Search

Objective: This study was conducted to clarify the expression characteristics of cell cycle exit and neuronal differentiation 1 (CEND1) in glioma and its effects on the proliferation, migration, invasion, and resistance to temozolomide (TMZ) of glioma cells. Materials and Methods: In this experimental study, CEND1 expression in glioma tissues and its relationship with patients’ survival were analyzed through bioinformatics. Quantitative real-time polymerase chain reaction (qRT-PCR) and immunohistochemistry were performed to detect CEND1 expression in glioma tissues. The cell counting kit-8 (CCK-8) method was adopted to detect cell viability and the effects of different concentrations of TMZ on the inhibition rate of glioma cell proliferation, and the median inhibitory concentration of TMZ (IC50 value) was calculated. 5-Bromo2'-deoxyuridine (BrdU), wound healing and Transwell assays were performed to evaluate the impacts of CEND1 on glioma cell proliferation, migration, and invasion. Besides, the Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, Gene Ontology (GO) analysis, and Gene Set Enrichment Analysis (GSEA) were applied to predict the pathways regulated by CEND1. Nuclear factor-kappa B p65 (NF-κB p65) and phospho-p65 (p-p65) expression were detected by Western blot. Results: CEND1 expression was reduced in glioma tissues and cells, and its low expression was significantly associated with the shorter survival of glioma patients. CEND1 knockdown promoted glioma cell growth, migration, and invasion, and increased the IC50 value of TMZ, whereas up-regulating CEND1 expression worked oppositely. Genes co-expressed with CEND1 were enriched in the NF-κB pathway, and knocking down CEND1 facilitated p-p65 expression, while CEND1 overexpression suppressed p-p65 expression. Conclusion: CEND1 inhibits glioma cell proliferation, migration, invasion, and resistance to TMZ by inhibiting the NFκB pathway. [ABSTRACT FROM AUTHOR]

Growth-regulating factors (GRFs) are involved in various developmental events, particularly leaf development. However, the functions of GRFs in woody plants remain elusive. In this study, functional characterization of GRF15 in Populus was performed. Most GRFs are preferentially expressed in young leaves. As GRF15 was expressed at the highest level and with highest ratio in Populus species with large leaves, this gene was investigated through transgenic analyses. Promotor-β-glucuronidase analysis revealed expression of GRF15 at the leaf expansion zone. Additionally, GRF15 was found to be localized in the nucleus and regulated by miR396. Leaf size and palisade cell size were significantly increased and decreased in GRF15 -overexpressing and dominant repression lines, respectively. Consistently, expression of EXPA11a, a homolog of cell-expansion marker EXPA11 in Arabidopsis, was strongly upregulated and downregulated in the GRF15- overexpressing and dominant repression lines, respectively, which was further manifested by activation of EXPA11a by GRF15 in transactivation assays. Therefore, GRF15 is required for leaf size control and primarily modulates cell expansion during leaf development in Populus. [ABSTRACT FROM AUTHOR]

Summary: Adventitious roots occur naturally in many species and can also be induced from explants of some tree species including Populus, providing an important means of clonal propagation. Auxin has been identified as playing a crucial role in adventitious root formation, but the associated molecular regulatory mechanisms need to be elucidated. In this study, we examined the role of PagFBL1, the hybrid poplar (Populus alba × P. glandulosa clone 84K) homolog of Arabidopsis auxin receptor TIR1, in adventitious root formation in poplar. Similar to the distribution pattern of auxin during initiation of adventitious roots, PagFBL1 expression was concentrated in the cambium and secondary phloem in stems during adventitious root induction and initiation phases, but decreased in emerging adventitious root primordia. Overexpressing PagFBL1 stimulated adventitious root formation and increased root biomass, while knock‐down of PagFBL1 transcript levels delayed adventitious root formation and decreased root biomass. Transcriptome analyses of PagFBL1 overexpressing lines indicated that an extensive remodelling of gene expression was stimulated by auxin signalling pathway during early adventitious root formation. In addition, PagIAA28 was identified as downstream targets of PagFBL1. We propose that the PagFBL1‐PagIAA28 module promotes adventitious rooting and could be targeted to improve Populus propagation by cuttings. [ABSTRACT FROM AUTHOR]

Parkinson's disease (PD) is a common central neurodegenerative disease in middle-aged and elderly people. The progressive degeneration and death of dopaminergic neurons leads to insufficient dopamine (DA) neurotransmitters. Acupuncture and moxibustion can alleviate the aging of neurons. Therefore, studying the neuroprotective effects of electroacupuncture (EA) in PD mice is particularly important. Intraperitoneal injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP, 20 mg/kg) was used to establish a PD mouse model, and lipopolysaccharide (LPS) was used to induce microglia polarization. Western blotting, terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL), Nissl staining and immunohistochemistry were used to detect neuronal apoptosis and injury, α-syn expression and microglial accumulation in PD mice. In addition, the levels of inflammatory factors were determined using enzyme-linked immunosorbent assay (ELISA). Flow cytometry was used to detect the Ca2+ content. The fluorescein isothiocyanate (FITC) labeling method was used to assess glucose uptake. A reagent kit was used to detect glucose and lactate levels. MPTP induced the selective loss of DA neurons in the SN of mice, altered Ca2+ homeostasis, and induced an inflammatory response. In addition, maintaining Ca2+ homeostasis depends on the activity of transient receptor potential channel 1 (TRPC1). EA therapy promotes TRPC1 expression, which has a negative regulatory effect on sodium–glucose cotransporter 1 (SGLT1). Under the action of EA, TRPC1 protein expression increased, Ca2+ concentrations increased, and the effect of SGLT1 was inhibited, thereby facilitating glucose metabolism, blocking the activation of the phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) pathway, restraining M1 polarization of microglia, and alleviating the PD process. EA promotes TRPC1/Ca2+ pathway activation, inhibits SGLT1-mediated regulation of glucose metabolism and PI3K/AKT pathway activation, inhibits microglial M1 polarization, and alleviates PD. • EA alleviates neuronal damage in PD mice by decreasing SGLT1 levels. • Downregulation of SGLT1 inhibits microglial M1 polarization by regulating glucose metabolism. • EA improves neuronal damage in PD mice through the TRPC1/Ca2+ pathway. [ABSTRACT FROM AUTHOR]