In vitro 3-D model based on extending time of culture for studying chronological epidermis aging

Santos, Morgan Dos; Metral, Élodie; Boher, Aurélie; Rousselle, Patricia; Thépot, Amélie; Damour, O.

doi:10.1016/j.matbio.2015.03.009

Cited by 55 publications

(61 citation statements)

References 55 publications

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“…their replicative limit (Replicative Senescence). Several other studies have shown that treatments similar to the preaging conditions used in this study induce senescence and DNA damage in vitro: Replicative senescence is induced through multiple population doublings in various cell types (24)(25)(26); senescence associated with oxidative stress was exemplified in literature (27,28); and the chronological aging in a skin tissue equivalent has been shown in vitro (29). As control, we prepared tissues using the cells isolated from young animals and simply passaged twice in regular cell culture conditions (Young).…”

Section: Resultsmentioning

confidence: 78%

A Tissue Engineered Model of Aging: Interdependence and Cooperative Effects in Failing Tissues

Acun

Vural

Zorlutuna

2017

Sci Rep

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Aging remains a fundamental open problem in modern biology. Although there exist a number of theories on aging on the cellular scale, nearly nothing is known about how microscopic failures cascade to macroscopic failures of tissues, organs and ultimately the organism. The goal of this work is to bridge microscopic cell failure to macroscopic manifestations of aging. We use tissue engineered constructs to control the cellular-level damage and cell-cell distance in individual tissues to establish the role of complex interdependence and interactions between cells in aging tissues. We found that while microscopic mechanisms drive aging, the interdependency between cells plays a major role in tissue death, providing evidence on how cellular aging is connected to its higher systemic consequences.

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Section: Resultsmentioning

confidence: 78%

A Tissue Engineered Model of Aging: Interdependence and Cooperative Effects in Failing Tissues

Acun

Vural

Zorlutuna

2017

Sci Rep

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“…This stability has allowed culture periods as long as 60 wk (Hibiya et al, 2017), which can be used to study chronological aging in vitro. For example, 120 d of culture of reconstituted human epidermis led to increased cellular senescence and morphological changes resembling those of chronological skin aging in vivo (Dos Santos et al, 2015). Furthermore, genomic stability has been reported to be higher in organoids than in traditional cell Figure 1.…”

Section: Discussionmentioning

confidence: 99%

Opportunities for organoids as new models of aging

Todhunter

LaBarge

et al. 2017

Journal of Cell Biology

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“…Image processing and analysis were performed using ImageJ software, focusing on the following parameters: epidermal thickness for HPS‐stained sections, number of Ki67 and TGIF1 nucleus‐positive cells, and stained areas of filaggrin, loricrin and K10 immunostaining. Quantifications were performed as described previously …”

Section: Methodsmentioning

confidence: 99%

MicroRNA‐23b‐3p regulates human keratinocyte differentiation through repression of TGIF1 and activation of the TGF‐ß–SMAD2 signalling pathway

Barbollat-Boutrand

Joly‐Tonetti

Santos³

et al. 2016

Experimental Dermatology

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MicroRNAs (miRNAs) are a class of short non-coding RNAs capable of repressing gene expression at the post-transcriptional level. miRNAs participate in the control of numerous cellular mechanisms, including skin homeostasis and epidermal differentiation. However, few miRNAs involved in these processes have been identified so far in human skin, and the gene networks they control remain largely unknown. Here, we focused on miR-23b-3p, a miRNA that is expressed during the late step of human keratinocyte differentiation. We report that miR-23b-3p silencing modulates epidermal differentiation in human skin reconstructs. The SMAD transcriptional corepressor TGIF1 was identified on bioinformatic analysis as a potential target of miR-23b-3p. Expression analysis and reporter gene assays confirmed direct regulation of TGIF1 expression by miR-23b-3p. Finally, we showed that miR-23-3p was able to activate TGF-ß signalling in human keratinocytes by increasing SMAD2 phosphorylation through TGIF1 repression. Taken together, these data identify miR-23b-3p as a new regulator of human epidermal differentiation in line with TGF-ß signalling.

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In vitro 3-D model based on extending time of culture for studying chronological epidermis aging

Cited by 55 publications

References 55 publications

A Tissue Engineered Model of Aging: Interdependence and Cooperative Effects in Failing Tissues

A Tissue Engineered Model of Aging: Interdependence and Cooperative Effects in Failing Tissues

Opportunities for organoids as new models of aging

MicroRNA‐23b‐3p regulates human keratinocyte differentiation through repression of TGIF1 and activation of the TGF‐ß–SMAD2 signalling pathway

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