| [1] PubMed ID: | 35088199 |
| Disease Name: | Myocarditis |
| Sample: | mice with AVMC |
| Dysfunction Pattern: | Expression(highly expressed) |
| Validated Method: | Flow Cytometry//qRT-PCR//ELISA |
| Description: | In the present study, we found that MALAT1 was highly expressed in mice with AVMC, and the expression was correlated positively with cardiac pathological scores, cardiac IL-17 mRNA expression, and the percentages of splenic Th17 cells. In conclusion, our results suggest that MALAT1 knockdown alleviates CVB3-induced AVMC in mice, which may be partially attributable to the decline in Th17 cells responses. |
| Causality: | Yes |
| Causal Description: | We further demonstrated that MALAT1 knockdown could significantly alleviate the severity of disease and inhibit the differentiation of Th17 cells, accompanying the reduced mRNA expression of RORγt and productions of Th17-related pro-inflammatory cytokines in vivo. Additionally, in vitro analysis showed that MALAT1 knockdown suppressed na?ve CD4+ T cells differentiation towards Th17 cells. |
| Clinical-realted Application: | In the present study, we found that MALAT1 was highly expressed in mice with AVMC, and the expression was correlated positively with cardiac pathological scores, cardiac IL-17 mRNA expression, and the percentages of splenic Th17 cells. |
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