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The RXFP3 receptor is functionally associated with cellular responses to oxidative stress and DNA damage
Jaana van Gastel1,2, Hanne Leysen1,2, Paula Santos-Otte3
1Receptor Biology Lab, Department of Biomedical Sciences, University of Antwerp, Antwerp, Belgium.
Aging
|December 4, 2019
Summary
The relaxin family peptide 3 receptor (RXFP3) and GIT2 protein regulate cellular responses to DNA damage and oxidative stress, offering potential targets for anti-aging therapies.
Area of Science:
- Cellular Biology
- Molecular Biology
- Aging Research
Background:
- DNA damage response (DDR) and oxidative stress are implicated in aging and related disorders.
- G protein-coupled receptor (GPCR) kinase interacting protein 2 (GIT2) is crucial in DNA damage and oxidative stress pathways.
- GIT2 influences the expression of the GPCR relaxin family peptide 3 receptor (RXFP3), suggesting a potential therapeutic target.
Purpose of the Study:
- To elucidate the functional relationship between RXFP3 and GIT2 in the context of oxidative stress and DDR.
- To explore the potential of the RXFP3-GIT2 system as a therapeutic target for mitigating age-related damage.
Main Methods:
- Affinity Purification-Mass Spectrometry was used to identify RXFP3 interacting partners under oxidative (H2O2) and DNA-damaging (camptothecin) stress.
- Analysis of GIT2 knockout (GIT2KO) mice tissues to assess GIT2 expression effects on RXFP3.
- Investigated the impact of RXFP3 stimulation on DNA damage markers (H2AX, BRCA1).
Main Results:
- Multiple proteins involved in DDR and cell cycle control were identified as RXFP3 interacting partners.
- RXFP3 expression levels were found to increase following DNA damage.
- Relaxin 3-mediated stimulation of RXFP3 reduced the phosphorylation of DNA damage markers H2AX and BRCA1, indicating moderation of DNA damage.
Conclusions:
- The study suggests an RXFP3-GIT2 system that plays a role in regulating cellular degradation following DNA damage.
- This RXFP3-GIT2 pathway represents a novel mechanism for potentially slowing the accumulation of age-related cellular damage.
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