«Eighty - two percent of the smooth muscle cells within advanced atherosclerotic lesions can not be identified using the typical methodology since the lesion cells down - regulate smooth
muscle cell markers.
Not exact matches
They injected this handcrafted virus into rats and found that the
marker gene was indeed active only in smooth
muscle cells.
But in the 1 September issue of the Journal of Clinical Investigation, cardiologist Michael Parmacek and his colleagues at the University of Chicago describe how they deleted two genes from the common cold virus to make it unable to cause any sniffling or fever, then replaced them with a
marker gene that turns out an easily detected protein and the SM22 promoter, which turns on expression of genes in smooth
muscle cells that surround arteries.
In order to locate all gene switches, the Freiburg research team used modern sequencing methods to examine the entire genome — DNA, epigenetic
markers and RNA — during the development, maturation and disease of human cardiac
muscle cells.
Last December, for instance, Chien's group reported finding
markers for heart
muscle stem
cells by tracing their development from embryonic tissue.
Once they were able to isolate skeletal
muscle cells using the newly identified surface
markers, the research team matured those
cells in the lab to create dystrophin - producing
muscle fibers.
Using the ERBB3 and NGFR surface
markers, the skeletal
muscle cells were isolated and then injected into mice at the same time a TGF Beta inhibitor was administered.
Skeletal
muscle cells isolated using the ERBB3 and NGFR surface
markers (right) restore human dystrophin (green) after transplantation significantly greater than previous methods (left).
The answer was yes: They found
cells with
markers from all three major body
cell types, called germ layers: ectoderm (such as nerve
cells), mesoderm (
muscle and blood vessel
cells), and endoderm (kidney
cells).
In order to locate all gene switches, the Freiburg research team used modern sequencing methods to examine the entire genome - DNA, epigenetic
markers and RNA - during the development, maturation and disease of human cardiac
muscle cells.
«But the desired
cells often lack a readily accessible surface
marker, or that
marker is not specific enough, as is the case for cardiac
muscle cells.
Red represents the cardiac
muscle marker troponin, and green is cadherin, which helps
cells stick to each other.
In fact, it turned out that these
cells expressed
markers characteristic of brain pericytes, such as PDGF receptor beta, smooth
muscle actin, NG2 and also CD146 not depicted here.
Perivascular
cells, including pericytes in the smallest blood vessels (e.g., microvessels) and ARCs around larger ones, express mesenchymal stem
cell markers and bear a multi-differentiation fate potential (differentiate into osteoblasts, chondrocytes, adipocytes, smooth
muscle cells and myocytes) similar to that documented for MSCs in vitro.
Infiltrating
cells in the myocardium and skeletal
muscle were positive for the T -
cell marker CD3 or the macrophage
marker CD68.
Whilst the supplements did not affect maximal oxygen uptake or the results of a 20 metre shuttle test, the results showed that
markers for the production of new
muscle mitochondria — the power supply for
cells — increased only in the group without supplements.
MyoD is normally only expressed in skeletal
muscle, and it was later found to be a transcription factor involved in the differentiation of
muscle cells and also a very early
marker of
muscle cell fate commitment.
In the same way, whereas NR supplementation increased
muscle stem
cell number in aged mice, thereby enhancing mitochondrial function and
muscle strength, it reduced the expression of
cell senescence and apoptosis
markers [233]; the state of senescence is important to protect against carcinogenesis [234].
Compression stockings improved all
markers of recovery except for creatine kinase (a
marker of
muscle cell damage).