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Updated: Nov 8, 2025
Imaging Mitochondrial Ca2+ Uptake in Astrocytes and Neurons using Genetically Encoded Ca2+ Indicators GECIs
Published on: January 22, 2022
Interaction between miRNA-155 targeting neuronal pacemaker ion channels and release of amino acid transmitters during
1Department of Neurology, Qingdao Hospital of Traditional Chinese Medicine (Qingdao Hiser Hospital), Qingdao, Shandong, China. 65090218@sdutcm.edu.cn.
Objective:
Cerebral hemorrhage can cause hemorrhagic stroke, leading to severe brain damage. MiRNA-155 is closely related to the development of stroke. However, the regulatory mechanism of miRNA-155 during cerebral ischemia has not yet been elucidated.
Materials And Methods:
SD rats were separated to sham operation group, model group, miRNA-155 inhibitor group and miRNA-155 agonist group followed by analysis of neural function, miRNA-155 and pacemaker ion channel hyperpolarization-activated, cyclic nucleotide-gated (HCN) expression by Real Time PCR. Meanwhile, Caspase 3 activity, glutamic acid (Glu) and γ-aminobutyric acid (GABA) content were also measured along with analysis of IL-6 and IL-1β secretion by ELISA as well as reactive oxygen species (ROS) content and superoxide dismutase (SOD) activity.
Results:
Compared to sham operation group, model group presented significantly elevated miRNA-155 level and Longa score, decreased HCN expression, elevated Caspase 3 activity and Glu content, and reduced GABA and SOD activity. Meanwhile, model group also had elevated IL-6 and IL-1β secretion, and ROS content (p<0.05). The miRNA-155 agonist group further exacerbated these changes (p<0.01). The miRNA-155 inhibitor group could inhibit miRNA-155 expression and significantly reverse the above pathological changes (p<0.05).
Conclusions:
miRNA-155 is increased in cerebral ischemia. Regulation of miRNA-155 expression can target neuronal pacing ion channel HCN channel to regulate the release of amino acid transmitters, thereby alleviating the progress of cerebral ischemia.
Insights
MicroRNA-155 (miRNA-155) exacerbates cerebral ischemia by affecting neuronal function and neurotransmitter release. Inhibiting miRNA-155 can reverse these damaging effects, offering a potential therapeutic target for stroke.
Area of Science:
- Neuroscience
- Molecular Biology
- Biochemistry
Background:
- Cerebral hemorrhage leads to stroke and brain damage.
- MicroRNA-155 (miRNA-155) is implicated in stroke development.
- The precise role of miRNA-155 in cerebral ischemia remains unclear.
Purpose of the Study:
- To investigate the regulatory mechanism of miRNA-155 in cerebral ischemia.
- To explore the relationship between miRNA-155 and hyperpolarization-activated cyclic nucleotide-gated (HCN) channels.
- To assess the therapeutic potential of modulating miRNA-155.
Main Methods:
- Establishment of a cerebral ischemia model in Sprague-Dawley rats.
- Groups included sham operation, model, miRNA-155 inhibitor, and miRNA-155 agonist.
- Analysis of neural function, gene/protein expression (miRNA-155, HCN), enzyme activity (Caspase 3, SOD), neurotransmitter levels (Glu, GABA), and inflammatory markers (IL-6, IL-1β) using RT-PCR, ELISA, and biochemical assays.
Main Results:
- Cerebral ischemia model showed increased miRNA-155, elevated Longa scores, reduced HCN expression, increased Caspase 3 activity, higher Glu, lower GABA, increased IL-6 and IL-1β, and elevated ROS with decreased SOD activity.
- miRNA-155 agonist worsened these pathological changes.
- miRNA-155 inhibition reversed these detrimental effects.
Conclusions:
- MicroRNA-155 (miRNA-155) levels are elevated in cerebral ischemia.
- Modulating miRNA-155 impacts neuronal HCN channels and neurotransmitter release.
- Targeting miRNA-155 offers a potential strategy to alleviate cerebral ischemia progression.
