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LincRNA-EPS Promotes Proliferation of Aged Dermal Fibroblast by Inducing CCND1
Liping Zhang1, Iris C Wang1,2, Songmei Meng1
1Department of Physiology, College of Medicine, University of Tennessee Health Science Center, Memphis, TN 38163, USA.
International Journal of Molecular Sciences
|July 27, 2024
Summary
Reduced long intergenic non-coding RNA (lincRNA)-EPS in aged skin cells impairs healing. Restoring lincRNA-EPS boosts cell division and Cyclin D1, offering a potential therapeutic target for wound repair.
Area of Science:
- Molecular Biology
- Cell Biology
- Dermatology
Background:
- Aging alters dermal fibroblast function, impacting skin wound healing.
- Reduced cell proliferation is characteristic of aged dermal fibroblasts.
- The role of long intergenic non-coding RNAs (lincRNAs), specifically LincRNA-EPS, in aged fibroblasts is not well understood.
Purpose of the Study:
- To investigate the role of LincRNA-EPS in aged dermal fibroblasts.
- To determine the effect of LincRNA-EPS on cell cycle regulator Cyclin D1 (CCND1) and cell proliferation.
- To explore the potential of LincRNA-EPS as a therapeutic target for age-related skin wound healing.
Main Methods:
- Primary dermal fibroblasts were isolated from young and aged mice.
- LincRNA-EPS was overexpressed using plasmid transfection.
- Cell proliferation was assessed via MTT assay, and gene expression was quantified using real-time PCR.
Main Results:
- Aged dermal fibroblasts showed decreased LincRNA-EPS expression, lower CCND1 levels, and reduced proliferation.
- Overexpression of LincRNA-EPS in aged fibroblasts upregulated CCND1 and significantly increased cell proliferation.
- LincRNA-EPS promotes CCND1 expression by sequestering miR-34a and targeting CCND1.
Conclusions:
- LincRNA-EPS is crucial for regulating CCND1 and promoting proliferation in aged dermal fibroblasts.
- Reduced LincRNA-EPS contributes to impaired wound healing in aged skin.
- LincRNA-EPS represents a promising therapeutic target for improving age-related skin wound healing.
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