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Bone marrow-derived mesenchymal stem cells from people with idiopathic pulmonary fibrosis (IPF) perform basic cellular functions, such as growth and division, worse than these cells of healthy people the same age , says a study.
The study, "Senescence of mesenchymal stem cells derived from the bone marrow of patients with idiopathic pulmonary fibrosis, "Posted in the newspaper Stem cell research and therapy, also drew attention to the "systemic consequences" of the disease.
Aging is a well-known risk factor for the REIT. Researchers have shown that the lung cells of patients with FPI show an increase in markers of cellular senescence – an inability to continue to divide and grow – which characterized aging.
The theory of cellular aging on senescence suggests that organisms, including people, age due to the accumulation of senescent cells physiologically less useful.
Senescence is the phenomenon by which normal and growing proliferating cells enter a process called cell cycle arrest, no longer divide and no longer produce cells at a healthy rate.
Mesenchymal stem cells (MSCs) have been used in the cellular treatment of various diseases because they have the ability to influence the immune system. It is also known that these cells have a protective effect against FPI. But we know that the normal functioning of MSCs decreases with age as they go into senescence.
Studies on animal models of lung lesions have shown that infusion of older bone marrow-derived MSCs (B-CSM) is less effective – in terms of protective activity – than infusion of MSCs derived from young donors .
The researchers sought to determine the differences between the characteristics of B-MSCs taken from healthy individuals and those from REI patients in the same age group.
They searched for markers of cellular senescence, as well as measures of mitochondrial function (measurement of cell viability) and DNA damage. In addition, the protective capacity of B-MSCs was studied by injecting them into an animal model of FPI.
The results indicated that B-MSCs of patients with FPI were more senescent than those of healthy people of the same age, with significant problems of mitochondrial function and increased accumulation of DNA damage – equivalent to a lower cell viability.
"We demonstrate for the first time that B-MSCs of patients with FPI are senescent with significant differences in mitochondrial function, the accumulation of DNA damage resulting in defects in critical cellular functions by compared to age-matched controls, "the team wrote.
Together, these aberrations resulted in failures in the critical functions of the cell versus the controls.
It is interesting to note that the study also revealed that senescent B-MSC IPFs can induce senescence in normal age fibroblasts by promoting inflammation.
"The consequences of having senescent B-MSCs are not completely understood, but the decrease in their ability to respond to normal activation and the risk of having a negative impact on the local niche by inducing inflammation." and senescence in neighboring cells suggests a new link. between B-MSC and the onset of the disease, "wrote his researchers.
Finally, the researchers showed that patients' B-MSCs were less effective at preventing fibrotic changes in an animal model of the disease, thus highlighting their lesser protective powers compared to B-MSCs of healthy people.
"The B-MSCs of patients with FPI are defective compared to controls of the same age," the researchers concluded. And they added:[d]Although the IPF is a disease with a respiratory phenotype and a major representation in the lungs, our results show systemic consequences of the disease. "
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