Yanlin Guo

Associate Professor

Teaching Interests

BSC 360: Cell Physiology

BSC 792: Cell Signaling

BSC492/692 Advanced Cell Biology

Research Interests

Cell signaling refers to the process by which a signal, such as a growth factor or an environmental stress, on the cell surface is converted into a specific cellular response. This process is mediated by various intracellular signaling pathways. Mitogen-activated protein (MAP) kinases are key signal-transducing enzymes that are responsible for the regulation of many cellular responses, such as changes in gene expression, proliferation, differentiation, and apoptosis. The research projects in my laboratory are broadly related to the study of molecular mechanisms by which endothelial cells assemble into blood vessels. We are particularly interested in the roles of p38 MAP kinases in the regulation of endothelial cell physiology and vascular biology. Our research utilizes various biochemical, molecular, and cellular approaches. By manipulating the expression and activity level of p38 MAP kinases, we have been investigating their functions in two different experimental models: 1) in conventional 2-dimensional (2D) cell culture dishes where cell proliferation, cell adhesion, and apoptosis are analyzed, 2) in 3D cell culture matrices made of extracellular matrix components where endothelial cells migrate, elongate, and coalesce to form tube structures, mimicking the steps of blood vessel formation in vivo. Our research has recently expended to the use of mouse embryonic stem cells (ESCs) as an in vitro differentiation model to study endothelial cell differentiation and vascular development.

We are also actively engaged in interdisciplinary collaborative research. In collaboration with Dr. Faqing Huang (Dept of Chemistry and Biochemistry) whose lab has developed a novel folate receptor [FR]-based siRNA delivery strategy specific to cancer cells, we are using folate-conjugated siRNA to target cancer cell markers. We expect that this strategy may specifically inhibit tumor cell growth, thus could be potentially used for the development of siRNA-based cancer therapy. In collaboration with Dr. Joshua Otaigbe (School of Polymer Sciences) whose group has extensive experience in synthesizing poly-urethane based biocompatible polymers, we have fabricated 3-demisional synthetic polymer matrices that support cell growth. We are now developing the methods that can direct stem cells differentiating to endothelial cells in synthetic biopolymer matrices, which may be used for vascular tissue engineering. 

Current Graduate Students | Publications

Representative Publications

Chakraborty, S, Kang, B, Huang, F and Guo,Y-L. Mouse embryonic stem cells lacking p38 alpha and p38 delta can differentiate to endothelial cells, smooth muscle cells, and epithelial cells. Differentiation, 2009, 78: 143-150. 
Rajan, S, Ye, J, Bai, S, Huang, F, and Guo, Y-L. NF-?B, but not p38 MAP kinase, is required for TNF-?-induced expression of cell adhesion molecules in endothelial cells. J Cell Biochem. 2008, 105:477-486 
Wang, W, Guo, Y-L, and Otaigbe, JU. Synthesis and characterization of novel biodegradable and biocompatible Poly (ester-urethane)s thin films prepared by homogeneous solution polymerization. Polymer. 2008, 49:4393-4398 
Liu, Y, Cao, DJ, Sainz, IM, Guo, Y-L, Colman, RW. The inhibitory effect of HKa in endothelial cell tube formation is mediated by disrupting the uPA-uPAR complex and inhibiting its signaling and internalization. Am J Physiol, 2008, 295: C257-C267 
Guo, Y-L, Ye, J, and Huang, F. p38? MAP kinase deficient mouse embryonic stem cells can differentiate to endothelial cells, smooth muscle cells and neurons. Dev. Dyn. 2007, 236: 3383-3392 
Guo, Y-L and Yang, B. Deletion of p38? MAP kinase results in an increased cell adhesion and cell viability in mouse embryonic stem cells. Stem Cells Dev. 2006, 15: 655-664