Identification of Shaker Potassium Channel Family Members and Functional Characterization of SsKAT1.1 in Stenotaphrum secundatum Suggest That SsKAT1.1 Contributes to Cold Resistance.

Stenotaphrum secundatum is an excellent shade-tolerant warm-season turfgrass. Its poor cold resistance severely limits its promotion and application in temperate regions. Mining cold resistance genes is highly important for the cultivation of cold-resistant Stenotaphrum secundatum. Although there have been many reports on the role of the Shaker potassium channel family under abiotic stress, such as drought and salt stress, there is still a lack of research on their role in cold resistance. In this study, the transcriptome database of Stenotaphrum secundatum was aligned with the whole genome of Setaria italica, and eight members of the Shaker potassium channel family in Stenotaphrum secundatum were identified and named SsKAT1.1, SsKAT1.2, SsKAT2.1, SsKAT2.2, SsAKT1.1, SsAKT2.1, SsAKT2.2, and SsKOR1. The KAT3-like gene, KOR2 homologous gene, and part of the AKT-type weakly inwardly rectifying channel have not been identified in the Stenotaphrum secundatum transcriptome database. A bioinformatics analysis revealed that the potassium channels of Stenotaphrum secundatum are highly conserved in terms of protein structure but have more homologous members in the same group than those of other species. Among the three species of Oryza sativa, Arabidopsis thaliana, and Setaria italica, the potassium channel of Stenotaphrum secundatum is more closely related to the potassium channel of Setaria italica, which is consistent with the taxonomic results of these species belonging to Paniceae. Subcellular location experiments demonstrate that SsKAT1.1 is a plasma membrane protein. The expression of SsKAT1.1 reversed the growth defect of the potassium absorption-deficient yeast strain R5421 under a low potassium supply, indicating that SsKAT1.1 is a functional potassium channel. The transformation of SsKAT1.1 into the cold-sensitive yeast strain INVSC1 increased the cold resistance of the yeast, indicating that SsKAT1.1 confers cold resistance. The transformation of SsKAT1.1 into the salt-sensitive yeast strain G19 increased the resistance of yeast to salt, indicating that SsKAT1.1 is involved in salt tolerance. These results suggest that the manipulation of SsKAT1.1 will improve the cold and salt stress resistance of Stenotaphrum secundatum.

Downregulation of lncRNA SNHG16 inhibits vascular smooth muscle cell proliferation and migration in cerebral atherosclerosis by targeting the miR-30c-5p/SDC2 axis.

Atherosclerosis (AS) is the basic lesion underlying the occurrence and development of cerebrovascular diseases. Abnormal proliferation of vascular smooth muscle cells (VSMCs) plays a crucial role in AS. We aimed to explore the role of SNHG16 in AS and the molecular mechanism of VSMC involvement in the regulation of AS. The expression levels of SNHG16, miR-30c-5p and SDC2 were detected by qRT-PCR. CCK-8, wound healing and Transwell assays were used to assess ox-LDL-induced VSMC proliferation, migration, and invasion, respectively. Western blot analysis was used to detect SDC2 and MEK/ERK pathway-related protein levels. A dual-luciferase reporter assay confirmed the binding of SNHG16 with miR-30c-5p and miR-30c-5p with SDC2. SNHG16 and SDC2 expression was upregulated in patients with AS and ox-LDL-induced VSMCs, while miR-30c-5p was downregulated. Ox-LDL-induced VSMC proliferation and migration were increased, and the MEK/ERK signalling pathway was activated. MiR-30c-5p was targeted to SNHG16 and SDC2. Downregulating SNHG16 or upregulating miR-30c-5p inhibited ox-LDL-induced VSMC proliferation and migration and inhibited MEK/ERK signalling pathway activation. In contrast, downregulating miR-30c-5p or upregulating SDC2 reversed the effects of downregulating SNHG16 or upregulating miR-30c-5p. Furthermore, downregulating SDC2 inhibited ox-LDL-induced proliferation and migration of VSMCs and inhibited activation of the MEK/ERK signalling pathway, while upregulating lncRNA SNHG16 reversed the effects of downregulating SDC2. Downregulation of SNHG16 inhibited VSMC proliferation and migration in AS by targeting the miR-30c-5p/SDC2 axis. This study provides a possible therapeutic approach to AS.

