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A Murine Pancreatic Islet Cell-based Screening for Diabetogenic Environmental Chemicals

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TRANSCRIPTIONAL AND PHOSPHO-PROTEOMIC SCREENS REVEAL STEM CELL ACTIVATION OF INSULIN-RESISTANCE AND TRANSFORMATION

R Mouzannar¹, J McCafferty, G Benedetto

¹UNC-Charlotte, Department of Biology and Bioinformatics Research Center, Charlotte, NC 28223.

International Journal of Genomics and Proteomics

|July 12, 2011

Summary

Even brief, non-toxic reactive oxidative species (ROS) exposure can trigger stem cell transformation. This study shows minimal ROS can induce insulin resistance and cancer signaling in stem cells, impacting disease development.

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Area of Science:

Cellular Biology
Oxidative Stress Research
Stem Cell Biology

Background:

Chronic elevated reactive oxidative species (ROS) are linked to diseases, cellular transformation, and tumor progression.
The impact of transient, minimally toxic ROS exposure on disease initiation remains unclear.

Purpose of the Study:

To investigate the transcriptional and phospho-proteomic responses of murine embryonic stem (ES) cells to brief, minimally toxic hydrogen peroxide (H2O2) exposure.
To determine if low-dose ROS can initiate disease or cellular transformation signaling.

Main Methods:

Murine embryonic stem (ES) cells were exposed to a single, brief, minimally toxic dose of hydrogen peroxide (H2O2).
Transcriptional and phospho-proteomic analyses were performed to assess cellular responses.
Responses were compared to those induced by acute H2O2 exposure and etoposide.

Main Results:

The cellular response to minimal H2O2 was distinct from acute H2O2 or etoposide.
Significant upregulation of oncogenes and downregulation of tumor suppressors were observed.
Insulin signaling induction, including insulin receptor hypophosphorylation, occurred, mirroring insulin resistance models and diabetic patients.

Conclusions:

Brief, non-toxic ROS exposure can induce insulin resistance and transformation signaling in stem cells.
Stem cells exhibit higher resistance to ROS and retain self-renewal signatures, suggesting greater potential for ROS-mediated mutagenesis.
These findings demonstrate a potential mechanism linking minimal ROS exposure to the development of diabetes and cancer.