AI Article Synopsis
- Sestrin2 plays a role in cellular responses to stress, but its impact on the cardiovascular system was previously unknown.
- In studies with macrophage cells, oxLDL was found to increase Sestrin2 expression, and silencing Sestrin2 led to higher cell apoptosis and reactive oxygen species production.
- The research indicates that the JNK/c-Jun signaling pathway is involved in the regulation of Sestrin2, suggesting that boosting its expression could be a potential treatment strategy for lipid-related cardiovascular issues.
Article Abstract
Sestrin2 is involved in a different cellular response to stress conditions. However, the function of Sestrin2 in the cardiovascular system remains unknown. In the present study, we tested whether Sestrin2 has a beneficial effect on macrophage cell apoptosis induced by oxidized low-density lipoprotein (oxLDL). We found that oxLDL induces expression of Sestrin2 in RAW264.7 cells in a time-dependent and dose-dependent manner. We also found that knockdown of Sestrin2 using small RNA interference promotes cell apoptosis and reactive oxygen species production induced by oxLDL. In addition, our results show that the c-Jun NH(2)-terminal kinase (JNK)/c-Jun pathway is activated by oxLDL. Inhibiting the activity of the JNK pathway abolishes the increase of Sestrin2 induced by oxLDL. These findings suggest that the inductive effect of Sestrin2 is mediated by the JNK/c-Jun pathway. Our results indicate that the induction of Sestrin2 acts as a compensatory response to oxLDL for survival, implying that stimulating expression of Sestrin2 might be an effective pharmacological target for the treatment of lipid-related cardiovascular diseases.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4390166 | PMC |
| http://dx.doi.org/10.1089/dna.2014.2627 | DOI Listing |
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