Biomedical Engineering Reference
In-Depth Information
revolutionize the DES market. A caveat for the use of stem cells for vascular repair
is that these cells may be the culprits in the development of restenosis. Scientists at
the Weill Cornell Medical College in New York are currently studying how stem
cells implant themselves in the wall of arteries and grow out of control following
angioplasty and contribute to development of re-stenosis. The researchers observed
that transforming growth factor beta (TGF-b), which stimulates tissue growth, is
released in high levels inside the artery following the trauma of angioplasty. This
could happen because TGF-b may attract stem cells to the injured area to heal the
wound, leading to the growth of dense tissue, which blocks the artery. If this
mechanism of restenosis is proven, one strategy would be to incorporate a TGF-b
antagonist in the DES to shut off this response.
Role of Cells in Cardiac Tissue Repair
Modulation of Cardiac Macrophages for Repair of Infarct
A new strategy has been investigated for the modulation of cardiac macrophages to
a reparative state at a predetermined time after MI with the aim to promote resolu-
tion of inflammation and elicit infarct repair (Harel-Adar et al.
2011
). Intravenous
injections of PS-presenting liposomes are employed to mimic the anti-inflamma-
tory effects of apoptotic cells. Following PS-liposome uptake by macrophages
in vitro and in vivo, the cells secrete high levels of anti-inflammatory cytokines
(TGF-b and IL-10) with upregulation of the expression of the mannose receptor
CD206, concomitant with downregulation of proinflammatory biomarkers, such as
TNF-a and the surface marker CD86. In a rat model of acute MI, targeting of
PS-presenting liposomes to infarct macrophages after injection via the femoral vein
was demonstrated by MRI. The treatment promotes angiogenesis, preserves small
scars, and prevents ventricular dilatation and remodeling. This strategy represents
a unique and accessible approach for MI repair.
Transplantation of Myoblasts for Myocardial Infarction
Cells taken from peripheral muscles and injected into infarcted areas of the myo-
cardium are incorporated into the myocardium and take on some characteristics of
cardiomyocytes. Most importantly, the cell transplants improve contractility in the
infarcted areas. To prevent the progression of events after experimental MI, autolo-
gous skeletal myoblasts (muscle precursor cells) have been transplanted into
infarcted myocardium of the rabbits induced by a cryoprobe. Follow-up histologi-
cal examination of the heart showed that islands of different sizes comprising
elongated, striated cells that retained characteristics of both skeletal and cardiac
cells were found in the area of the infarction. In rabbits in which myoblasts were
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