Cyclin-dependent kinase inhibitor p16INK4a and telomerase may co-modulate endothelial progenitor cells senescence

Yang, Deguang; Liu, Ling; Zheng, Xiao‐Yan

doi:10.1016/j.arr.2008.02.001

Cited by 48 publications

(38 citation statements)

References 85 publications

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“…Our data also showed that shikonin increased expression of p16, further contributing to inhibition of phosphorylation of Rb in both K1 and FTC133 cells, and NAC dramatically abolished this effect. These observations suggest that shikonin inhibits cell growth by modulating the activity of the p16/Rb/E2 factor (E2F) pathway, as supported by previous studies showing that ROS-induced upregulation of p16 is one of the mechanisms regulating senescence, which keeps the balance between regeneration and cancer (34,35). Given that metastasis is the major cause of cancer-related death, we investigated the effect of shikonin on cell migration and invasion in this study.…”

Section: Discussionmentioning

confidence: 70%

Shikonin Inhibits Thyroid Cancer Cell Growth and Invasiveness Through Targeting Major Signaling Pathways

Yang

Guan

et al. 2013

The Journal of Clinical Endocrinology & Metabolism

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Section: Discussionmentioning

confidence: 70%

Shikonin Inhibits Thyroid Cancer Cell Growth and Invasiveness Through Targeting Major Signaling Pathways

Yang

Guan

et al. 2013

The Journal of Clinical Endocrinology & Metabolism

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“…Cellular senescence of endothelial progenitor cells (EPCs), vascular endothelial cells (VECs) and vascular smooth muscle cells (VSMCs) have all been suggested to have causal roles in the development of atherosclerosis (Yang et al, 2008, Minamino et al, 2008, Matthews et al, 2006. This may be due to an impaired ability to replace damaged/lost cells due to senescent EPCs, the reduced proliferative capacity of these tissues owing to the presence of senescent cells, the altered cellular phenotype of the senescent cells, the changed tissue microenvironment of the artery due to the different spectrum of proteins secreted by senescent cells, or a combination of all four.…”

Section: Discussionmentioning

confidence: 99%

“…Many studies have investigated the potential role of cellular senescence in the development and progression of disease, including atherosclerosis (Burton, 2009, Erusalimsky, 2009). Senescence in endothelial progenitor cells (EPCs), vascular endothelial cells (VECs) and vascular smooth muscle cells (VSMCs) have all been implicated in the development and progression of atherosclerosis (Yang et al, 2008, Minamino et al, 2008, Matthews et al, 2006. However, the majority the of work on cellular senescence has been carried out on fibroblasts, with limited understanding of the phenotype of many other cell types, especially those linked to age-related pathology.…”

Section: Introductionmentioning

confidence: 99%

Microarray analysis of senescent vascular smooth muscle cells: A link to atherosclerosis and vascular calcification

Burton¹,

Giles²,

Sheerin³

et al. 2009

Experimental Gerontology

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International audienceLittle is known about the senescent phenotype of human vascular smooth muscle cells (VSMCs) and the potential involvement of senescent VSMCs in age-related vascular disease, such as atherosclerosis. As such, VSMCs were grown and characterised to generate senescent VSMCs needed for microarray analysis (Affymetrix). Comparative analysis of the transcriptome profiles of early (14 CPD) and late (39-42 CPD) passage VSMCs found a total of 327 probesets called as differentially expressed: 149 are up-regulated in senescence and 178 repressed (-value < 0.5%, minimum effect size of at least 2-fold differential regulation, explore data at www.madras.cf.ac.uk/vsmc). Data mining shows a differential regulation of genes at senescence associated with the development of atherosclerosis and vascular calcification. These included genes with roles in inflammation (IL1β, IL8, ICAM1, TNFAP3, ESM1 and CCL2), tissue remodelling (VEGF, VEGFβ, ADM and MMP14) and vascular calcification (MGP, BMP2, SPP1, OPG and DCN). The microarray data for IL1β, IL8 and MGP were validated by either, ELISA, Western blot analysis or RT-PCR. These data thus provide the first evidence for a role of VSMC senescence in the development of vascular calcification and provides further support for the involvement of senescent VSMCs in the progression of atherosclerosis

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“…Primary diploid cells have limited lifespan before reaching permanent growth arrest called replicative senescence. 42 We here show that onset of replicative senescence in EPCs is delayed compared to HUVECs. However, after 60-80 days of continuous culture, they are also prone to loss of proliferation rate.…”

Section: Discussionmentioning

confidence: 82%

Immortalized Functional Endothelial Progenitor Cell Lines from Umbilical Cord Blood for Vascular Tissue Engineering

Sobhan

Seervi²,

Joseph³

et al. 2012

Tissue Engineering Part C: Methods

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Endothelial progenitor cells (EPCs) play a significant role in multiple biological processes such as vascular homeostasis, regeneration, and tumor angiogenesis. This makes them a promising cell of choice for studying a variety of biological processes, toxicity assays, biomaterial-cell interaction studies, as well as in tissueengineering applications. In this study, we report the generation of two clones of SV40-immortalized EPCs from umbilical cord blood. These cells retained most of the functional features of mature endothelial cells and showed no indication of senescence after repeated culture for more than 240 days. Extensive functional characterization of the immortalized cells by western blot, flow cytometry, and immunofluorescence studies substantiated that these cells retained their ability to synthesize nitric oxide, von Willebrand factor, P-Selectin etc. These cells achieved unlimited proliferation potential subsequent to inactivation of the cyclin-dependent kinase inhibitor p21, but failed to form colonies on soft agar. We also show their enhanced growth and survival on vascular biomaterials compared to parental cultures in late population doubling. These immortalized EPCs can be used as a cellular model system for studying the biology of these cells, gene manipulation experiments, cell-biomaterial interactions, as well as a variety of tissue-engineering applications.

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Cyclin-dependent kinase inhibitor p16INK4a and telomerase may co-modulate endothelial progenitor cells senescence

Cited by 48 publications

References 85 publications

Shikonin Inhibits Thyroid Cancer Cell Growth and Invasiveness Through Targeting Major Signaling Pathways

Shikonin Inhibits Thyroid Cancer Cell Growth and Invasiveness Through Targeting Major Signaling Pathways

Microarray analysis of senescent vascular smooth muscle cells: A link to atherosclerosis and vascular calcification

Immortalized Functional Endothelial Progenitor Cell Lines from Umbilical Cord Blood for Vascular Tissue Engineering

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