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Cognitive dysfunction often exists in neurodegenerative diseases such as Parkinson's disease and Alzheimer's disease.
miR-128b, miR-132, miR-34c and other miRNAs are directly involved in the regulation of cognitive disorders.
Among them, miR-128 is abnormally expressed in neuropsychiatric diseases such as depression, anxiety, Parkinson's disease, and Alzheimer's disease.
miR-218 was originally thought to be a tumor-related miRNA, which can be used as a prognostic biomarker for a variety of tumors, including miR-218-1 and miR-218-2, which are located in the tumor suppressor genes SLIT2 and SLIT3, respectively Zizhong.
In recent years, more and more researches have focused on miRNAs.
On April 6, 2021, researcher Jun Yao from the School of Life Sciences of Tsinghua University published an article in PNAS, revealing that miR-218 regulates cognitive dysfunction by activating the downstream molecule complement protein C3.
They found that miR-218 is lowly expressed in the cerebellum and midbrain, and is highly expressed in the hippocampus.
After further knocking out miR-218-1 and miR-218-2 using CRISPR-Cas9 technology, we found the learning and memory ability of mice after miR-218-2 knockout through behavioral studies such as water maze, elevated experiment, and tail suspension experiment.
Disorders appeared, but they did not show anxiety or depression-like mood disorders, and none of the above behavior disorders appeared after miR-218-1 was knocked out.
The morphological changes of hippocampal neurons when miR-218-1 is knocked out.
In terms of morphology, the length of dendrites of hippocampal neurons is reduced after miR-218-1 is knocked out, but the dendritic spine density at the top and base increases, and presynaptic The diameter of the vesicle decreases and moves away from the active area.
This indicates that miR-218 can affect the distribution and transport properties of presynaptic vesicles.
Electrophysiological experiments found that the tiny excitatory postsynaptic currents of hippocampal neurons were reduced after miR-218-1 was knocked out, which indicated that the release of presynaptic vesicles was reduced.
Injecting miR-218 precursors into the hippocampus can enhance the learning and memory abilities of wild-type mice.
At the same time, the tiny excitatory postsynaptic currents increase.
These results indicate that miR-218 can regulate learning and memory in both directions: less, learning and memory impairment; more, strong learning and memory ability.
In order to find the molecular mechanism by which miR-218 directly regulates learning and memory, the researchers discovered through single-cell sequencing that miR-218-2 knockout mouse hippocampal brain regions C3, Mmp13 (matrix metalloproteinase 13), Gdnf (glial cell-derived) The expression of neurotrophic factor) is up-regulated, and over-expression of miR-218 will cause the down-regulation of the candidate molecular target protein.
The three most potential molecular target proteins mentioned above were selected from thousands of changed genes, and then C3, Mmp13, and Gdnf were specifically silenced by shRNA interference technology, and it was found that only after knocking down C3, the expression similar to miR- The role of 218.
This indicates that complement C3 may act as a medium for miR-218 to regulate learning and memory.
In order to further verify the role of complement C3, they injected C3 recombinant protein into the hippocampus of wild-type mice, the small excitatory synaptic currents were weakened, and showed learning and memory impairment; and in the hippocampus of miR-218-2 knockout mice After injection of C3a receptor inhibitors into the brain area, the small excitatory currents are enhanced, and learning and memory can be improved.
In general, this article uses electrophysiology, CRISPR-Cas9 technology, shRNA interference, pharmacology and other means to further reveal in more detail the molecular mechanism of miR-218 regulating presynaptic function through complement C3 and mediating learning and memory.
[References] 1.
https://doi.
org/10.
1073/pnas.
2021770118 The pictures in the article are all from the references
Cognitive dysfunction often exists in neurodegenerative diseases such as Parkinson's disease and Alzheimer's disease.
miR-128b, miR-132, miR-34c and other miRNAs are directly involved in the regulation of cognitive disorders.
Among them, miR-128 is abnormally expressed in neuropsychiatric diseases such as depression, anxiety, Parkinson's disease, and Alzheimer's disease.
miR-218 was originally thought to be a tumor-related miRNA, which can be used as a prognostic biomarker for a variety of tumors, including miR-218-1 and miR-218-2, which are located in the tumor suppressor genes SLIT2 and SLIT3, respectively Zizhong.
In recent years, more and more researches have focused on miRNAs.
On April 6, 2021, researcher Jun Yao from the School of Life Sciences of Tsinghua University published an article in PNAS, revealing that miR-218 regulates cognitive dysfunction by activating the downstream molecule complement protein C3.
They found that miR-218 is lowly expressed in the cerebellum and midbrain, and is highly expressed in the hippocampus.
After further knocking out miR-218-1 and miR-218-2 using CRISPR-Cas9 technology, we found the learning and memory ability of mice after miR-218-2 knockout through behavioral studies such as water maze, elevated experiment, and tail suspension experiment.
Disorders appeared, but they did not show anxiety or depression-like mood disorders, and none of the above behavior disorders appeared after miR-218-1 was knocked out.
The morphological changes of hippocampal neurons when miR-218-1 is knocked out.
In terms of morphology, the length of dendrites of hippocampal neurons is reduced after miR-218-1 is knocked out, but the dendritic spine density at the top and base increases, and presynaptic The diameter of the vesicle decreases and moves away from the active area.
This indicates that miR-218 can affect the distribution and transport properties of presynaptic vesicles.
Electrophysiological experiments found that the tiny excitatory postsynaptic currents of hippocampal neurons were reduced after miR-218-1 was knocked out, which indicated that the release of presynaptic vesicles was reduced.
Injecting miR-218 precursors into the hippocampus can enhance the learning and memory abilities of wild-type mice.
At the same time, the tiny excitatory postsynaptic currents increase.
These results indicate that miR-218 can regulate learning and memory in both directions: less, learning and memory impairment; more, strong learning and memory ability.
In order to find the molecular mechanism by which miR-218 directly regulates learning and memory, the researchers discovered through single-cell sequencing that miR-218-2 knockout mouse hippocampal brain regions C3, Mmp13 (matrix metalloproteinase 13), Gdnf (glial cell-derived) The expression of neurotrophic factor) is up-regulated, and over-expression of miR-218 will cause the down-regulation of the candidate molecular target protein.
The three most potential molecular target proteins mentioned above were selected from thousands of changed genes, and then C3, Mmp13, and Gdnf were specifically silenced by shRNA interference technology, and it was found that only after knocking down C3, the expression similar to miR- The role of 218.
This indicates that complement C3 may act as a medium for miR-218 to regulate learning and memory.
In order to further verify the role of complement C3, they injected C3 recombinant protein into the hippocampus of wild-type mice, the small excitatory synaptic currents were weakened, and showed learning and memory impairment; and in the hippocampus of miR-218-2 knockout mice After injection of C3a receptor inhibitors into the brain area, the small excitatory currents are enhanced, and learning and memory can be improved.
In general, this article uses electrophysiology, CRISPR-Cas9 technology, shRNA interference, pharmacology and other means to further reveal in more detail the molecular mechanism of miR-218 regulating presynaptic function through complement C3 and mediating learning and memory.
[References] 1.
https://doi.
org/10.
1073/pnas.
2021770118 The pictures in the article are all from the references
