UV, stress and aging

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Abstract

Skin is a model of choice in studies on aging. Indeed, skin aging can be modulated by internal and external factors, reflecting its complexity. Two types of skin aging have been identified: intrinsic, mainly genetically determined and extrinsic—also called "photo-aging"—resulting on the impact of environmental stress and more precisely of UV rays. Simplified in vitro models, based on cellular senescence, have been developed to study the relationship between UV and aging. These models vary on the cell type (fibroblasts or keratinocytes, normal or immortalized) and the type of UV used (UVA or UVB).

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DNA damage foci at dysfunctional telomeres.

Hiroyuki Takai, Agata Smogorzewska, Titia de Lange (2003)

We report cytologic and genetic data indicating that telomere dysfunction induces a DNA damage response in mammalian cells. Dysfunctional, uncapped telomeres, created through inhibition of TRF2, became associated with DNA damage response factors, such as 53BP1, gamma-H2AX, Rad17, ATM, and Mre11. We refer to the domain of telomere-associated DNA damage factors as a Telomere Dysfunction-Induced Focus (TIF). The accumulation of 53BP1 on uncapped telomeres was reduced in the presence of the PI3 kinase inhibitors caffeine and wortmannin, which affect ATM, ATR, and DNA-PK. By contrast, Mre11 TIFs were resistant to caffeine, consistent with previous findings on the Mre11 response to ionizing radiation. A-T cells had a diminished 53BP1 TIF response, indicating that the ATM kinase is a major transducer of this pathway. However, in the absence of ATM, TRF2 inhibition still induced TIFs and senescence, pointing to a second ATM-independent pathway. We conclude that the cellular response to telomere dysfunction is governed by proteins that also control the DNA damage response. TIFs represent a new tool for evaluating telomere status in normal and malignant cells suspected of harboring dysfunctional telomeres. Furthermore, induction of TIFs through TRF2 inhibition provides an opportunity to study the DNA damage response within the context of well-defined, physically marked lesions.

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Making sense of latent TGFbeta activation.

Justin Annes, John Munger, Daniel Rifkin (2003)

TGFbeta is secreted as part of a latent complex that is targeted to the extracellular matrix. A variety of molecules, 'TGFbeta activators,' release TGFbeta from its latent state. The unusual temporal discontinuity of TGFbeta synthesis and action and the panoply of TGFbeta effects contribute to the interest in TGF-beta. However, the logical connections between TGFbeta synthesis, storage and action are obscure. We consider the latent TGFbeta complex as an extracellular sensor in which the TGFbeta propeptide functions as the detector, latent-TGFbeta-binding protein (LTBP) functions as the localizer, and TGF-beta functions as the effector. Such a view provides a logical continuity for various aspects of TGFbeta biology and allows us to appreciate TGFbeta biology from a new perspective.

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How cells read TGF-beta signals.

J Massagué (2000)

Cell proliferation, differentiation and death are controlled by a multitude of cell-cell signals, and loss of this control has devastating consequences. Prominent among these regulatory signals is the transforming growth factor-beta (TGF-beta) family of cytokines, which can trigger a bewildering diversity of responses, depending on the genetic makeup and environment of the target cell. What are the networks of cell-specific molecules that mould the TGF-beta response to each cell's needs?

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Author and article information

Journal

Journal ID (nlm-ta): Dermatoendocrinol

Journal ID (iso-abbrev): Dermatoendocrinol

Journal ID (publisher-id): DERM

Title: Dermato-endocrinology

Publisher: Landes Bioscience

ISSN (Print): 1938-1972

ISSN (Electronic): 1938-1980

Publication date (Print): 01 July 2012

Publication date PMC-release: 01 July 2012

Volume: 4

Issue: 3

Pages: 236-240

Affiliations

Research Unit of Cellular Biology (URBC); NARILIS; University of Namur (FUNDP); Namur, Belgium

Author notes

[* ]Correspondence to: Florence Debacq-Chainiaux, Email: florence.chainiaux@ 123456fundp.ac.be

Article

Publisher ID: 2012DE0198R Publisher Item ID: 23652

DOI: 10.4161/derm.23652

PMC ID: 3583883

PubMed ID: 23467762

SO-VID: 39643ef5-3db2-426e-9a7f-e1bd9c4939db

License:

This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.

UV, stress and aging

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Karger: Dermatology

Most cited references 55

DNA damage foci at dysfunctional telomeres.

Making sense of latent TGFbeta activation.

How cells read TGF-beta signals.

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