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The pathogenesis of chronic venous disorder (CVeD) remains partially understood. A marked wall remodeling has been shown with potential accelerated tissue senescence. Selleckchem MSC-4381 We have investigated the expression of peroxisome proliferator-activated receptor (PPAR) isoforms transcription factor EB (TFEB) as regulatory molecules of cellular homeostasis and makers of peroxisomal and lysosomal biogenesis. We have also quantified p16 expression as a cellular senescence marker. In specimens of maior safena vein from 35 CVeD and 27 healthy venous controls (HV), we studied the expression of PPAR-α, PPAR-β/δ, PPAR-γ, TFEB and p16 by RT-qPCR and immunohistochemical techniques. We have demonstrated a reduced gene and protein expression of the PPAR-α and PPAR-β/δ isoform as well as that of TFEB in the venous wall of CVeD patients, suggesting an altered peroxisomal and lysosomal biogenesis associated with an increased cellular senescence shown by increased p16 expression.KAIKObase was established in 2009 as the genome database of the domesticated silkworm Bombyx mori. It provides several gene sets and genetic maps as well as genome annotation obtained from the sequencing project of the International Silkworm Genome Consortium in 2008. KAIKObase has been used widely for silkworm and insect studies even though there are some erroneous predicted genes due to misassembly and gaps in the genome. In 2019, we released a new silkworm genome assembly, showing improvements in gap closure and covering more and longer gene models. Therefore, there is a need to include new genome and new gene models to KAIKObase. In this article, we present the updated contents of KAIKObase and the methods to generate, integrate and analyze the data sets. Database URL https//kaikobase.dna.affrc.go.jp.Cervical cancer is one of the most diagnosed malignancies among females. The 5-fluorouracil (5-Fu) is a widely used chemotherapeutic agent against diverse cancers. Despite the initially encouraging progresses, a fraction of cervical cancer patients developed 5-Fu resistance. We detected that NEAT1 was significantly upregulated in cervical cancer tissues and cell lines. Moreover, NEAT1 was positively associated with 5-Fu resistance. Furthermore, expression of NEAT1 was significantly upregulated in 5-Fu resistant CaSki cervical cancer cells. Knocking down NEAT1 by shRNA dramatically promoted the sensitivity of 5-Fu resistant CaSki cells. We observed a negative correlation between lncRNA-NEAT1 and miR-34a in cervical cancer patient tissues. Overexpression of miR-34a significantly sensitized 5-Fu resistant cells. Bioinformatical analysis uncovered that NEAT1 functions as a competitive endogenous RNA (ceRNA) of miR-34a in cervical cancer cells via sponging it at multiple sites to suppress expression of miR-34a. This negative association between NEAT1 and miR-34a was further verified in cervical cancer tissues. We found the 5-Fu resistant cells displayed significantly increased glycolysis rate. Overexpression of miR-34a suppressed cellular glycolysis rate and sensitized 5-Fu resistant cells through direct targeting the 3'UTR of LDHA, a glycolysis key enzyme. Importantly, knocking down NEAT1 successfully downregulated LDHA expressions and glycolysis rate of cervical cancer cells by upregulating miR-34a, a process could be further rescued by miR-34a inhibition. Finally, we demonstrated inhibition of NEAT1 significantly sensitized cervical cancer cells to 5-Fu through the miR-34a/LDHA pathway. In summary, this study suggests a new molecular mechanism for the NEAT1-mediated 5-Fu resistance via the miR-34a/LDHA-glycolysis axis.Sepsis is a common cause of deaths of patients in intensive care unit. The study aims to figure out the role of long non-coding RNA (lncRNA) GAS5 in the myocardial depression in mice with sepsis. Cecal ligation and puncture (CLP) was applied to induce sepsis in mice, and then the heart function, myocardium structure, and the inflammatory response were evaluated. Differentially expressed lncRNAs in mice with sepsis were identified. Then gain- and loss-of-functions of GAS5 were performed in mice to evaluate its role in mouse myocardial depression. The lncRNA-associated microRNA (miRNA)-mRNA network was figured out via an integrative prediction and detection. Myocardial injury was observed by overexpression of high-mobility group box 1 (HMGB1) in septic mice with knockdown of GAS5 expression. Activity of NF-κB signaling was evaluated, and NF-κB inhibition was induced in mice with sepsis and overexpression of GAS5. Collectively, CLP resulted in myocardial depression and injury, and increased inflammation in mice. GAS5 was highly expressed in septic mice. GAS5 inhibition reduced myocardial depression, myocardial injury and inflammation responses in septic mice. GAS5 was identified to bind with miR-449b and to elevate HMGB1 expression, thus activating the NF-κB signaling. HMGB1 overexpression or NF-κB inactivation reduced the GAS5-induced myocardial depression and inflammation in septic mice. Our study suggested that GAS5 might promote sepsis-induced myocardial depression via the miR-449b/HMGB1 axis and the following NF-κB activation.An-Chuan Granule (ACG), a traditional Chinese medicine (TCM) formula, is an effective treatment for asthma but its pharmacological mechanism remains poorly understood. In the present study, network pharmacology was applied to explore the potential mechanism of ACG in the treatment of asthma. The tumor necrosis factor (TNF), Toll-like receptor (TLR), and Th17 cell differentiation-related, nucleotide-binding oligomerization domain (NOD)-like receptor, and NF-kappaB pathways were identified as the most significant signaling pathways involved in the therapeutic effect of ACG on asthma. A mouse asthma model was established using ovalbumin (OVA) to verify the effect of ACG and the underlying mechanism. The results showed that ACG treatment not only attenuated the clinical symptoms, but also reduced inflammatory cell infiltration, mucus secretion and MUC5AC production in lung tissue of asthmatic mice. In addition, ACG treatment notably decreased the inflammatory cell numbers in bronchoalveolar lavage fluid (BALF) and the levels of pro-inflammatory cytokines (including IL-6, IL-17, IL-23, TNF-alpha, IL-1beta and TGF-beta) in lung tissue of asthmatic mice.
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