Biomedical Engineering Reference
In-Depth Information
-tropomyosin) 10 in various
embryonic and adult stem and progenitor cells such as mobilized peripheral blood
mononuclear cells [ 1406 ].
Except left ventriculomyocytes, most cardiac cells (vascular smooth and cardiac
myocytes and nodal and endothelial cells) are derived from multipotent progenitors
that express gene Islet-1 (Isl1) [ 1407 ]. A small quantity of cells that express stem
cell markers such as stem cell factor receptor (SCFR), stem cell antigen SCA1, and
multidrug resistance protein MDR1, have been identified in the human heart [ 1408 ].
However, SCFR
factor NKx2-5, myocardin, troponin-I, and sarcomeric
α
+
cells can be scouting cells of the immune system.
11.4.1.1
Cardiac Stem Cells
Cardiac stem cells divide either symmetrically or asymmetrically. 11 Myocardium
contains stem cell niches [ 1409 ]. Cardiac stem cells are smaller then mature
cardiomyocytes. Cardiac stem cells and supporting cells are connected by gap and
adherens junctions. Integrins of primitive and committed cells within the niche
attach these cells to extracellular matrix proteins (fibronectin and laminin) that
transduce mechanical signals for differentiation regulation.
Stem cells may regenerate the myocardium, especially after myocardial infarc-
tion and in ischemic cardiomyopathy, because the heart is a weakly regenerative
organ. Progenitor cells secrete paracrine factors and may contribute to vasculogen-
esis and tissue repair and remodeling [ 1410 ].
In the heart, resident stem cells can lead to endothelial and smooth muscle
cells as well as cardiomyocytes [ 1411 ]. The heart may contain various populations
of resident myocardial progenitors with different expression modes that may
differentiate into cardiomyocytes and endothelial cells. 12
Although cardiogenic progenitor cells maintain myocardial turnover, they do
not lead to heart regeneration. Consequently, injured adult hearts form scars
without cardiomyocyte proliferation. Appropriate differentiation of stem cell and
induction of the division cycle of resident cardiomyocytes can be stimulated with
suitable factors. Cytokine treatment (e.g., colony-stimulating factor CSF3) improves
infarction repair, but can also increase mortality [ 1412 ]. Cell delivery can be done
either by intracoronary infusion or direct intramyocardial injection during grafting
or using endovascular procedures. Periostin activates plasmalemmal
α
α
α
V -,
1 -,
3 -,
α
and
5 -integrins, and induces re-entry of cardiomyocytes into the cell cycle [ 1413 ].
10 These markers are supposed to be better than markers of late cardiogenic differentiation without
an important role in cardiac fate, such as
-myosin heavy chain and atrial natriuretic factor.
11 Asymmetric division predominates. Replicating cardiac stem cell gives birth to one daughter
cardiac stem cell and one daughter committed cell (cardiomyocyte, endothelial cell, or smooth
myocyte).
12 In vitro, these observations may correspond to culture artifacts.
α
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