RGD Reference Report - microRNA-195 attenuates neuronal apoptosis in rats with ischemic stroke through inhibiting KLF5-mediated activation of the JNK signaling pathway. - Rat Genome Database

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microRNA-195 attenuates neuronal apoptosis in rats with ischemic stroke through inhibiting KLF5-mediated activation of the JNK signaling pathway.

Authors: Chang, Lisha  Zhang, Wan  Shi, Songxin  Peng, Yanbo  Wang, Dali  Zhang, Li  Zhang, Jiang 
Citation: Chang L, etal., Mol Med. 2020 Apr 9;26(1):31. doi: 10.1186/s10020-020-00150-w.
RGD ID: 45073134
Pubmed: PMID:32272873   (View Abstract at PubMed)
PMCID: PMC7146986   (View Article at PubMed Central)
DOI: DOI:10.1186/s10020-020-00150-w   (Journal Full-text)


BACKGROUND: Accumulating evidence has implicated the regulation of microRNAs (miRs) in ischemia stroke. The current study aimed to elucidate the role of microRNA-195 (miR-195) in neuronal apoptosis and brain plasticity in rats with ischemic stroke via the JNK signaling pathway/KLF5 axis.
METHODS: Ischemic stroke rat models were established by middle cerebral artery occlusion (MCAO), and oxygen deprivation (OGD) models were constructed in rat neuronal cells, followed by gain- or loss-of-function of miR-195 and/or KLF5 in rats and cells. Infarct volume, neuronal loss and ultrastructure, the expression of GAP-43, SYP and KLF5 protein as well as cell apoptosis were determined in the rats. Caspase-3 activity as well as the expression of miR-195, KLF5, GAP-43, SYP, JNK, phosphorylated JNK, Bax and Bcl-2 was measured in the cells.
RESULTS: The infarct size, expression of GAP-43 and SYP protein and apoptotic cells were increased in the miR-195-/- MCAO rats, while reductions were detected in the miR-195 mimic MCAO and KLF5-/- MCAO rats. Bcl-2 expression was increased, Bax and Caspase-3 expression as well as the ratio of phosphorylated JNK/JNK was decreased in response to miR-195 overexpression or KLF5 knockdown. Interestingly, the silencing of KLF5 reversed the effects exerted by the miR-195 inhibitor on the expression of Bcl-2, phosphorylated JNK/JNK, Bax and Caspase-3.
CONCLUSIONS: Collectively, our study unraveled that miR-195 could down-regulate KLF5 and block the JNK signaling pathway, ultimately inhibiting neuronal apoptosis in rats with ischemic stroke.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  

Phenotype Annotations    Click to see Annotation Detail View

Mammalian Phenotype

Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
Mir195Ratabnormal neuron number  IMP in hippocampusRGD 
Klf5Ratabnormal postsynaptic density morphology  IMP  RGD 
Mir195Ratabnormal postsynaptic density morphology  IMP  RGD 
Klf5Ratabnormal protein level  IMP Syp and Gap43RGD 
Mir195Ratabnormal protein level  IMP Syp and Gap43RGD 
Klf5Ratdecreased neuron number  IMP in hippocampusRGD 
Objects Annotated

Genes (Rattus norvegicus)
Klf5  (KLF transcription factor 5)
Mir195  (microRNA 195)

Genes (Mus musculus)
Klf5  (Kruppel-like transcription factor 5)
Mir195a  (microRNA 195a)

Genes (Homo sapiens)
KLF5  (KLF transcription factor 5)
MIR195  (microRNA 195)


Additional Information