The Weill Cornell researchers» process was more direct: Four transcription factors prompted adult
mouse endothelial cells, which line the inside of blood vessels, to turn into HSCs.
Not exact matches
In experiments conducted on human lung
endothelial cells and in
mice, the researchers showed that NS1 caused permeability of the endothelium, which lines the walls of blood and lymph vessels.
However, when the researchers knocked out SIRT1 in
endothelial cells of 10 - month - old
mice, then put them on a four - week treadmill running program, they found that the exercise did not produce the same gains seen in normal 10 - month - old
mice on the same training plan.
To do that, they deleted the gene for SIRT1, which encodes the major mammalian sirtuin, in
endothelial cells of
mice.
The researchers also found that SIRT1 activity in
endothelial cells is critical for the beneficial effects of exercise in young
mice.
A team from Cold Spring Harbor Laboratory in Long Island, N.Y., reports that it staved off full - blown metastasis in
mice by preventing mini-tumors in the lungs from recruiting stem
cells called
endothelial progenitors, which assemble into blood vessels to nourish the malignancy.
By blocking these in lung
endothelial cells, the researchers were able to slow lung tumor growth in
mice and also reduce the spread of metastatic tumors.
In these studies, they used
mice that had been specially bred to express a fluorescent green protein in their
endothelial cells.
Fibroblasts (red) express
endothelial markers (green), making the heart
cells in
mice appear yellow.
To explore this idea, they induced heart attacks in
mice and then studied the fibroblasts to see if the
cells expressed markers characteristic of
endothelial cells.
To verify that the process worked, the
endothelial cells with the inversion - corrected genes were transplanted into F8 deficient
mice (
mice with hemophilia A) and the
mice started producing the F8 clotting factor on their own, which essentially cured them of hemophilia A.
Now, a multidisciplinary research team led by David Eckmann, MD, PhD, Horatio C. Wood Professor of Anesthesiology and Critical Care at the Perelman School of Medicine at the University of Pennsylvania and professor of Bioengineering in Penn's School of Engineering and Applied Science, has found that when delivered by a microscopic transporter called a nanocarrier, steroids can access the hard - to - reach lung
endothelial cells that need it most and are successful at preventing inflammation in
mice.
This experiment uses quantitative PCR to detect the expression level of POSTN in CD34 + / CD31 − pulmonary fibroblasts, CD31 +
endothelial cells, and CD45 + immune
cells isolated from lungs of
mice with macrometastases, which is a replication of the experiment reported in Figure 2H.
To overcome these limitations, we used two - color flow cytometry to identify and select microvascular
endothelial cells from primary cultures obtained from different organs of
mice whose tissues harbor a temperature - sensitive SV40 large T antigen (H - 2Kb - tsA58
mice; ImmortoMice).
B, CSCs isolated from 231BrM infected with lentivirus of miR7 or KLF4 expression plasmids were seeded on top of
mouse brain
endothelial cells or Matrigel.
Tissue - specific microvascular
endothelial cell lines from H - 2K (b)- tsA58
mice for studies of angiogenesis and metastasis
Each of the
endothelial cell lines established from the H - 2Kb - tsA58 transgenic
mice was capable of generating vascular - like channels on Matrigel within 12 h.
When primary cultures from these
mice are stimulated with proinflammatory cytokines, the
endothelial cell fraction responds by up - regulating the inducible
endothelial cell adhesion molecules, E-selectin and VCAM - 1.
A, CSCs isolated from 231BrM and MB231 with the ectopic expression of miR7 and miR7 - LNA were seeded on top of
mouse brain
endothelial cells or Matrigel.
The immortalized
mouse brain microvascular
endothelial cells (mBrEC) were supplied by Dr. Isaiah J. Fidler (M.D. Anderson Cancer Center, Houston, TX; ref.
However, unlike HUVECs or other commercially available
endothelial cell lines, the
endothelial cells generated from the H - 2Kb - tsA58
mice retained their ability to mobilize these adhesion molecules despite undergoing numerous population doublings (currently 30 passages).
The immortalized
endothelial cell lines established from H - 2Kb - tsA58
mice provide, for the first time, a
cell culture system to examine factors regulating angiogenesis and tumor
cell arrest in different organ systems.
The
endothelial cells in insulin - receptor knockout
mice expressed more of the VCAM - 1 adhesion molecule that helps white blood
cells grab onto the growing plaques, and blood vessels gathered four times as many white blood
cells.
The present demonstration of T
cell - mediated apoptosis of allogeneic corneal
cells from CD4 KO
mice is consistent with previous findings, which noted the presence of apoptotic keratocytes and corneal
endothelial cells in rejected corneal allografts in humans and rats respectively (5, 32).
In our study, CD8 − T
cells from CD4 KO rejector
mice failed to display CTL or DTH activity, yet they were capable of inducing donor - specific apoptosis of corneal
endothelial cells.
The results of a typical experiment are shown in Figure 3 and demonstrate that even though spleen
cells from CD4 KO
mice could adoptively transfer corneal allograft rejection, they did not display conventional CTL activity against either BALB / c corneal epithelial or
endothelial cells.
The scientists began with a line of
mice in which the gene for the insulin receptor has been knocked out in
endothelial cells only.
However, in vitro assays using spleen
cells from CD4 KO
mice that had rejected BALB / c corneal allografts failed to detect CTL activity against donor corneal epithelial or
endothelial cells.
The extensive apoptosis of allogeneic corneal
endothelial cells by CD8 − T
cells from CD4 KO
mice was perplexing, as this
cell population should not contain CD4 +
cells.
Spleen
cells were isolated 7 — 14 days after C57BL / 6 CD4 KO
mice had rejected BALB / c corneal allografts and were tested for anti - BALB / c CTL in a conventional 4 - hr 51Cr - release assay using BALB / c corneal epithelial and
endothelial target
cells.
Production of factor VIII by human liver sinusoidal
endothelial cells transplanted in immunodeficient uPA
mice.
mouse liver, IHC - P, high background in
endothelial cells.
Vascular
endothelial growth factor (VEGF) expressed by neural progenitor
cells (NPCs)(cyan) stimulates the growth of blood vessels (red) in the
mouse embryonic hindbrain, and provides regulatory factors to promote the self - renewal of neural progenitors.
Three recent experimental studies focused on low consumption / exposure.949596 In one study, 29 smokers each consumed a single cigarette, immediately after which they had a significant decrease in blood vessel output power and significant increase in blood vessel ageing level and remaining blood volume 25 minutes later, as markers of atherosclerosis.94 In another study, human coronary artery
endothelial cells were exposed to the smoke equivalent to one cigarette, which led to activation of oxidant stress sensing transcription factor NFR2 and up - regulation of cytochrome p450, considered to have a role in the development of heart disease.95 These effects were not seen when heart
cells were exposed to the vapour from one e - cigarette.95 A study exposed adult
mice to low intensity tobacco smoke (two cigarettes) for one to two months and found adverse histopathological effects on brain
cells.96
It also helped protect against oxidative damage that leads to brain
cell death, and reduced injury to brain
endothelial cells in
mice with high - fat diets.