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MicroRNA-155 influences cell damage in ischemic stroke via TLR4/MYD88 signaling pathway
Wei Chen1, Lingtong Wang1, Zhaoping Liu2
1Department of Neurology, Linhai Second People's Hospital, Taizhou, 317016, Zhejiang, China.
Abstract:
Cerebral ischemic stroke (CIS) is extremely harmful, and its treatment should be underpinned by understanding its pathogenic mechanism. This study was designed to determine the involvement of miR-155 in CIS development via the TLR4/MyD88 signaling pathway. First, we quantified serum miR-155 in patients with CIS and healthy individuals, and found high expression of miR-155 in such patients and a decrease in it in the patients after therapy (P < 0.05). Serum miR-155 demonstrated a favorable function in predicting the development and prognosis of CIS (P < 0.001). We also conducted a mouse assay, and found that knocking out miR-155 can improve the neurological function of mice and suppress protein TLR4 and MyD88 (all P < 0.05). Finally, we carried out a cell assay, and found enhancement in the activity of SH-SY5Y cells, decrease in their apoptosis, and protein TLR4 and MyD88 in them after suppression of miR-155 (all P < 0.05). Furthermore, we also found complete reverse by TLR4/MyD88 pathway inhibitor on the influence of increasing miR-155 on cells (P > 0.05). Therefore, with an increase in cases with CIS, miR-155 takes a part in the development of cell damage by activating TLR4/MyD88, and it is probably the key to diagnosing and treating CIS.
Insights
MicroRNA-155 (miR-155) plays a key role in cerebral ischemic stroke (CIS) development by activating the TLR4/MyD88 pathway. Suppressing miR-155 may offer a novel diagnostic and therapeutic strategy for CIS.
Area of Science:
- Neuroscience
- Molecular Biology
- Immunology
Background:
- Cerebral ischemic stroke (CIS) poses a significant health burden, necessitating a deeper understanding of its underlying pathogenic mechanisms for effective treatment.
- MicroRNAs (miRNAs) are emerging as critical regulators in various biological processes, including neurological disorders.
Purpose of the Study:
- To investigate the role of microRNA-155 (miR-155) in the pathogenesis of CIS.
- To elucidate the involvement of the Toll-like receptor 4 (TLR4)/MyD88 signaling pathway in miR-155-mediated CIS development.
Main Methods:
- Serum levels of miR-155 were quantified in CIS patients and healthy controls, and changes post-therapy were assessed.
- A mouse model of CIS was utilized to evaluate the effects of miR-155 knockout on neurological function and key pathway proteins.
- In vitro cell assays using SH-SY5Y cells were performed to examine the impact of miR-155 modulation and TLR4/MyD88 pathway inhibition on cellular activity, apoptosis, and protein expression.
Main Results:
- CIS patients exhibited significantly higher serum miR-155 levels, which decreased after therapy. Serum miR-155 proved to be a valuable predictor of CIS development and prognosis.
- miR-155 knockout in mice improved neurological function and suppressed TLR4 and MyD88 protein levels.
- Suppression of miR-155 in SH-SY5Y cells enhanced cell activity, reduced apoptosis, and decreased TLR4 and MyD88 expression. Inhibition of the TLR4/MyD88 pathway reversed the effects of miR-155 overexpression on cells.
Conclusions:
- miR-155 contributes to cellular damage in CIS by activating the TLR4/MyD88 signaling pathway.
- miR-155 represents a potential key target for the diagnosis and treatment of cerebral ischemic stroke.
