miRNA-144 induces microglial autophagy and inflammation following intracerebral hemorrhage
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Updated: Mar 9, 2026
Detection of MicroRNAs in Microglia by Real-time PCR in Normal CNS and During Neuroinflammation
Published on: July 23, 2012
Anyong Yu1, Tianxi Zhang1, Wenyi Zhong1
1Department of Emergency, The First Affiliated Hospital of Zunyi Medical College, Guizhou 563003, China.
Abstract:
Autophagic activation mediated inflammation contributes to brain injury of intracerebral hemorrhage (ICH). MiRNAs play a key role in inflammation, which negatively and posttranscriptionally regulate gene expression and function. Modulating the mTOR signal, a central regulator of autophagy, could be of great significance for ICH. However, the specific of miRNA is unknown. In the current study, we detected the miRNA-144 expression, autophagic activity and inflammation of microglia in ICH. We also knocked down endogenous miRNA-144 to regulate autophagy and inflammation in ICH. In addition, we assessed the neurological damge in ICH mice. We found that ICH promoted miRNA-144 expression but downregulated mTOR expression. In addition, upregulation of mTOR attenuated microglial autophagy and inflammation in ICH. Furthermore, downregulation of miRNA-144 also inhibited inflammation, brain edema and improved neurological functions in ICH mice. Taken together, our findings suggested that miRNA-144 was a crucial regulator of autophagy via regulation of mTOR, and represented a promising therapeutical strategy for ICH.
Insights
This study reveals miRNA-144 exacerbates brain injury in intracerebral hemorrhage (ICH) by activating autophagy and inflammation. Downregulating miRNA-144 shows therapeutic potential for ICH treatment.
Area of Science:
- Neuroscience
- Molecular Biology
- Cell Biology
Background:
- Autophagic activation and inflammation are key contributors to brain injury following intracerebral hemorrhage (ICH).
- MicroRNAs (miRNAs) are critical regulators of inflammatory processes, acting posttranscriptionally.
- The mTOR signaling pathway is a central regulator of autophagy and a potential therapeutic target for ICH.
Purpose of the Study:
- To investigate the role of miRNA-144 in regulating autophagy and inflammation in the context of ICH.
- To explore the relationship between miRNA-144, mTOR signaling, and microglial activity in ICH.
- To assess the therapeutic potential of modulating miRNA-144 for ICH treatment.
Main Methods:
- Detection of miRNA-144 expression, autophagic activity, and microglial inflammation in ICH models.
- Knockdown of endogenous miRNA-144 to modulate autophagy and inflammation.
- Assessment of neurological damage and brain edema in ICH mouse models.
Main Results:
- ICH promoted miRNA-144 expression while downregulating mTOR.
- Upregulation of mTOR attenuated microglial autophagy and inflammation in ICH.
- Downregulation of miRNA-144 inhibited inflammation, reduced brain edema, and improved neurological function in ICH mice.
Conclusions:
- miRNA-144 is a critical regulator of autophagy through mTOR signaling in ICH.
- Targeting miRNA-144 presents a promising therapeutic strategy for mitigating brain injury in intracerebral hemorrhage.
