Teaching Interests
BSC 360: Cell Physiology
Signal Transduction
BSC 792: Cell Signaling
Research Interests
My research has focused on the study
of cell signaling; especially on the MAP kinase
pathways. The recent studies have centered on the
cellular mechanisms that regulate angiogenesis, the
process of new blood vessel formation. Angiogenesis is
crucial for normal physiological processes, such as
embryogenesis and wound healing. It also occurs under
pathological conditions, such as cancer and
cardiovascular diseases. The goal of our research is to
understand the molecular mechanisms by which endothelial
cells, the building blocks of blood vessels, assemble
into blood vessels. Specifically, our research projects,
supported by grants from the American Heart Association
and the National Institutes of Health, focus on the
following areas:
- The roles of p38 MAP kinases in
the regulation of endothelial cell physiology and
angiogenesis
p38 MAP kinases (p38) regulate endothelial cell
proliferation, morphogenesis, and survival. However,
the molecular mechanisms of p38a and p38b, two major
isoforms expressed in endothelial cells, are not
clear. By manipulating their expression and activity
levels, we are analyzing their functions in two
different experimental settings: a) in 2D cell
culture dishes where cell proliferation is the major
cellular activity, b) in 3D cell culture matrix
where endothelial cell differentiate into
vessel-like structures.
- The roles of p38a in the
regulation of mouse embryonic stem cell
differentiation.
38a is the most widely expressed isoform of p38
family. Its pivotal role in growth and development
is best demonstrated by the fact p38a knockout
(38a-/-) mice is embryonic lethal. However, the
embryonic stem cells (38a-/-ES cells) are viable. We
are using p38a-/-ES cells as a “loss–of–function”
tool to study this enzyme in the regulation of ES
cell differentiation into endothelial cells.
- Development of 3-dimensional (3D)
cell culture systems as in vitro
angiogenesis models
When cultured in a 3D collagen or fibrin matrix (two
major components of basement membrane supporting
blood vessel growth), endothelial cells migrate,
elongate, and coalesce to form tube structures,
mimicking the steps of angiogenesis. The 3D cell
culture as in vitro angiogensis model allow us to
study signaling events, cell morphogenesis, and to
test the effects of agents that inhibit or promote
angiogenesis.
Current Graduate
Students |
Publications
Representative Publications
Guo, Y-L and Yang, B. Deletion of p38a MAP kinase results in an increased cell adhesion and
cell viability in mouse embryonic stem cells. Stem
Cells Dev. 2006, 15: 655-664
Yang, B.H., Cao, D.J.,
Colman, R.W. and Guo, Y-L. Different roles of ERK and
p38 MAP kinases during tube formation from endothelial
cells in 3-dimensional cell culture. J. Cell Physiol.
2004, 200:360-369
Wang, S., Hasham, M.G.,
Isordia-salas, I., Tsygankov, A.Y., Colman, R.W. and
Guo, Y-L. Up-regulation of cdc2 and cyclin A during
apoptosis of endothelial cells induced by cleaved high
molecular weight kininogen. Am. J. Physiol.
2003, 284: H1917-H1923
Guo, Y-L, Kang, B., Han.,
J, Williamson. J.R. p38beta MAP kinase protects rat
mesangial cells from TNF-alpha-induced apoptosis. J.
Cell Biochem. 2001, 82: 556-565
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