Telomerase activity and telomere on stem progeny senescence

Brazvan, Balal; Ebrahimi-Kalan, Abbas; Velaei, Kobra; Mehdipour, Ahmad; Serej, Zeynab Aliyari; Ebrahimi, Ayyub; Ghorbani, Mohammad; Cheraghi, Omid; Charoudeh, Hojjatollah Nozad

doi:10.1016/j.biopha.2018.02.073

Cited by 26 publications

(13 citation statements)

References 114 publications

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“…Because telomerase is helpful to lengthen telomere during DNA duplicate, its activity is an important parameter to evaluate cellular senescence [26]. Results showed that hyper-osmolarity culture significantly decreased telomerase activity compared with the in situ -osmolarity culture, whereas the NAC partly increased telomerase activity of NP cells in the hyper-osmolarity culture (Figure 3).…”

Section: Resultsmentioning

confidence: 99%

Hyper-osmolarity environment-induced oxidative stress injury promotes nucleus pulposus cell senescence in vitro

Yang

et al. 2019

Bioscience Reports

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Nucleus pulposus (NP) cell senescence is involved in disc degeneration. The in situ osmolarity within the NP region is an important regulator of disc cell’s biology. However, its effects on NP cell senescence remain unclear. The present study was aimed to investigate the effects and mechanism of hyper-osmolarity on NP cell senescence. Rat NP cells were cultured in the in situ-osmolarity medium and hyper-osmolarity medium. The reactive oxygen species (ROS) scavenger N-acetylcysteine (NAC) was added along with the medium to investigate the role of oxidative injury. Cell cycle, cell proliferation, senescence associated β-galactosidase (SA-β-Gal) activity, telomerase activity, expression of senescence markers (p16 and p53) and matrix molecules (aggrecan and collagen II) were tested to assess NP cell senescence. Compared with the in situ-osmolarity culture, hyper-osmolarity culture significantly decreased cell proliferation and telomerase activity, increased SA-β-Gal activity and cell fraction in the G0/G1 phase, up-regulated expression of senescence markers (p16 and p53) and down-regulated expression of matrix molecules (aggrecan and collagen II), and increased intracellular ROS accumulation. However, addition of NAC partly reversed these effects of hyper-osmolarity culture on cellular senescence and decreased ROS content in NP cells. In conclusion, a hyper-osmolarity culture promotes NP cell senescence through inducing oxidative stress injury. The present study provides new knowledge on NP cell senescence and helps us to better understand the mechanism of disc degeneration.

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Section: Resultsmentioning

confidence: 99%

Hyper-osmolarity environment-induced oxidative stress injury promotes nucleus pulposus cell senescence in vitro

Yang

et al. 2019

Bioscience Reports

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“…Most HSCs are in quiescent state under homeostasis, and cycle infrequently for self-renewal or to differentiate into multipotent progenitors (MPPs) and more committed progenitors, with limited self-renewal potential. Hematopoiesis is carefully regulated by both extrinsic and intrinsic mechanism(s), which balance quiescence, self-renewal and differentiation to support normal multi-lineage reconstitution [1][2][3]. In 1978, Ray Schofield first introduced the important regulatory role of bone marrow niche for HSCs.…”

Section: Introductionmentioning

confidence: 99%

Role of microvascular endothelial cells on proliferation, migration and adhesion of hematopoietic stem cells

et al. 2020

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Background: The present study investigated the effects of microvascular endothelial cells (MECs) on the chemotaxis, adhesion and proliferation of bone marrow hematopoietic stem cells (HSCs) ex vivo. Methods and Results: MECs were collected from the lung tissue of C57BL/6 mice, and HSCs were isolated with immunomagnetic beads from bone marrow of GFP mice. MECs and HSCs were co-cultured with or without having direct cell–cell contact in Transwell device for the measurement of chemotaxis and adhesion of MECs to HSCs. Experimental results indicate that the penetration rate of HSCs from the Transwell upper chamber to lower chamber in ‘co-culture’ group was significantly higher than that of ‘HSC single culture’ group. Also, the HSCs in co-culture group were all adherent at 24 h, and the co-culture group with direct cell–cell contact had highest proliferation rate. The HSC number was positively correlated with vascular endothelial growth factor (VEGF) and stromal cell-derived factor-1 (SDF-1) levels in supernatants of the culture. Conclusions: Our study reports that MECs enhance the chemotaxis, adhesion and proliferation of HSCs, which might be related to cytokines SDF-1 and VEGF secreted by MECs, and thus MECs enhance the HSC proliferation through cell–cell contact. The present study revealed the effect of MECs on HSCs, and provided a basis and direction for effective expansion of HSCs ex vivo.

