BME Seminar Series
Presents
Robert Strieter, M.D.
Professor and Chair
of the Department of Medicine,
University of Virginia
The Role of Circulating Mesenchymal Progenitor
Cells (Fibrocytes) in Promotion of Fibrosis and Adipose Tissue
Friday, January 26, 2007
2:00 - 3:00 p.m.
BME Lecture Hall (Room 1041), MR-5
ABSTRACT
Historically, tissue repair was thought to be primarily related to
local cellular events with the exception of platelet degradation and
recruitment of leukocytes during the coagulation and inflammatory phases
of repair. However, recent studies have challenged this paradigm,
and have demonstrated the existence of populations of circulating adult
progenitor cells that behave as cells that can differentiate into
endothelial cells, muscle cells, neural cells, hepatic cells,
osteoblasts, myofibroblasts. The mesenchymal progenitor cells are
believed to reside primarily in the bone marrow and are mobilized to
enter the pool of circulating blood cells when exposed to specific
environmental cues, traffic to specific tissue sites, and within their
new tissue microniche and in response to specific environmental cues
differentiate into specific cellular lineages. The function of
these cells may be critical for maintenance of homeostasis of peripheral
organs, or they can be recruited to participate in repair following
tissue injury. My presentation will focus on a circulating pool of
cells that are mesenchymal progenitor cells with evidence for plasticity
to differentiate into myofibroblasts and adipocytes. Our findings
demonstrate that under conditions of evolving pulmonary fibrosis and in
response to TGF-b, these cells can differentiate into myofibroblasts and
play a major role in promoting fibrosis. However, if these cells
are exposed to different microenvironmental cues and in the absence of
TGF-beta, they can differentiate into adipocytes and form adipose tissue,
which is relevant to their contribution to form adipose tissue relevant
to the metabolic syndrome. These findings support the notion that
developing strategies to target the trafficking of these cells to
specific tissue sites, as well as modulating their differentiation may
serve as novel therapeutic interventions to attenuate their role in
promoting fibrosis and adiposity.