WRKY transcription factor family in lettuce plant (Lactuca sativa): Genome-wide characterization, chromosome location, phylogeny structures, and expression patterns.

WRKY transcription factors (TF) have been identified in many plant species and play critical roles in multiple stages of growth and development and under various stress conditions. As one of the most popular vegetable crops, asparagus lettuce has important medicinal and nutritional value. However, study of WRKY TFs family in asparagus lettuce is limited. With the lettuce (Lactuca sativa L.) genome publication, we identified 76 WRKY TFs and analyzed structural characteristics, phylogenetic relationships, chromosomal distribution, interaction network, and expression profiles. The 76 LsWRKY TFs were phylogenetically classified as Groups I, II (IIa-IIe), and III. Cis element analysis revealed complex regulatory relationships of LsWRKY genes in response to different biological progresses. Interaction network analysis indicated that LsWRKY TFs could interact with other proteins, such as SIB (sigma factor binding protein), WRKY TFs, and MPK. The WRKYIII subfamily genes showed different expression patterns during the progress of asparagus lettuce stem enlargement. According to qRT-PCR analysis, abiotic stresses (drought, salt, low temperature, and high temperature) and phytohormone treatment could induce specific LsWRKYIII gene expression. These results will provide systematic and comprehensive information on LsWRKY TFs and lay the foundation for further clarification of the regulatory mechanism of LsWRKY, especially LsWRKYIII TFs, involved in stress response and the progress of plant growth and development.

TRIM21 negatively regulates Corynebacterium pseudotuberculosis-induced inflammation and is critical for the survival of C. pseudotuberculosis infected C57BL6 mice.

Corynebacterium pseudotuberculosis, a facultative intracellular bacterium, is an important zoonotic pathogen responsible for chronic inflammatory diseases. TRIM21, an E3 ubiquitin-protein ligase, plays pivotal roles in inflammation regulation. However, its role during C. pseudotuberculosis infection is unclear. Here, we found that TRIM21 expression was significantly increased in C. pseudotuberculosis-infected macrophages. Following infection by C. pseudotuberculosis, we observed a significantly higher number of bacteria and a higher degree of LDH release from Trim21-/- macrophages compared to wild-type (WT) macrophages, suggesting that TRIM21 limits C. pseudotuberculosis replication in macrophages and protects the infected cells from death. Further in vivo experiments showed a significantly higher mortality, higher bacterial load, much more severe abscess formation, and lesions in the organs of C. pseudotuberculosis-infected Trim21-/- mice compared to those of the infected WT mice, suggesting that TRIM21 plays critical roles in protecting against C. pseudotuberculosis infection. Moreover, the secretory levels of IL-1α, IL-1ß, IL-6, and TNF-α were significantly higher in C. pseudotuberculosis-infected Trim21-/- macrophages compared to infected WT macrophages; the levels of these cytokines were also higher in the sera, organs, and ascites of C. pseudotuberculosis-infected Trim21-/- mice compared to infected WT mice. These findings suggest that TRIM21 negatively regulates the secretion of pro-inflammatory cytokines in macrophages, sera, organs, and ascites of mice following C. pseudotuberculosis infection. Collectively, the present study demonstrates that TRIM21 plays a vital role in preventing C. pseudotuberculosis infection, which may be related to the negative regulation of pro-inflammatory cytokines production by TRIM21 during this pathogen infection.

Long noncoding RNA NBAT1 suppresses hepatocellular carcinoma progression via competitively associating with IGF2BP1 and decreasing c-Myc expression.

Hepatocellular Carcinoma (HCC) is the second leading cause of cancer-related deaths. Neuroblastoma associated transcript 1 (NBAT1) is a newly identified long noncoding RNA (lncRNA), which has been reported to play an important role in human cancers. However, the functional role and underlying mechanism of NBAT1 in HCC remains unclear. Here, we found that the expression of NBAT1 was decreased in HCC tissues and cells; as well, the decreased expression of NBAT1 was also associated with tumor size and clinical TNM stages. NBAT1 overexpression, both in vitro and in vivo studies, inhibited tumorigenesis through apoptosis augmentation and cell cycle blockade. Mechanistically, NBAT1 bound to IGF2BP1 and inhibited the interaction between IGF2BP1 and c-Myc mRNA, thus suppressing the stability of c-Myc mRNA. Collectively, NBAT1 is associated with HCC tumorigenesis and could be a therapeutic target for HCC treatment.

