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Related Experiment Video

Updated: May 14, 2026

Detection of Nuclear Blebbing and DNA Leakage in Mammalian Cells by Immunofluorescence

Detection of Nuclear Blebbing and DNA Leakage in Mammalian Cells by Immunofluorescence

Published on: January 17, 2025

Longwave UV light induces the aging-associated progerin.

Hirotaka Takeuchi¹, Thomas M Rünger

¹Department of Dermatology, Boston University School of Medicine, Boston, Massachusetts, USA.

The Journal of Investigative Dermatology

|February 9, 2013

Summary

Ultraviolet A (UVA) radiation accelerates skin aging by inducing progerin, a protein linked to Hutchinson-Gilford progeria syndrome (HGPS). This UVA-induced progerin accumulation causes abnormal nuclear shapes, contributing to photoaging.

Related Experiment Videos

Last Updated: May 14, 2026

Detection of Nuclear Blebbing and DNA Leakage in Mammalian Cells by Immunofluorescence

Detection of Nuclear Blebbing and DNA Leakage in Mammalian Cells by Immunofluorescence

Published on: January 17, 2025

Area of Science:

Cell Biology
Dermatology
Genetics

Background:

Hutchinson-Gilford progeria syndrome (HGPS) involves premature aging due to LMNA gene mutations, leading to progerin accumulation and nuclear abnormalities.
Progerin accumulation is also observed in normal intrinsic aging, suggesting a link between HGPS and the aging process.

Purpose of the Study:

To investigate whether UV exposure accelerates progerin accumulation and abnormal nuclear shapes, contributing to skin photoaging.
To elucidate the mechanism by which UVA induces progerin expression and its role in photoaging.

Main Methods:

Cultured neonatal and aged fibroblasts were exposed to UVA or UVB radiation.
Progerin expression, nuclear morphology, and the role of oxidative damage were assessed.
The effect of a singlet oxygen quencher (sodium azide) was evaluated.

Main Results:

UVA, but not UVB, induced progerin expression and HGPS-like abnormal nuclear shapes in fibroblasts.
Aged cells showed a greater response to UVA compared to neonatal cells.
Progerin induction by UVA was mediated by oxidative damage and alternative splicing, suppressed by sodium azide.

Conclusions:

UVA exposure accelerates intrinsic aging processes by inducing progerin accumulation and nuclear abnormalities in skin cells.
Photoaging is partly a consequence of damage-accelerated intrinsic aging, mediated by UVA-induced oxidative stress.
This study reveals a novel pathway contributing to skin photoaging.