 13-25. PMID: 21061914 (* Corresponding author)
Qi, L.*, Yang, L. and Chen, H. 2011. Detecting and quantitating physiological ER stress in mammals. Methods in Enzymology. 490: 137- 46. PMID: 21266248 (* Corresponding author)
Sha, H., He, Y., Yang, L. and Qi, L.* 2011. Stressed Out About Obesity: IRE1α-XBP1 Pathway in Metabolism. Trends Endocrinol Metab. 22: 374-381. PMID: 21703863 (* Corresponding author)
Francisco, A.B., Singh, R., Sha, H., Yan, X., Qi, L., Lei, X. and Qiaoming Long. 2011. Haploid insufficiency of suppressor enhancer Lin12 1 like (SEL1L) predisposes mice to high fat diet-induced hyperglycemia. J. Biol. Chem. 286: 22275-82. PMID: 21536682
Xia, S., Sha, H.B., Yang, L., Ji, Y., Ostrand-Rosenberg, S. and Qi, L.* 2011. Gr-1+ CD11b+ myeloid-derived suppressor cells suppress inflammation and promote insulin sensitivity in obesity. J. Biol. Chem. 286: 23591-9. PMID: 21592961 (* Corresponding author)
Xue, Z., He, Y, Ye, K., Gu, Z., Mao, Y. and Qi, L.* 2011. A Conserved Structural Determinant Located at the Interdomain Region of Mammalian IRE1α. J. Biol. Chem. 286:30859-66. PMID: 21757700 (* Corresponding author)
Mao, T., Shao, M., Qiu, Y., Huang, J., Zhang, Y., Song, B., Wang, Q., Jiang, L., Liu, Y., Han, J., Cao, P., Li, J., Gao, X., Rui, L., Qi, L., Li, W. and Liu, Y. 2011. PKA Phosphorylation Couples Hepatic IRE1α to Glucagon Signaling in Glucose Metabolism. Proc. Natl. Acad. Sci. USA. 108: 15852-7. PMID: 21911379
Ji, Y., Sun, S., Xu, A., Bhargava, P., Lam, K., Gao B., Lee, C., Kersten, S., and Qi, L.* 2012. Activation of Natural Killer T Cells Promotes M2 Macrophage Polarization in Adipose Tissue and Improves Systemic Glucose Tolerance via the Interleukine-4 (IL-4)/STAT6 Protein Signaling Axis in Obesity. J. Biol. Chem. 287: 13561-13571 PMID: 22396530 (* Corresponding author)
Sun, S., Ji, Y., Kerstern, S. and Qi, L.* 2012. Mechanisms of Inflammatory Responses in Obese Adipose Tissue. Annu. Rev. Nutr. 32, Mar 9. [Epub ahead of print] PMID: 22404118 (* Corresponding author)
Sun, S., Ji, Y., Xia, S. and Qi, L.* 2012. The ATP-P2X7 Signaling Axis is Dispensable for Obesity-Associated Inflammasome Activation in Adipose Tissue. Diabetes. 61: 1471-8 PMID: 22415881 (* Corresponding author)
Ji, Y., Sun, S., Xia, S., Yang, L., Li, X., and Qi, L.* 2012. Short-Term High-fat-Diet Challenge Promotes Alternative Macrophage Polarization in Adipose Tissue via Natural Killer T Cells and Interleukine-4. J. Biol. Chem. 287: 24378-86. PMID: 22645141 (* Corresponding author)
He, Y., Beatty, A., Han, X., Ma, X., Adelstein, R., Yates, J. R., Kemphues, K., and Qi, L.* 2012. Novel Role of Non-Muscle Myosin IIB in IRE1α Signaling Upon ER Stress. Dev. Cell. 23: 1141-1152 PMID: 23237951 (* Corresponding author)
Stanya, K.J., Jacobi, D., Liu, S., Bhargava, P., Gangl, M.R., Mizgerd, J.P., Qi, L., Shi, H., McKenzie, A.N.J., Lee, C.H. 2012. Direct control of hepatic glucose production by Interleukin-13 in mice. J Clin Invest. Dec 21. doi:pii: 64941. 10.1172/JCI64941. PMID: 23257358 [Epub ahead of print]