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Cells
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Cellular Plasticity in Ageing
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Cellular Plasticity in Ageing

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Aging".

Deadline for manuscript submissions: closed (20 September 2022) | Viewed by 2521

Special Issue Editor

Dr. Han Li

E-Mail Website
Guest Editor
Cellular Plasticity and Disease Modelling, Department of Developmental and Stem Cell Biology, CNRS UMR 3738, Institut Pasteur, 25 Rue du Dr Roux, 75015 Paris, France
Interests: cellular senescence; in vivo reprogramming; cellular plasticity; tissue regeneration; cancer; ageing

Special Issue Information

Dear Colleagues,

Ageing is characterized by gradual functional decline and is associated with a dramatic increase in the risk of many diseases. Moreover, it has been recognized that ageing may be the underlying driving force behind many disorders. Cellular plasticity is the ability of a cell to acquire a new identity and adopt an alternative fate. Breakthroughs in the cellular reprogramming field have revealed that terminal differentiated cells can be experimentally induced to change their identities, highlighting the remarkable plasticity of differentiated cells both in vitro and in vivo and the exciting implications for regenerative medicine. Moreover, recent studies have demonstrated that certain somatic cells can acquire plasticity under physiological and pathological conditions, contributing significantly to tissue repair and disease development, especially tumorigenesis. 

This Special Issue is focused on cellular plasticity in ageing and seeks original research and review articles with a focus on:

  1. Mechanisms for cellular plasticity regulation.
  2. The impact of ageing on cellular plasticity in the context of tissue regeneration and cancer.
  3. How to modulate plasticity for rejuvenation on the cellular, tissue, and organism level.

Dr. Han Li
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • ageing
  • cellular plasticity
  • stem cell
  • tissue regeneration
  • cancer
  • rejuvenation
  • reprogramming
  • cellular senescence
  • regenerative medicine

Published Papers (1 paper)

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Research

17 pages, 4819 KiB  
Article
Paracrine Senescence of Mesenchymal Stromal Cells Involves Inflammatory Cytokines and the NF-κB Pathway
by Lun-Yin Chou, Chun-Te Ho and Shih-Chieh Hung
Cells 2022, 11(20), 3324; https://doi.org/10.3390/cells11203324 - 21 Oct 2022
Cited by 13 | Viewed by 1975
Abstract
It has been known that senescence-associated secretory phenotype (SASP) triggers senescence of the surrounding normal cells. However, SASP signaling regarding mesenchymal stromal cell aging remains to be fully elucidated. Therefore, the present study aimed to clarify the molecular mechanism of late (passage) MSC-induced [...] Read more.
It has been known that senescence-associated secretory phenotype (SASP) triggers senescence of the surrounding normal cells. However, SASP signaling regarding mesenchymal stromal cell aging remains to be fully elucidated. Therefore, the present study aimed to clarify the molecular mechanism of late (passage) MSC-induced paracrine SASP-mediated senescence of early (passage) MSCs during ex vivo expansion. Here, we conducted an extensive characterization of senescence features in bone-marrow (BM)-derived MSCs from healthy human donors. Late MSCs displayed an enlarged senescent-like morphology, induced SASP-related proinflammatory cytokines (IL-1α and IL-8), and reduced clonogenic capacity and osteogenic differentiation when compared to early MSCs. Of note, paracrine effects of SASP-related IL-1α and IL-8 from late MSCs induced cellular senescence of early MSCs via an NF-κB-dependent manner. Moreover, cellular senescence of early MSCs was promoted by the synergistic action of IL-1α and IL-8. However, inhibition of NF-κB by shRNA transfection or using inhibitors in early MSCs blocked early MSCs cellular senescence caused by paracrine SASP of late MSCs. In conclusion, these findings reveal that late MSCs display features of senescence and that, during ex vivo expansion, SASP-related proinflammatory cytokines contribute to activate a cellular senescence program in early MSCs that may ultimately impair their functionality. Full article
(This article belongs to the Special Issue Cellular Plasticity in Ageing)
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