PTPRN2 CpG Methylation Biomarker for Oxidative Stress Detection
Find Innovative SolutionsGenerate Solutions
Solution Overview
Problem
Existing methods fail to effectively detect oxidative stress in cells, particularly due to UV light exposure and aging, which can lead to cellular damage and DNA fragmentation, without using genomic samples.
Innovation Solution
A method utilizing differential methylation of CpG sites in the Protein Tyrosine Phosphatase Receptor Type N2 (PTPRN2) gene to identify oxidative stress, specifically through determining the methylation status of pre-selected CpG sites using bisulfite sequencing or TET-assisted pyridine borane sequencing.
Engineering Contradictions & Design Principles
Engineering Contradiction Analysis
1Measurement precision
If existing methods are used for early detection of oxidative stress, then detection capability is limited, but the inability to use genomic samples prevents accurate and specific detection of OS in cells
Solution Approach 1:
The invention changes the detection parameter from general oxidative stress markers to specific DNA methylation patterns at CpG sites in the PTPRN2 gene. This parameter change enables accurate detection of oxidative stress using genomic samples, as methylation status serves as a specific biomarker that reflects oxidative stress conditions while being detectable in DNA-based assays
2Measurement precision
If differential methylation of PTPRN2 is used to detect oxidative stress, then detection precision is improved, but the complexity of the method increases due to requiring specific genomic analysis
Solution Approach 1:
The invention extracts and focuses on a specific, detectable feature (DNA methylation status at CpG sites in PTPRN2) from the complex biological system. By isolating this particular epigenetic marker, the method achieves high detection precision while simplifying the overall approach to a single biomarker assay rather than requiring analysis of multiple complex parameters
Solution Approach 2:
The invention uses DNA methylation patterns as a copy or surrogate marker of oxidative stress damage. Instead of directly measuring oxidative stress parameters, the method detects the epigenetic copy left by oxidative stress on the PTPRN2 gene, which serves as a stable and detectable representation of the stress condition
Applied Scientific Principles
This section explains which scientific principles are used to turn an abstract innovation direction into a practical engineering solution.
Function Achieved in This Case
Enables early detection of oxidative stress caused by UV light exposure and aging, allowing for timely intervention to prevent further cellular damage, with the biomarker being inheritable and applicable across generations.
Implementation Method 1
determining the methylation status of pre-selected CpG sites using bisulfite sequencing or TET-assisted pyridine borane sequencing
Implementation Method 2
determining the methylation status of pre-selected CpG sites using bisulfite sequencing or TET-assisted pyridine borane sequencing
Data Source
Figure 1~2
Figure 3~4
Figure 5~6
AI summary
The present invention is related to a method of identifying oxidative stress (OS) caused by ageing and/or Ultraviolet (UV) light exposure in a test cell, comprising (a) determining the methylation status of at least one CpG site in Protein Tyrosine Phosphatase Receptor Type N2 (PTPRN2), and/or the regulatory region of PTPRN2 in a DNA sample obtained from the test cell, (b) comparing the methylation status of the CpG site of PTPRN2 from (a) with that of a control without OS caused by ageing and/or UV light exposure, wherein a difference in the methylation status of the CpG site of PTPRN2, and/or the regulatory region of PTPRN2 in the test cell compared to the CpG site in the control is indicative of the test cell having OS caused by exposure of the cell to UV light and/or ageing.