Critical roles of NLRP3 inflammasome in IL-1ß secretion induced by Corynebacterium pseudotuberculosis in vitro.

Corynebacterium pseudotuberculosis is a prominent human and animal pathogen causing chronic inflammatory diseases. Interleukin-1ß (IL-1ß) is involved in the response to such pathogenic infections. However, the mechanism by which IL-1ß is secreted during C. pseudotuberculosis infection remains unclear. This study aimed to investigate the mechanism underlying IL-1ß secretion by macrophages infected with C. pseudotuberculosis. Herein, we firstly revealed that nucleotide-binding oligomerization domain-like receptor family, pyrin domain containing 3 (NLRP3), apoptosis-associated speck-like protein containing a CARD (ASC) and caspase-1 (Casp1) play critical roles in IL-1ß secretion rather than IL-1ß precursor (pro-IL-1ß) expression in C. pseudotuberculosis-infected macrophages. Toll like receptor 4 (TLR4) is partially involved in IL-1ß secretion, while absent in melanoma 2 (AIM2) is not involved in IL-1ß secretion by C. pseudotuberculosis-infected macrophages. In addition, nuclear factor kappa B (NF-κB) and p38 mitogen-activated protein kinases (p38 MAPK) inhibitors almost attenuated IL-1ß secretion, implying that NF-κB and p38MAPK pathway are involved in IL-1ß secretion in C. pseudotuberculosis-infected macrophages. Furthermore, C. pseudotuberculosis were significantly more numerous in Nlrp3-/-, Asc-/-, and Casp-1-/- macrophages than in WT macrophages at 24 h after infection (P < 0.05), indicating that NLRP3 inflammasome components limit C. pseudotuberculosis replication in macrophages. Together, these data provide novel insights into the mechanisms underlying IL-1ß secretion in C. pseudotuberculosis-infected macrophages and further the current understanding of the host pro-inflammatory immune response against this pathogen.

The relationship between serum hepatitis B virus DNA level and liver histology in patients with chronic HBV infection.

BACKGROUND: There is no consensus regarding the relationship between HBV DNA and liver fibrosis, and the relationship between HBV DNA and the degree of liver cirrhosis has not been reported in patients with chronic HBV infection. METHODS: From January 2011 to December 2016, liver biopsies were performed on 396 patients with chronic hepatitis B and cirrhosis. Assessments of liver fibrosis and cirrhosis were based on the Laennec staging system. RESULTS: Serum levels of HBV DNA were correlated with fibrosis and cirrhosis (KW = 73.946, P<0.001). Serum HBV DNA level was correlated with mild fibrosis, moderate to severe fibrosis and cirrhosis (P = 0.009, P<0.001, and P<0.001, respectively). The HBeAg-positive group and HBeAg-negative group showed significant differences in HBV DNA levels, and the rates of mild fibrosis, severe fibrosis and cirrhosis were significantly different between these two groups (F = 17.585, P<0.001 and F = 6.017, P = 0.003, respectively). The replication status of the serum HBV DNA affected fibrosis formation as well as cirrhosis (χ2 = 53.76, P<0.001). In the HBeAg-positive group, the sensitivity, specificity and AUC values of HBV DNA as a predictor for mild fibrosis and cirrhosis were 64.3%, 78.94% and 0.818, respectively, and 81.0%, 69.2%, and 0.871, respectively. In the HBeAg-negative group, the sensitivity, specificity and AUC values of HBV DNA for liver sclerosis prediction were 48%, 76.8% and 0.697, respectively. CONCLUSIONS: Different HBV DNA levels had different effects on the formation of fibrosis and sclerosis in liver tissues. HBV DNA levels can predict mild fibrosis and cirrhosis in liver tissue, which is enhanced in HBeAg-positive patients.