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High-probability grants
According to our matching algorithm, Liya Pi is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2016 — 2020 |
Pi, Liya |
K01Activity Code Description: For support of a scientist, committed to research, in need of both advanced research training and additional experience. |
Connective Tissue Growth Factor: An Intriguing Therapeutic Target in Alcoholic Liver Disease
? DESCRIPTION (provided by applicant): The goal of this Mentored Scientist Award (K01) application is to promote the development of the applicant into a multi-disciplinarily trained independent principal investigator. The strengths of the application are brought together by three major areas of emphasis as follows. 1) Credentials of the applicant. Dr. Pi's application builds upon her previous track-record of productivity with a concentrated determination to establish scientific independence through a change in research direction. The applicant's short-term goals encompass the acquisition of technical skills, initiation and establishment of an independent line of research, and to enhance professional skills (i.e. scientific writing, mentorin of trainees, grant writing, oral communication). Long-term goals are centered on becoming a leader in regenerative medicine, achieving a tenure-track position, training future scientists, and involvement in society and faculty leadership. 2) Training environment. Dr. Pi has received full commitment and the support of Drs. Bryon Petersen (mentor) and Gregory Schultz (co-mentor) to implement and complete the training necessary to advance outstanding junior faculty. Dr. Petersen is recognized as a world leader in the fields of stem cell biology and liver regeneration. Dr. Schultz complements the candidate's new direction of research by bringing renowned experience of understanding mechanism of fibrotic disorders. Dr. Pi has selected Drs. Lewin, Srivastava, and Gao as additional members due to their remarkable commitment and experience in developing the next generation of successful academic scientists. Dr. Pi will use the results obtained during the award period to justify and extend the scope of the project by formulating an independent New Investigator R01 application to advance into a tenure track position in academia. 3). Innovative models and research. The central hypothesis to be tested is that: Connective tissue growth factor (CTGF) is an important therapeutic target for alcoholic liver disease (ALD). The spectrum of ALD encompasses steatohepatitis, fibrosis to end-stage cirrhosis and liver cancer. The goal of this proposal is to understand the molecular mechanism of ALD and identify therapeutic targets that reverse alcoholic fibrosis and prevent cirrhosis. So far, there is no FDA approved treatment for any fibrotic disorder. CTGF overexpression, together with transforming growth factor (TGF)-ß, has been found in various kinds of fibrotic disorders. Our research has identified CTGF as a key molecule in the regulation of liver repair and hepatic progenitor cell (HPC) activation. We have developed several genetic mouse tools and will use them to determine the function of CTGF in ALD by testing: 1) whether CTGF can potentiate hepatocyte injury and inflammation during the early phase of alcoholic liver injury; 2) whether CTGF plays an important role in progression of alcoholic fibrosis and HPC activation; 3) whether targeting CTGF and TGF-ß utilizing RNA interference and adeno- associated virus (AAV) delivery system reduces alcoholic fibrosis. This project will employ a multidisciplinary approach, including liver pathophysiology, AAV and RNA-based therapies to test the central hypothesis.
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1 |
2020 — 2021 |
Pi, Liya |
R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Regulation of the Pro-Fibrotic Connective Tissue Growth Factor in Alcoholic Liver Disease: Mechanisms and Targeting Approaches
Project Summary / Abstract: Alcoholic liver disease is a major health and financial concern worldwide. Liver fibrosis and its advanced form, cirrhosis, can occur in virtually all types of chronic liver disease (CLD) including alcohol-induced liver injury. According to the American Liver Foundation, 5.5 million Americans are currently afflicted with CLD or cirrhosis, and the National Institutes of Health (NIH) reports cirrhosis as the 12th leading cause of death due to disease in America. Hepatic progenitor cells (HPCs) are the source of an alternative regenerative mechanism when hepatocyte proliferation is inhibited due to severe liver damage. HPC are closely associated with activated myofibroblast cells (MF) and correlate with severity of liver fibrosis in many CLD. No FDA approved treatment is currently available for any fibrotic disorder. There is an urgent need for the development of anti-fibrotic drugs to control progression of fibrosis while in reversible stages. Connective tissue growth factor (Ctgf) is a profibrotic mediator and modulates cell-cell and cell-matrix signaling through binding to a variety of growth factors, matrix protein, and cell surface proteins including integrins. It is a target gene of the transcriptional coactivator Yes-associated protein (Yap) and acts as an enhancer of transforming growth factor (Tgf)-?, promoting liver fibrosis and HPC activation in chronic liver disease. Our studies demonstrated fine-tuned regulation of Ctgf via hepatocyte nuclear factor (Hnf)4? antagonism of Yap and TGF-?1 signaling in regenerating hepatocytes whereas Ctgf deficiency reduces hepatic inflammation, hepatocyte proliferation and collagen synthesis. Adamts7 (a disintegrin and metalloproteinase with thrombospondin type I repeat 7) was identified as a novel enzyme for Ctgf turnover during liver injury. The Ctgf binding protein-extracellular matrix protein (ECM)1- was identified to inhibit Tgf-? activation and exhibited anti-fibrotic potential. The multifaceted regulations of Ctgf during fibrosis offers important translational opportunities for diagnosis and follow-up of hepatic fibrogenesis as well as intriguing targets for therapeutic interventions. Utilizing a noninvasive imaging technique we recently developed, in Aim 1, the function of Adamts7 in regulating fibrotic responses during alcohol-induced liver injury will be examined. In Aim 2, the anti-fibrotic effects of ECM1 on alcoholic liver injury and HPC activation will be assessed. This study will provide new mechanistic insights during alcoholic liver disease. The knowledge we obtain will help identify molecular targets to enhance liver regeneration and reduce liver fibrosis.
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1 |