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Describing a Transcription Factor Dependent Regulation of the MicroRNA Transcriptome
Published on: June 15, 2016
MicroRNA-29a promotes apoptosis of monocytes by targeting STAT3 during sepsis
1Department of ICU, Shengli Hospital of Shandong University, Shandong, China.
Abstract:
Sepsis is a major cause of morbidity and mortality in critically ill patients. The sepsis syndrome results from a dysregulated inflammatory response to infection that leads to multiple-organ failure, but the underlying mechanisms remain poorly understood. More and more reports show that microRNAs (miRNAs) play an important role in sepsis. In the progression of this syndrome, cells change their behavior in response to cytokines stimulated by sepsis, such as interleukin-10 (IL-10). IL-10 can activate JAK2-STAT3 in the cells to protect them from damage. miR-29a is a potential miRNA directly targeting STAT3. In this study, we investigate the role of miR-29a in targeting STAT3 during sepsis. When cells were treated with IL-10, STAT3 was activated in monocytes, as determined using western blotting. It was verified that STAT3 was a new target gene of miR-29a. miR-29a could inhibit IL-10-induced cytokine release by targeting JAK-STAT3 in monocytes. In conclusion, this study demonstrates for the first time that miR-29a inhibits STAT3 in human monocytes during sepsis.
Insights
MicroRNAs (miRNAs) like miR-29a play a key role in sepsis. This study shows miR-29a targets STAT3, inhibiting inflammation in monocytes during sepsis.
Area of Science:
- Molecular Biology
- Immunology
- Critical Care Medicine
Background:
- Sepsis is a life-threatening condition causing organ failure due to dysregulated inflammation.
- MicroRNAs (miRNAs) are increasingly recognized for their role in sepsis pathogenesis.
- Interleukin-10 (IL-10) activates the JAK2-STAT3 pathway, offering cellular protection during sepsis.
Purpose of the Study:
- To investigate the role of miR-29a in targeting STAT3 during sepsis.
- To elucidate the mechanism by which miR-29a influences IL-10-induced responses in monocytes.
Main Methods:
- Western blotting was used to assess STAT3 activation in monocytes treated with IL-10.
- Experimental verification confirmed STAT3 as a direct target gene of miR-29a.
- The impact of miR-29a on IL-10-induced cytokine release was analyzed.
Main Results:
- Interleukin-10 (IL-10) treatment activated STAT3 in human monocytes.
- STAT3 was identified as a novel target gene of miR-29a.
- miR-29a was shown to inhibit IL-10-induced cytokine release by targeting the JAK-STAT3 pathway in monocytes.
Conclusions:
- This study establishes miR-29a as an inhibitor of STAT3 in human monocytes during sepsis.
- miR-29a plays a regulatory role in the inflammatory response to sepsis via the JAK-STAT3 pathway.
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