Objective: Hippocampal neuron apoptosis contributes to autism, while METTL3 has been documented to possess great potentials in neuron apoptosis. Our study probed into the role of METTL3 in neuron apoptosis in autism and to determine the underlying mechanism. Methods: Bioinformatics analysis was used to analyze expressed genes in autism samples. Institute of Cancer Research mice were treated with valproic acid to develop autism models. The function of METTL3 in autism-like symptoms in mice was analyzed with behavioral tests and histological examination of their hippocampal tissues. Primary mouse hippocampal neurons were extracted for in vitro studies. Downstream factors of METTL3 were explored and validated. Results: METTL3, MALAT1, and Wnt/β-catenin signaling were downregulated, while SFRP2 was upregulated in the hippocampal tissues of a mouse model of autism. METTL3 stabilized MALAT1 expression by promoting m6A modification of MALAT1. MALAT1 promoted SFRP2 methylation and led to reduced SFRP2 expression by recruiting DNMT1, DNMT3A, and DNMT3B to the promoter region of SFRP2. Furthermore, SFRP2 facilitated activation of the Wnt/β-catenin signaling. By this mechanism, METTL3 suppressed autism-like symptoms and hippocampal neuron apoptosis. Conclusion This research suggests that METTL3 can reduce autism-like symptoms and hippocampal neuron apoptosis by regulating the MALAT1/SFRP2/Wnt/β-catenin axis.

Objective: To study the effects of long non-coding RNA linc-01135 on the osteogenic differentiation of inflammatory PDLSCs(P-PDLSCs) under 12％ static mechanical strain loading. Methods: Cells were isolated and cultured from the healthy and periodontitis samples respectively to obtain healthy PDLSCs(H-PDLSCs) and P-PDLSCs. RT-PCR were used to identify the expression level of linc-01135. Lentiviruses were used to upregulate and downregulate the expression of linc-01135, and the osteogenesis gene expression were analyzed by RT-PCR and the osteogenesis differentiation capability were evaluated by alizarin red staining. Results: linc-01135 expression in P-PDLSCs was lower than that in H-PDLSCs. When the expression of linc-01135 was upregulated in P-PDLSCs before 12％ SMS loading, the expression level of RUNX2, ALP, OPG was significantly increased. In contrast, the expression of RUNX2, ALP, OPG was significantly decreased when the expression of linc-01135 was suppressed. Alizarin red staining proved the same trend. Conclusion: linc-01135 can promote the osteogenic differentiation capability of P-PDLSCs under 12％SMS loading.

Portal hypertension is a serious complication of liver cirrhosis resulting from the increases in portal vascular resistance and portal blood inflow. Both etiological and non-etiological therapies can effectively reduce portal venous pressure to a certain degree, but with an unsatisfactory effect in improving prognosis. New therapeutic drugs targeting the reduction in intrahepatic vascular resistance may help to achieve the reversal of portal hypertension. Based on the pathogenesis of cirrhotic portal hypertension, this article summarizes the current pharmacotherapies from the aspects of etiological and non-etiological therapies, so as to provide a comprehensive theoretical and evidence-based basis for clinical treatment options.