Multidimensional amphibian diversity and community structure along a 2 600 m elevational gradient on the eastern margin of the Qinghai-Tibetan Plateau.

Mountain systems harbor an evolutionarily unique and exceptionally rich biodiversity, especially for amphibians. However, the associated elevational gradients and underlying mechanisms of amphibian diversity in most mountain systems remain poorly understood. Here, we explored amphibian phylogenetic and functional diversity along a 2 600 m elevational gradient on Mount Emei on the eastern margin of the Qinghai-Tibetan Plateau in southwestern China. We also assessed the relative importance of spatial (area) and environmental factors (temperature, precipitation, solar radiation, normalized difference vegetation index, and potential evapotranspiration) in shaping amphibian distribution and community structure. Results showed that the phylogenetic and functional diversities were unimodal with elevation, while the standardized effect size of phylogenetic and functional diversity increased linearly with elevation. Phylogenetic net relatedness, nearest taxon index, and functional net relatedness index all showed a positive to negative trend with elevation, indicating a shift from clustering to overdispersion and suggesting a potential change in key processes from environmental filtering to competitive exclusion. Overall, our results illustrate the importance of deterministic processes in structuring amphibian communities in subtropical mountains, with the dominant role potentially switching with elevation. This study provides insights into the underlying assembly mechanisms of mountain amphibians, integrating multidimensional diversity.

Cyanidin inhibits EMT induced by oxaliplatin via targeting the PDK1-PI3K/Akt signaling pathway.

Anthocyanins have been shown to exhibit antitumor activity in several cancers in vitro and in vivo. Oxaliplatin is widely used as an anti-cancer drug. However, a large proportion of patients receiving platinum-based anti-cancer drug treatments will relapse because of metastasis and drug resistance. The aim of this study is to discover an effective anthocyanin that possesses the combinational anti-metastatic effects of oxaliplatin. Our results showed that cyanidin, one of the main constituents of anthocyanins, widely found in black rice, black bean, Hawthorn and other foods, could reverse drug resistance and enhance the effects of oxaliplatin on hepatic cellular cancer (HCC). Cyanidin inhibited migration and reversed EMT biomarker changes induced by low dose OXA. Moreover, 3-phosphoinositide-dependent protein kinase 1 (PDK1) can be considered a potential target and cyanidin significantly increased OXA sensitivity and inhibited the EMT induced by OXA via PI3K/Akt signaling in HCC.

Suppression of NF-κB signaling and P-glycoprotein function by gambogic acid synergistically potentiates adriamycin -induced apoptosis in lung cancer.

Gambogic acid (GA) has been approved by the Chinese Food and Drug Administration for the treatment of lung cancer in clinical trials. However, whether GA has chemosensitizing properties when combined with other chemotherapy agents in the treatment of lung cancer is not known. Here we investigated the effects of GA combined with adriamycin (ADM), a common chemotherapy agent, in regard to their activities and the possible mechanisms against lung cancer in vitro and in vivo. Cell viability results showed that sequential GA-ADM treatment was synergistic, while the reverse sequence and simultaneous treatments were antagonistic or additive, in lung cancer cells and ADM resistant cells, but not in normal cells. The combined use of GA and ADM synergistically displayed apoptosis-inducing activities in lung cancer cells. Moreover, GA in combination with ADM could promote PARP cleavage, enhance caspases activation and decrease the expression of anti-apoptotic proteins in lung cancer cells. The combined use of GA and ADM decreased the expression of P-glycoprotein and increased the accumulation of ADM in lung cancer cells. Furthermore, it was found that, prior to ADM treatment, GA could inhibit NF-κB signaling pathways, which have been validated to confer ADM resistance. The critical role of NF-κB was further confirmed by using PDTC, a NF-κB inhibitor, which significantly increased apoptosis induction by the combination of GA and ADM and inhibited ADM-induced ABCB1 upregulation. Importantly, our results indicated that the combination of GA and ADM exerted enhanced anti-tumor effects on A549 xenograft models through inhibiting NF-κB and P-glycoprotein, and attenuated ADM-induced cardiotoxicity. Collectively, these findings indicate that GA sensitizes lung cancer cells to ADM in vitro and in vivo, providing a rationale for the combined use of GA and ADM in lung cancer chemotherapy.