They found that reducing the level of VEGF - A in
mouse kidney cells caused kidney failure very similar to that seen in women suffering from preeclampsia.
Not exact matches
He conducted his postdoctoral research at Brigham and Women's Hospital / Harvard Medical School, where he researched the role of the Wnt signaling pathway in
mouse models of
kidney disease, and was part of a team that discovered a stem
cell subtype responsible for solid organ fibrosis.
Single -
cell transcriptomics of the
mouse kidney reveals potential cellular targets of
kidney disease
Two years ago, he and his colleagues reported in Aging
Cell that cutting the calories ingested by
mice by 30 % for up to 4 weeks protected the rodents»
kidneys when their blood supply was cut off and then restored.
After giving the
cells a week to get used to each other, the scientists implanted the chimeric concoction into the protective tissue surrounding the
kidneys of living
mice.
«Just one transplant of the human EPO - producing
cells treated
kidney anaemia in
mice, keeping their haemoglobin levels in the normal range for the remaining 7 - month lifespan of the animals,» says Kenji Osafune, of Kyoto University in Japan, who led the team.
The team then transplanted these
cells into the
kidney cavities of
mice with a form of
kidney anaemia.
To demonstrate the capabilities of SpDamID in the current study, the authors analyzed Notch - mediated transcriptional activation in
mouse kidney progenitor
cells (mK4
cells).
Cells were transplanted to the kidney capsule and photo was taken two weeks later by which time the beta cells are making insulin and have cured the diabetes in the m
Cells were transplanted to the
kidney capsule and photo was taken two weeks later by which time the beta
cells are making insulin and have cured the diabetes in the m
cells are making insulin and have cured the diabetes in the
mouse.
The
cells were implanted into an adult
mouse, beneath a membrane that surrounds the
kidney.
In the
mouse study, the insulin - producing
cells were placed under the
kidney capsule — a thin membrane layer that surrounds the
kidney — where they developed into an organ - like structure with its own blood supply.
Using
cell models and genetically engineered
mice, the authors then could reproduce
kidney disease changes upon expression of APOL1 gene variants, but the disease required the presence suPAR.
To confirm that these
cells were, in fact, stem
cells, the scientists transferred them into the
kidneys of adult
mice.
«
Mice engineered with rare
kidney disease shed light on how
cells repair broken DNA.»
In this cross section of a
kidney from a young FAN1 knockout
mouse,
cell nuclei are stained purple.
In observing
kidney cells from the FAN1 knockout
mice, the researchers noticed that their nuclei were abnormally large.
Through studies conducted in
mice, Oliver M. Steinmetz, MD (University Hospital Hamburg Eppendorf, in Germany) and his colleagues have shown that the messenger protein IL - 6, which is rapidly produced at high levels during an acute inflammatory form of
kidney disease, potently dampens activation of tissue - destructive immune
cells called macrophages.
«We isolated
kidney progenitor
cells from
mice and searched for the most favorable culture conditions,» said Assistant Professor Shunsuke Tanigawa of Kumamoto University.
After transplanting the human iPS
cell - based
kidney tissue into a
mouse body, glomeruli connecting to
mouse kidney capillaries formed.
The team found deep conservation of certain processes that likely reflects similar underlying regulatory processes between
mouse and man, but there were also significant differences in gene expression during
kidney development, as well as in the timing, scale, organization, and molecular profile of key
cell types and
cell structures.
The test drug slowed the growth of
kidney cysts in two
mouse models and in
cell cultures of human
kidney cysts, the study showed.
«Our stem
cells also survive outside of
mice, in a culture, so we can also manipulate them in a laboratory,» said Abad, adding that: «The next step is studying if these new stem
cells are capable of efficiently generating different tissues such as that of the pancreas, liver or
kidney.»
«Massive single -
cell survey of
kidney cell types reveals new paths to disease: Study of over 57,000
cells from
mouse kidneys help identify human renal disorders.»
Using
mice bred to lack some types of lymphoid
cells, among other features, researchers were able to show that those
mice still had high levels of suPAR and proteinuria, indicating that lymphoid
cells were not the perpetrators of
kidney disease.
Four weeks after transplanting these
cells into the
kidney cavities of
mice with a form of
kidney anaemia, the treated animals had blood EPO levels 20 times higher than those in controls (Science Translational Medicine, doi.org/cdmx).
The study is published in the scientific journal Oncoimmunology and describes how a
cell type in the blood, the neutrophil, causes
kidney dysfunction in
mice with cancer.
They showed that it slowed the growth of human lung cancer
cells but not
kidney cancer
cells in these
mice.
Rare stem
cells (in red) that give rise to scar - tissue secreting myofibroblast
cells, here found near the blood vessels of a
mouse kidney (in green).
COS - 7 African green monkey
kidney cells, C2C12
mouse myoblastic
cells, MC3T3 - E1 human osteoblastic
cells, and U-2 OS human osteosarcoma
cells were obtained from ATCC.
In
mice with
kidney and cardiac fibrosis, the ablation of these
cells resulted in reduction in fibrosis and rescued heart function.
The scientists got another surprise when they followed up on this finding with
mouse experiments that exposed specialized
kidney cells called «podocytes», a key component of the blood filtering, to high levels of glucose.
Recently, we showed that bortezomib treatment in
mice bearing breast and
kidney tumors provided host survival benefit by amplifying tumor
cell caspase8 activation, CD8T
cell effector molecules via increased NotchNFkB crosstalk and Fas ligandmediated lysis of tumor
cells.
A new study establishes that the injection of a collagen - based biomaterial can mobilize endogenous stem
cells to promote
kidney regeneration in a
mouse model
By age 2, the
mice had some rat
cells in their
kidney, lung, pancreas, liver, and brain.
On the other hand, there are many other tissues — notably, the
kidney and articular cartilage — where p16Ink4a - expressing senescent
cells appear to be a contributing factor to human and murine degenerative aging, but which were not evaluated in treated or control
mice in this study, and it would be of interest to see the effects of ablation of p16Ink4a - positive senescent
cells.
Studying
cells from the stomach and pancreas in humans and
mice, as well as
mouse kidney and liver
cells, and
cells from more than 800 tumor and precancerous lesions in people, the researchers found when tissue is injured by infections or trauma, mature
cells can revert back to a stem -
cell state in which they divide repeatedly.
Thus, upon activation by ActD, AKT becomes an inducer of p53 tumor suppression instead of being a survival factor, as consistently shown in human embryonic
kidney cell lines (293 and 293T), human hepatoma
cell line (HepG2), and
mouse hepatoma
cell line (Hepa - 1c1c7).