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Understanding the adaptive changes in maize kernels under high-temperature stress during grain formation stage is critical for developing strategies to alleviate the negative effects on yield and quality. In this study, we subjected waxy maize (Zea mays L. sinensis Kulesh) to four different temperature regimes from 1–15 d after pollination (DAP), namely normal day/normal night (control), hot day/normal night, normal day/hot night, and hot day/hot night. Compared to the control, the three high-temperature treatments inhibited kernel development and starch deposition. To understand how the kernels responded to high-temperature stress, their transcriptomes, proteomes, and metabolomes were studied at 10 DAP and 25 DAP. This showed that genes and proteins related to kernel development and starch deposition were up- and down-regulated, respectively, at 10 DAP, but this pattern was reversed at 25 DAP. Metabolome profiling under high-temperature stress showed that the accumulation patterns of metabolites at 10 DAP and 25 DAP were inversely related. Our multiomics analyses indicated that the response to high-temperature stress of signaling pathways mediated by auxin, abscisic acid, and salicylic acid was more active at 10 DAP than at 25 DAP. These results confirmed that high-temperature stress during early kernel development has a carry-over effect on later development. Taken together, our multiomics profiles of developing kernels under high-temperature stress provide insights into the processes that underlie maize yield and quality under high-temperature conditions. [ABSTRACT FROM AUTHOR]

In this study, the expression of Cripto-1 and the role of macrophage polarization in immune response after allogeneic transfusion were analyzed by constructing a mouse model of allogeneic transfusion. In order to analyze the effects of miR-449a on the PI3K/AKT/NF-κB signaling pathway and the expression of downstream related regulatory factors under normal and abnormal conditions, we adopt in vitro and in vivo experiments separately. The molecular mechanism of PI3K/AKT/NF-κB signaling pathway was analyzed by blocking or activating gene expression and western blotting. Experiment in vitro has confirmed that inhibition of miR-449a increased the protein expression of Cripto-1. In vivo experiments confirmed that allogeneic transfusion reduced the expression of Cripto-1, which further inhibited NF-κB signaling pathway through AKT/PI3K phosphorylation, regulated macrophage polarization, inhibited M1 polarization of macrophages, promoted M2 polarization, and thus affected immune response of the body. [ABSTRACT FROM AUTHOR]

Objective. To explore the role and mechanism of interleukin-8-mediated autophagy regulation of gastric cancer (GC) cells in GC. Methods. After cell culture, the SGC7901 cell line was separated into the control group and IL-8 (20 ng/mL) group, IL-8 (40 ng/mL) group, and IL-8 (60 ng/mL) group, to verify the effects of the PI3K/Akt signal path on the modulation of autophagy in GC cells. Western blot detected autophagy markers, ATG12-ATG5 complexes, autophagy-associated pathways, and apoptosis-associated factors in GC cells. Transwell was utilized to identify invasion capability. Results. Compared with the control group, the expression of LC3II, Atg5, ATG7, Beclin1, Bax, C-cas3, C-cas9, P-PI3K, P-Akt, and ATG12-ATG5 was remarkably elevated in the IL-8 (60 ng/mL) group, IL-8 (20 ng/mL) group, and the IL-8 (40 ng/mL) group. The expression of P62 and Bcl-2 in the IL-8 (60 ng/mL) group was also lower than that of the IL-8 (20 ng/mL) group and IL-8 (40 ng/mL) group, in contrast to the controls. The invasive quantity of GC SGC7901 cells in the IL-8 (60 ng/mL) group was also remarkably higher in contrast to the IL-8 (20 ng/mL) and IL-8 (40 ng/mL) groups. The relative expressions of LC3II, Atg5, ATG7, Beclin1, Bax, C-cas3, C-cas9, P-PI3K, P-Akt, and ATG12-ATG5 complex proteins in LY294002 group were considerably elevated. LC3II, Atg5, ATG7, Beclin1, Bax, C-cas3, C-cas9, P-PI3K, P-Akt, and ATG12-ATG5 were decreased in the IL-8 + LY294002 group. The relative expressions of P62 and Bcl-2 proteins in the IL-8 + LY294002 group were remarkably elevated, and the invasion of SGC7901 cells in the IL-8 group was elevated. In contrast to the IL-8 group, the invasion quantity of gastric cancer SGC7901 cells in the IL-8 + LY294002 group was considerably decreased. Conclusion. IL-8 promotes autophagy and aggression and suppresses apoptosis of GC SGC7901 cells by regulating PI3K/AKT pathway phosphorylation. [ABSTRACT FROM AUTHOR]

