A prospect of cell immortalization combined with matrix microenvironmental optimization strategy for tissue engineering and regeneration

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Abstract

Cellular senescence is a major hurdle for primary cell-based tissue engineering and regenerative medicine. Telomere erosion, oxidative stress, the expression of oncogenes and the loss of tumor suppressor genes all may account for the cellular senescence process with the involvement of various signaling pathways. To establish immortalized cell lines for research and clinical use, strategies have been applied including internal genomic or external matrix microenvironment modification. Considering the potential risks of malignant transformation and tumorigenesis of genetic manipulation, environmental modification methods, especially the decellularized cell-deposited extracellular matrix (dECM)-based preconditioning strategy, appear to be promising for tissue engineering-aimed cell immortalization. Due to few review articles focusing on this topic, this review provides a summary of cell senescence and immortalization and discusses advantages and limitations of tissue engineering and regeneration with the use of immortalized cells as well as a potential rejuvenation strategy through combination with the dECM approach.

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Extension of life-span by introduction of telomerase into normal human cells.

A. G. Bodnar, M. Ouellette, M Frolkis … (1998)

Normal human cells undergo a finite number of cell divisions and ultimately enter a nondividing state called replicative senescence. It has been proposed that telomere shortening is the molecular clock that triggers senescence. To test this hypothesis, two telomerase-negative normal human cell types, retinal pigment epithelial cells and foreskin fibroblasts, were transfected with vectors encoding the human telomerase catalytic subunit. In contrast to telomerase-negative control clones, which exhibited telomere shortening and senescence, telomerase-expressing clones had elongated telomeres, divided vigorously, and showed reduced straining for beta-galactosidase, a biomarker for senescence. Notably, the telomerase-expressing clones have a normal karyotype and have already exceeded their normal life-span by at least 20 doublings, thus establishing a causal relationship between telomere shortening and in vitro cellular senescence. The ability to maintain normal human cells in a phenotypically youthful state could have important applications in research and medicine.

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Cellular survival: a play in three Akts.

S. R. Datta, A Brunet, M Greenberg (1999)

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Bmi-1 is required for maintenance of adult self-renewing haematopoietic stem cells.

In-kyung Park, Dalong Qian, Mark J. Kiel … (2003)

A central issue in stem cell biology is to understand the mechanisms that regulate the self-renewal of haematopoietic stem cells (HSCs), which are required for haematopoiesis to persist for the lifetime of the animal. We found that adult and fetal mouse and adult human HSCs express the proto-oncogene Bmi-1. The number of HSCs in the fetal liver of Bmi-1-/- mice was normal. In postnatal Bmi-1-/- mice, the number of HSCs was markedly reduced. Transplanted fetal liver and bone marrow cells obtained from Bmi-1-/- mice were able to contribute only transiently to haematopoiesis. There was no detectable self-renewal of adult HSCs, indicating a cell autonomous defect in Bmi-1-/- mice. A gene expression analysis revealed that the expression of stem cell associated genes, cell survival genes, transcription factors, and genes modulating proliferation including p16Ink4a and p19Arf was altered in bone marrow cells of the Bmi-1-/- mice. Expression of p16Ink4a and p19Arf in normal HSCs resulted in proliferative arrest and p53-dependent cell death, respectively. Our results indicate that Bmi-1 is essential for the generation of self-renewing adult HSCs.

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Author and article information

Contributors

Zuoqin Yan: zuoqin_yan@163.com

Ming Pei: 304-293-1072 , mpei@hsc.wvu.edu

Journal

Journal ID (nlm-ta): Cell Biosci

Journal ID (iso-abbrev): Cell Biosci

Title: Cell & Bioscience

Publisher: BioMed Central (London )

ISSN (Electronic): 2045-3701

Publication date (Electronic): 5 January 2019

Publication date PMC-release: 5 January 2019

Publication date Collection: 2019

Volume: 9

Electronic Location Identifier: 7

Affiliations

[1 ]ISNI 0000 0001 2156 6140, GRID grid.268154.c, Stem Cell and Tissue Engineering Laboratory, Department of Orthopaedics, , West Virginia University, ; PO Box 9196, 64 Medical Center Drive, Morgantown, WV 26506-9196 USA

[2 ]ISNI 0000 0004 1755 3939, GRID grid.413087.9, Department of Orthopaedics, , Zhongshan Hospital of Fudan University, ; 180 Fenglin Road, Shanghai, 200032 China

[3 ]ISNI 0000 0004 1764 5163, GRID grid.413855.e, Department of Orthopaedics, , Chengdu Military General Hospital, ; Chengdu, 610083 Sichuan China

[4 ]ISNI 0000 0001 2156 6140, GRID grid.268154.c, WVU Cancer Institute, Robert C. Byrd Health Sciences Center, , West Virginia University, ; Morgantown, WV 26506 USA

Article

Publisher ID: 264

DOI: 10.1186/s13578-018-0264-9

PMC ID: 6321683

PubMed ID: 30627420

SO-VID: 81e4c354-fb60-49ab-a22e-c3701225a5c7

License:

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

History

Date received : 18 September 2018

Date accepted : 21 December 2018

Funding

Funded by: FundRef http://dx.doi.org/10.13039/100000069, National Institute of Arthritis and Musculoskeletal and Skin Diseases;

Award ID: AR067747-01A1

Award Recipient : Ming Pei

Funded by: FundRef http://dx.doi.org/10.13039/100001765, Musculoskeletal Transplant Foundation;

Award ID: Established Investigator Award

Award Recipient : Ming Pei

Funded by: FundRef http://dx.doi.org/10.13039/501100001809, National Natural Science Foundation of China;

Award ID: 81672157

Award ID: 81601889

Award Recipient : Song Chen Zuoqin Yan

Custom metadata

ScienceOpen disciplines: Cell biology

Keywords: cell senescence,decellularized cell-deposited extracellular matrix,differentiation,immortalization,proliferation,sv40,tissue engineering

Data availability:

ScienceOpen disciplines: Cell biology

Keywords: cell senescence, decellularized cell-deposited extracellular matrix, differentiation, immortalization, proliferation, sv40, tissue engineering

A prospect of cell immortalization combined with matrix microenvironmental optimization strategy for tissue engineering and regeneration

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Abstract

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Stress signalling in stem cells

Most cited references 323

Extension of life-span by introduction of telomerase into normal human cells.

Cellular survival: a play in three Akts.

Bmi-1 is required for maintenance of adult self-renewing haematopoietic stem cells.

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