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“…A number of studies have reported the increased detection of replicative senescence markers in BM-MSCs following culture in high glucose conditions, such as enhanced telomere shortening, positive SA-β-galactosidase staining and elevated expression of tumour suppressor (p53) and cyclin-dependent kinase inhibitor (p21 waf1 , p16 INK4a ) senescence marker genes [30–32, 37]. Consequently, we next asked whether the levels of these and other relevant telomere maintenance markers, rat telomerase (rTERT) and telomerase RNA (TR) [38], changed in CB-MSCs, following expansion over ~ 350 days in culture under normoglycaemic and hyperglycaemic conditions.…”

Section: Resultsmentioning

confidence: 99%

Effects of high glucose conditions on the expansion and differentiation capabilities of mesenchymal stromal cells derived from rat endosteal niche

Al-Qarakhli

Yusop

Waddington

et al. 2019

BMC Mol and Cell Biol

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BackgroundMesenchymal stromal cells in the endosteal niche lining compact bone (CB-MSCs) represent a heterogeneous population, all of which contribute to bone repair and remodelling. Hyperglycaemia associated with type 2 diabetes mellitus (T2DM) can delay and impair the bone healing process. Therefore, this study investigated the influences of high (25 mM) glucose conditions on CB-MSC populations isolated from male Wistar rats, versus normal (5.5 mM) glucose conditions; in terms of proliferation (population doublings, PDs), senescence characteristics, stem cell marker expression, colony forming efficiencies (CFEs); and osteogenic/adipogenic differentiation, following extended culture in vitro.ResultsCB-MSCs under both normoglycaemic and hyperglycaemic conditions demonstrated similar morphologies and rapid exponential growth to >300PDs, although high glucose conditions promoted more rapid and persistent proliferation beyond ~50PDs, with few indications of senescence. Limited senescence was confirmed by minimal SA-β-galactosidase staining, low senescence marker (p53, p21waf1, p16INK4a) expression and positive telomere maintenance marker (rTERT, TR) expression. However, telomere lengths varied throughout culture expansion, with hyperglycaemia significantly reducing telomere lengths at PD50 and PD200. Furthermore, CB-MSCs expanded in normal and high glucose conditions remained non-transformed, exhibiting similar MSC (CD73/CD90/CD105), multipotency (CD146) and embryonic (Slug, Snail) markers throughout extended culture, but negligible hematopoietic (CD34/CD45) or pluripotency (Nanog, Oct4) markers. Hyperglycaemia significantly increased CFEs at PD50 and PD100, which decreased at PD200. CB-MSC osteogenic differentiation was also inhibited by hyperglycaemia at PD15, PD100 and PD200, but not at PD50. Hyperglycaemia inhibited CB-MSC adipogenic differentiation to a lesser extent at PD15 and PD50, with reduced adipogenesis overall at PD100 and PD200.ConclusionThis study demonstrates the limited negative impact of hyperglycaemia on the proliferative and stem cell characteristics of heterogeneous CB-MSC populations, although minor sub-population(s) appear more susceptible to these conditions leading to impaired osteogenic/adipogenic differentiation capabilities. Such findings potentially highlight the impact of hyperglycaemia on CB-MSC bone repair capabilities in situ.

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Telomerase activity and telomere on stem progeny senescence

Cited by 26 publications

References 114 publications

Hyper-osmolarity environment-induced oxidative stress injury promotes nucleus pulposus cell senescence in vitro

Hyper-osmolarity environment-induced oxidative stress injury promotes nucleus pulposus cell senescence in vitro

Role of microvascular endothelial cells on proliferation, migration and adhesion of hematopoietic stem cells

Effects of high glucose conditions on the expansion and differentiation capabilities of mesenchymal stromal cells derived from rat endosteal niche

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