Sentences with phrase «in cell senescence»

«In fact, the CDKN2A takes part in the p53 signalling pathway, one of the most important ones in the cell senescence regulation,» adds Lucía.

The research group studied the role of oxidative stress (see «The Two Faces of Oxygen») in cell senescence, and at Packer's request, Smith began teaching Pereira - Smith cell culture techniques.

Not exact matches

On the contrary, senescence is decreased in activated hepatic stellate cells (HSCs), the supportive cells which, when triggered by alcohol or other liver insults, begin to produce excessive fibrotic material.

Austad recalls one conversation in which Muller made an insightful connection about telomeres, the DNA - and - protein caps at the ends of chromosomes that shorten with every cell division, eventually pushing cells into a nondividing state called senescence.

Telemere, the chromosome ends, is playing an inevitable role in maintaining the life including germ cells or cell senescence.

Through the mTOR signalling pathway, it is involved in the regulation of many cellular processes, including cell survival, metabolism, proliferation, differentiation, and senescence.

If we introduced stem cells with nice, long telomeres in the first place, we could let them wind down and eventually be lost to apoptosis, senescence, or other sources of damage — and just top our tissues up with more stem cells before enough of those cells were lost to begin to impair tissue function.

When researchers suppressed the ARF gene in mole - rat cells during the reprogramming process to iPSCs, the cells stopped proliferation with sign of cellular senescence, while the opposite happens with mouse cells.

Intermittent dosing with rapamycin selectively breaks the cascade of inflammatory events that follow cellular senescence, a phenomena in which cells cease to divide in response to DNA damaging agents, including many chemotherapies.

If senescence was happening too fast in the cells of Werner patients, it might mean that a biochemical gas pedal was stuck on the floor.

Results show that one night of partial sleep deprivation activates gene expression patterns in peripheral blood mononuclear cells (PBMCs) consistent with increasing accumulation of damage that initiates cell cycle arrest and increases susceptibility to senescence.

Senescence is associated with normal aging, and senescent cells accumulate in aged tissues, which impair the normal functions of the tissue and contribute to age - related diseases.

Clipped H3.3 may be a marker of cells that stop proliferating and has implications for cancer, in particular cancers like melanoma that have a senescence phase.»

These loci are known to be involved in various processes including cell senescence, autoimmunity and cell signaling, and also with Alzheimer's disease.

An alternative approach is to cause rapid cell aging and induce premature senescence, which we believe could become a new frontier in cancer drug development.»

Building on this «telomere hypothesis,» Geron's big idea was that tinkering with telomerase in cells could stave off their senescence — and prevent aging.

But if supplies of these materials run low, the cell will enter a suspended state called senescence and cell division will stop, freezing the advance of the virus, according to new findings from a Duke University research team that appear in Proceedings of the National Academy of Sciences.

Stuck in senescence, this cell can no longer grow or divide.

Working with researchers at the University of Tübingen, Germany, they mutated Arid1b in mice and human cells, and this stopped the cells from entering senescence.

Rattan joined the Clark group in 1984 and started exploring what happens when skin, bone, and connective tissue cells grow old and enter a state of limbo — called senescence — in which they neither divide nor die (see «More Than a Sum of Our Cells&raqcells grow old and enter a state of limbo — called senescence — in which they neither divide nor die (see «More Than a Sum of Our Cells&raqCells»).

Senescence is triggered when a cell grows abnormally fast and, once induced, it acts to keep the cell in limbo, such that it is alive but can no longer grow or divide.

Approaching aging from the perspective of senescence at the levels of cells and organs, the author discusses aging diseases in the context of the tissues that they impact.

Senescence impairs lung function in two ways: It prevents lung cells from dividing when they need to be replaced.

In addition to their cell - intrinsic effects, senescent cells develop the ability to negatively influence healthy neighboring cells and immune cells by secreting senescence - associated set of cytokines and mediators known as the SASP.

In fact, KLF4 blocks senescence and apoptosis by repressing transcription of P53, whereas it can activate P21 - dependent cell - cycle arrest, and therefore, KLF4 can function both as a tumor suppressor and an oncogene (33, 34).

This series addresses the contribution of cellular senescence to cardiovascular, neurodegenerative, and arthritic disorders as well as the senescent phenotypes in various tissues and cell types.

In this way they were able to reactivate the senescence program and stop the growth of the breast cancer cells.

In this study, the researchers addressed in more detail why cells treated with palbociclib enter senescencIn this study, the researchers addressed in more detail why cells treated with palbociclib enter senescencin more detail why cells treated with palbociclib enter senescence.

The breast cancer drug palbociclib arrests cells in G1 phase by CDK4 / 6 inhibition, but also causes cellular senescence.

In this study these cells were treated with a combination of gamma secretase inhibitor and BRAF inhibitor, a reduction in cell growth and an increase in senescence was observed in these resistant cellIn this study these cells were treated with a combination of gamma secretase inhibitor and BRAF inhibitor, a reduction in cell growth and an increase in senescence was observed in these resistant cellin cell growth and an increase in senescence was observed in these resistant cellin senescence was observed in these resistant cellin these resistant cells.

Senescence cell clearance, like senolytics gives, 15 - 30 % improvement in Average Lifespan and Healthspan, but nill on Maximum Lifespan extension.

These findings are in agreement with other studies on cell morphology [3, 4] and senescence [5], and the authors hope to advance these studies by separately analyzing subpopulations derived from the same bone marrow sample, and also surveying the grade of cell maturity (surface receptor analysis) and cytoskeleton composition of the cells during cell tracking.

