Age-Related Alterations Affecting the Chondrogenic Differentiation of Synovial Fluid Mesenchymal Stromal Cells in an Equine Model

Mazzotti, Eleonora; Teti, Gabriella; Falconi, Mirella; Chiarini, Francesca; Barboni, Barbara; Mazzotti, Antonio; Muttini, Aurelio

doi:10.3390/cells8101116

Cited by 17 publications

(14 citation statements)

References 64 publications

(85 reference statements)

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“…Autophagy is an intracellular catabolic process that involves cell metabolism and the recycling of damaged and dysfunctional organelles and proteins [20][21][22]. e role of autophagy in lung cancer remains controversial.…”

Section: Discussionmentioning

confidence: 99%

Qiyusanlong Formula Induces Autophagy in Non-Small-Cell Lung Cancer Cells and Xenografts through the mTOR Signaling Pathway

Gao

Wang

Yang

et al. 2021

Evidence-Based Complementary and Alternative Medicine

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Objective. Qiyusanlong (QYSL) formula has been used in the clinic for more than 20 years and has been proved to have pronounced efficacy in the treatment of non-small-cell lung cancer (NSCLC). This work aims to evaluate the molecular mechanism of QYSL formula action on NSCLC, specifically in relation to autophagy induction. Methods. In vitro, CCK-8 was used to detect the effect of QYSL serum on cell viability in A549 cells. In vivo, A549 cells were implanted subcutaneously in nude mice to establish a xenograft model. TUNEL staining was used to measure cell apoptosis and TEM to observe the autophagy-related morphological changes in vitro and in vivo. Western blotting, RT-qPCR, and immunofluorescence were used to measure autophagy-related proteins. In addition, rapamycin (an inhibitor of mTOR and inducer of autophagy) and MHY1485 (an activator of mTOR and inhibitor of autophagy) were used to determine whether QYSL-induced autophagy was regulated by the mTOR pathway. Results. QYSL serum inhibited the cell viability of A549 cells in a concentration‐dependent manner. In vivo, the QYSL formula inhibited xenograft growth. The QYSL formula promoted apoptosis in A549 cells and induced autophagosome formation in vitro and in vivo. In addition, the QYSL formula downregulated the expression of mTOR and p62, while it upregulated the expression of ATG-7 and Beclin-1 and increased the LC3-II/LC3-I ratio. QYSL serum inhibited p-mTOR in a similar manner to rapamycin while reducing the activating effects of MHY1485 on p-mTOR. Conclusion. The QYSL formula has anti-lung cancer effects and promotes autophagy through the mTOR signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Qiyusanlong Formula Induces Autophagy in Non-Small-Cell Lung Cancer Cells and Xenografts through the mTOR Signaling Pathway

Gao

Wang

Yang

et al. 2021

Evidence-Based Complementary and Alternative Medicine

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“…Moreover, MSCs is considered as a potential approach for cartilage repair and regeneration [ 99 ]. However, aging can seriously compromise MSCs’ characteristics and ability, particularly in chondrogenic differentiation [ 100 ]. The data from Mazzotti et al exhibited a reduced efficiency in the chondrogenic differentiation of aged equine synovial fluid MSCs (SfMSCs) compared to young SfMSCs.…”

Section: Conclusion and Future Prospectsmentioning

confidence: 99%

“…The data from Mazzotti et al exhibited a reduced efficiency in the chondrogenic differentiation of aged equine synovial fluid MSCs (SfMSCs) compared to young SfMSCs. Interestingly, mitophagy was distinctly observed only in aged SfMSCs, implying activation of mitophagy in aged MSCs [ 100 ]. Oxidative stress is closely involved in the fate of MSCs and the pathogenesis of age-related diseases.…”

Section: Conclusion and Future Prospectsmentioning

confidence: 99%

Mitophagy in degenerative joint diseases

et al. 2020

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Mitochondrial dysfunction is involved in aging and multiple degenerative diseases, including intervertebral disc degeneration (IVDD) and osteoarthritis (OA). Thus, the maintenance of mitochondria homeostasis and function is important. Mitophagy, a process that selectively clears damaged or dysfunctional mitochondria through autophagic machinery, functions to maintain mitochondrial quality control and homeostasis. IVDD and OA are similar joint diseases involving the degradation of cartilaginous tissues that are mainly caused by oxidative stress, cell apoptosis and extracellular matrix (ECM) degradation. Over the past decade, accumulating evidence indicates the essential role of mitophagy in the pathogenesis of IVDD and OA. Importantly, strategies by the regulation of mitophagy exert beneficial effects in the pre-clinical experiments. Given the importance and novelty of mitophagy, we provide an overview of mitophagy pathways and discuss the roles of mitophagy in IVDD and OA. We also highlight the potential of targeting mitophagy for the treatment of degenerative joint diseases.

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“…From a mechanistical point of view, in aging skeleton BM-MSCs show progressively decreased expression of the forkhead box protein P1 (FOXP1) gene, able to counteract expression of p16 [79], the archetypical cyclin dependent inhibitor (CKI) associated with senescence, also known to participate in terminal differentiation onset of several cellular lineages [99]. Indeed, MSCs derived from subjects with increasing age have a lower proliferation and differentiation capacity [100]. At the same time, MSCs derived from adipose tissue of obese subjects have lower self-renewal properties because of increased oxidative and metabolic stress.…”

Section: In Vivo Msc Senescencementioning

confidence: 99%

Molecular Mechanisms Contributing to Mesenchymal Stromal Cell Aging

Neri

Borzı̀

2020

Biomolecules

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Mesenchymal stem/stromal cells (MSCs) are a reservoir for tissue homeostasis and repair that age during organismal aging. Beside the fundamental in vivo role of MSCs, they have also emerged in the last years as extremely promising therapeutic agents for a wide variety of clinical conditions. MSC use frequently requires in vitro expansion, thus exposing cells to replicative senescence. Aging of MSCs (both in vivo and in vitro) can affect not only their replicative potential, but also their properties, like immunomodulation and secretory profile, thus possibly compromising their therapeutic effect. It is therefore of critical importance to unveil the underlying mechanisms of MSC senescence and to define shared methods to assess MSC aging status. The present review will focus on current scientific knowledge about MSC aging mechanisms, control and effects, including possible anti-aging treatments.

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Age-Related Alterations Affecting the Chondrogenic Differentiation of Synovial Fluid Mesenchymal Stromal Cells in an Equine Model

Cited by 17 publications

References 64 publications

Qiyusanlong Formula Induces Autophagy in Non-Small-Cell Lung Cancer Cells and Xenografts through the mTOR Signaling Pathway

Qiyusanlong Formula Induces Autophagy in Non-Small-Cell Lung Cancer Cells and Xenografts through the mTOR Signaling Pathway

Mitophagy in degenerative joint diseases

Molecular Mechanisms Contributing to Mesenchymal Stromal Cell Aging

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