Cerebral infarction is a common disease with a higher disability and fatality rates. The incidence rates of cerebral infarction or cerebral ischemic stroke gradually increase with aging and cerebrovascular disease progression. This study is aimed at evaluating the effects of HMGA2 on cerebral infarction-induced brain tissue damage and its underlying mechanisms. Adult Sprague Dawley rats were pretreated with sh-HMGA2 before cerebral infarction operation. The effect of HMGA2 on the arrangement, distribution, and morphological structure of neurons and the cell apoptosis ratio in brain tissue were detected via hematoxylin and eosin staining, brain-water content, TTC staining, and TUNEL staining. The results from ELISA assay, qPCR, and western blot indicated that downregulation of HMGA2 mitigated inflammatory stress via regulating the expression of TLR4/NF-κB. In addition, results showed that suppressed HMGA2 attenuated the neurological dysfunction of brain injury rats and markedly reduced infarct volume. HMGA2 might be able to alleviate the damage associated with cerebral infarction-induced inflammatory response and cell apoptosis. Moreover, downregulation of HMGA2 had a protective effect on the brain damage derived from cerebral infarction by mediating the TLR4/NF-κB pathway. In conclusion, the current study demonstrated that downregulation of HMGB2 decreased the infarct size, inflammatory responses, and apoptosis in cerebral injury and further had neuroprotective effects against cerebral infarction-induced brain damage. Finally, these results indicated that the downregulation of the TLR4/NF-κB pathway after ischemia by HMGB2 inhibition is a potential mechanism of the neuroprotective effect of cerebral injury. [ABSTRACT FROM AUTHOR]

To investigate the potential link between aberrant mitochondrial energy metabolism mediated by the AMPK/SIRT1 pathway and the etiology of anxiety disorders. The anxiety rat model was established by uncertain empty water bottle（UEWB）stress. Rats were submitted behavioral tests on the seventh, fourteenth, and twenty-first days and had the prefrontal cortex and amygdala removed for biochemical tests. The morphological alterations of the mitochondria in the medial prefrontal cortex and amygdala were examined by using a transmission electron microscope. Expression levels of AMPK, SIRT1, PGC-1, NRF-1 and NRF-2 were tested by western-blot analysis. ATP, respiratory chain complex and caspase enzyme expressions were tested by neurochemical and biochemical assays. Rats showed anxiety-like behavior after being exposed to the uncertain empty water bottle (UEWB) stress model. In model rats, mitochondrial structure is damaged, mitochondrial energy metabolism is decreased, and the expression of proteins associated with AMPK/SIRT1 pathway is significantly reduced in the brain. The level of mitochondrial energy metabolism correlates with anxiety-like behavior. The main mechanism of anxiety disorder is a disturbance of mitochondrial energy metabolism, which might be related to AMPK/SIRT1 pathway. • Uncertain empty water bottle stress model induces anxiety-like behavior in animals. • Mitochondrial structures are disrupted in anxious animals. • Disruption of mitochondrial energy metabolic function is associated with anxiety-like behavior. • Inhibition of AMPK/SIRT1 pathway may be a regulatory mechanism for decreased mitochondrial function. [ABSTRACT FROM AUTHOR]

IFNLR1 has been recently identified to be related to autosomal dominant nonsyndromic sensorineural hearing loss (ADNSHL). It is reported to be expressed in the inner ear of mice and the lateral line of zebrafish. However, it remains unclear how defects in this gene lead to hearing loss. To elucidate the global gene expression changes in zebrafish when the expression of ifnlr1 is downregulated. Transcriptome analysis was performed on ifnlr1 morpholino knockdown zebrafish and the control zebrafish using RNA-seq technology. The results show that 262 differentially expressed genes (DEGs) were up-regulated while 146 DEGs were down-regulated in the E4I4–Mo zebrafish larvae compared to the control-Mo. Six pathways were significantly enriched, including steroid biosynthesis pathway, adipocytokine signaling pathway, cytokine-cytokine receptor interaction pathway, p53 signaling pathway, AGE-RAGE signaling pathway in diabetic complications, and terpenoid backbone biosynthesis pathway. Among them, three pathways (steroid biosynthesis pathway, cytokine-cytokine receptor interaction pathway and p53 signaling pathway) are immune-associated. The transcriptome analysis results contribute to the groundwork for future research on the pathogenesis of IFNLR1 -associated hearing loss. [ABSTRACT FROM AUTHOR]