P. Charles Lin, Ph.D.
We seek to elucidate the mechanisms that govern vascular formation and homeostasis. Vascular networks form to satisfy the metabolic demands of tissue growth during development. When we reach adulthood, the vasculature becomes quiescent. However, disease conditions disturb this delicate balance and reactivate endothelium. What distinguishes physiological from pathological angiogenesis in diseases is an important question. It has significant implications for therapeutic interventions. We propose that inflammation distinguishes pathological from physiological angiogenesis. To this end, we tend to take an inflammatory angle to study angiogenesis. Understanding the interaction between inflammation and pathological angiogenesis allows us the possibility to preferentially target angiogenesis in disease conditions and spare normal blood vessels.
1) vascular biology, 2) tumor microenvironment, 3) inflammation, 4) metastasis, 5) angiogenesis
Vascular biology plays a vital role in the progression of many debilitating diseases, including cancer, diabetes, and heart disease. Vascular disease is the most common cause of death and disability in Western societies. Understanding the vascular system is critical in the war against these diseases. Research in Dr. Lin's laboratory centers on the mechanisms that govern blood vessel formation and vascular homeostasis. Vascular networks form to satisfy the metabolic demands of tissue growth during development. When we reach adulthood, the vascular endothelium becomes quiescent. However, under disease conditions, this delicate balance is disturbed and endothelium is reactivated.
What distinguishes physiological angiogenesis during normal growth from pathological angiogenesis in diseases is an important question, which has major implications in therapeutic interventions. We believe a major difference is inflammation. We further hypothesize that tissue injury/insult leads to inflammation, which triggers pathological angiogenesis. To this end, we are focusing on the interaction between inflammation and pathological angiogenesis, which offer the potential to preferentially target angiogenesis in disease conditions and spare normal blood vessels. Research in the lab combines genetic and biochemical approaches, in vitro, three-dimensional organotypic culture and animal models as well as non-invasive imaging technology, to dissect the molecular mechanisms of vascular formation and homeostasis during disease progression.
Selected Key Publications
Expansion of myeloid immune suppressor Gr+CD11b+ cells in tumor-bearing host directly promotes tumor angiogenesis.Cancer Cell. 6(4): 409-21, 2004. [ Journal Article ]
- Blood. 108(4): 1260-6, 2006. [ Journal Article ]
Abrogation of TGF beta signaling in mammary carcinomas recruits Gr-1+CD11b+ myeloid cells that promote metastasis.Cancer Cell. 13(1): 23-35, 2008. [ Journal Article ]
- J Exp Med. 207(1): 77-84, 2010. [ Journal Article ]
- Cancer Cell. 25(4): 501-15, 2014. [ Journal Article ]
Dr. P. Charles Lin received his Ph.D. in Cell and Molecular Biology (1988) at the Peking Union Medical College, Institute of Chinese Medical Sciences, Beijing, China. In 1992, he joined the Department of Medicine, Duke University Medical Center as a Research Associate. In 1999, Dr. Lin was appointed Assistant Professor at Vanderbilt University Medical Center. In 2005, he became Associate Professor with Tenure at the Department of Radiation Oncology, Department of Cancer Biology, and Department of Cell & Development Biology at Vanderbilt University School of Medicine. Dr. Lin established the Vascular Biology Section at the Center for Cancer Research in August, 2010.
|Jaewoo Hong Ph.D.||Postdoctoral Fellow (CRTA)|
|Wooram Jung Ph.D.||Postdoctoral Fellow (Visiting)|
|Jingyi Liu Ph.D.||Research Fellow (Visiting)|
|Lois L. McKennett||Animal Technician (Contr)|
|Yongfen Min Ph.D.||Research Fellow|
|Peng Qu Ph.D.||Research Fellow|