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Published on: April 22, 2017
Regulation of tissue transglutaminase gene expression as a molecular model for retinoid effects on proliferation and
E A Chiocca1, P J Davies, J P Stein
1Department of Internal Medicine, University of Texas Medical School, Houston 77225.
Abstract:
Retinoids (structural and functional analogs of vitamin A) are potent antiproliferative agents whose mode of action is poorly understood. It has been suggested that the molecular events that underscore their action involve alterations in gene expression, but no gene has yet been shown to be directly regulated by these molecules. Several years ago, we found that retinoic acid caused an accumulation of the enzyme tissue transglutaminase in murine peritoneal macrophages and in human promyelocytic leukemia (HL-60) cells. We now report that this induction is caused by an increase in the mRNA for this enzyme. Retinoic acid is the only mediator of this induction, since its effects do not depend on the presence of serum proteins. The induction of tissue transglutaminase mRNA is not due to an increase in its stability but to an increase in the relative transcription rate of its gene. We present a model to correlate the retinoid induction of tissue transglutaminase with retinoid effects on cellular growth and differentiation.
Insights
Retinoids, vitamin A analogs, increase tissue transglutaminase mRNA by boosting gene transcription. This finding offers insights into retinoid action on cell growth and differentiation.
Area of Science:
- Molecular Biology
- Cell Biology
- Biochemistry
Background:
- Retinoids are vitamin A analogs with antiproliferative effects.
- The precise molecular mechanisms of retinoid action, particularly gene regulation, remain unclear.
- Previous studies indicated retinoids increase tissue transglutaminase enzyme levels.
Purpose of the Study:
- To elucidate the molecular mechanism behind retinoid-induced accumulation of tissue transglutaminase.
- To determine if retinoids directly regulate gene expression of tissue transglutaminase.
- To establish a model linking retinoid-induced tissue transglutaminase expression to cellular effects.
Main Methods:
- Quantification of tissue transglutaminase mRNA levels in response to retinoic acid.
- Assessment of mRNA stability and gene transcription rates.
- Cellular studies using murine peritoneal macrophages and human promyelocytic leukemia (HL-60) cells.
Main Results:
- Retinoic acid significantly increases tissue transglutaminase mRNA levels.
- This induction is mediated solely by retinoic acid, independent of serum proteins.
- The increase in mRNA results from enhanced gene transcription, not altered mRNA stability.
- Retinoid effects are not dependent on serum proteins.
Conclusions:
- Retinoic acid directly upregulates tissue transglutaminase gene transcription.
- This provides a direct link between retinoid action and specific gene expression changes.
- A model is proposed to connect retinoid-induced tissue transglutaminase expression with cellular growth and differentiation.
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