Some of the leading folk in the cellular senescence research community today published the results from a very encouraging life span study, extending life in mice via a method of removing senescent cells.

Moreover, there are yet other cell types — such as visceral adipose tissue macrophages and cytotoxic CD8 + T - cells — in which the age - related supernumerary accumulation of dysfunctional and apoptosis - resistant cells appears to play a highly deleterious role on tissue function, but where the cells are not «senescent» cells in the classical sense of p16Ink4a expression and the senescence - associated secretory profile observed in senescent fibroblasts.

In the presentation, Dr. Gudkov discusses findings from a study published earlier this month in the journal Aging, which identified a subset of immune cells, which the authors called senescence - associated macrophages (SAMsIn the presentation, Dr. Gudkov discusses findings from a study published earlier this month in the journal Aging, which identified a subset of immune cells, which the authors called senescence - associated macrophages (SAMsin the journal Aging, which identified a subset of immune cells, which the authors called senescence - associated macrophages (SAMs).

* The principle caveat would be that the interaction of senescence with defective mitotic checkpoint function within such cells, and the effects upon their neighbors of their state and of their senescence - associated secretory phenotype, would very likely cause some phenomena that would not be observed in p16Ink4a - senescent cells or in their effects on neighbors.

Cardiovascular disease and renal disease for example are accelerated in patients with diabetes and AGEs have been shown to induce senescence in cell types related to these diseases, such as endothelial progenitor cells, vascular endothelial cells and renal cells.

In response, the cells underwent changes indicative of senescence, ceasing cell division and churning out key SASP factors.7 Notably, astrocytes were much more vulnerable to paraquat than skin cells: astrocytes went senescent at a lower concentration of the toxin than was required for skin cells, and the doses that turned skin cells senescent killed astrocytes outright.7

Sure enough, when the researchers examined the brains of PD patients, they found more cells exhibiting signs of senescence than in people without the disease — and especially astrocytes, as they had expected.7 This was true even after matching patients for age, meaning that PD subjects had even more senescent astrocytes in their SNcs than is typical for people their age (ranging in this case from 50 — 92 years at autopsy)-- and remember, aging already drives an increase in the burden of these cells as compared with young people, even in those who have yet to develop Parkinson's disease.7

With their deep expertise in the biology of senescent cells, the Campisi lab will be focused on fundamental research into questions like how senescent cells vary in their susceptibility and resistance to immune clearance (depending on factors like their tissues of residence or the pathway that led them into senescence); the targets and mechanisms used by NK cells to clear senescent cells; and why subsets of senescent cells might persist when their similarly - situated neighbors are cleared out (and what might allow us to overcome that resistance).

(20) It was this emerging line of research that van Deursen's collaborator Dr. James Kirkland presented at the fifth annual Strategies for Engineered Negligible Senescence Conference (SENS5) in September of this year, (18) and it was his expertise in the senescence of adipose tissue that he contributed to the new report on the effects of ablating sSenescence Conference (SENS5) in September of this year, (18) and it was his expertise in the senescence of adipose tissue that he contributed to the new report on the effects of ablating ssenescence of adipose tissue that he contributed to the new report on the effects of ablating such cells.

When BubR1H / H; INK - ATTAC mouse bone marrow cells were pushed into senescence in vitro by the PPAR - γ - activating drug rosiglitazone, a subpopulation of the cells exhibited high levels of INK - ATTAC expression and GFP, coupled with SAβ - gal staining; subsequent to treatment with the INK - ATTAC activating drug, these cells rapidly entered into apoptosis, and within 48 h were either destroyed or in the cell death process.

(14,15)-RRB- have found age - related satellite cell attrition consistent with the senescence of a subset thereof; moreover, one such study (15) reported that decreases in the number and quality of satellite cells with aging are reliably associated with elevated expression of p16Ink4a (contrary to (14)-RRB-, and with secretory and proteomic abnormalities consistent with a rising burden of senescent cells.

To impute aging phenotypes directly to p16Ink4a - expressing senescent cells, van Deursen and colleagues with expertise in the aging and senescence of the relevant tissues developed and tested the effects of a pharmacologically - inducible system for the ablation of p16Ink4a - expressing cells.

A great deal of evidence has now been amassed that stromal cell senescence plays an important role in laying the groundwork for tumor metastasis, promoting cell proliferation with inflammatory cytokines, encouraging angiogenesis, and degrading the tumor - suppressive action of an intact extracellular matrix.

In particular, they are focused on studying the functional role and molecular mechanisms of cellular senescence in both of these events, and how a deregulation of normal epithelial stem cell proliferation is involveIn particular, they are focused on studying the functional role and molecular mechanisms of cellular senescence in both of these events, and how a deregulation of normal epithelial stem cell proliferation is involvein both of these events, and how a deregulation of normal epithelial stem cell proliferation is involved.

The gene remains completely dormant and harmless in a mouse's cell until it is «armed» by the activation of the key senescence gene, p16INK / 4a, which rarely occurs except in senescent cells.

Senescent cells lose their normal function in the tissue, cease dividing, and begin secreting a deadly mix of inflammatory and tissue - degrading factors collectively known as the senescence - associated secretory phenotype (SASP) that damages and deranges local tissues.

He presented his finding that mitochondrial dysfunction can induce senescence in cultured cells at the SENS6 Conference at the University of Cambridge.

In the third stage, senescence, cells stop dividing entirely.