Osa-miR11117 Targets OsPAO4 to Regulate Rice Immunity against the Blast Fungus Magnaporthe oryzae.

The intricate regulatory process governing rice immunity against the blast fungus Magnaporthe oryzae remains a central focus in plant-pathogen interactions. In this study, we investigated the important role of Osa-miR11117, an intergenic microRNA, in regulating rice defense mechanisms. Stem-loop qRT-PCR analysis showed that Osa-miR11117 is responsive to M. oryzae infection, and overexpression of Osa-miR11117 compromises blast resistance. Green fluorescent protein (GFP)-based reporter assay indicated OsPAO4 is one direct target of Osa-miR11117. Furthermore, qRT-PCR analysis showed that OsPAO4 reacts to M. oryzae infection and polyamine (PA) treatment. In addition, OsPAO4 regulates rice resistance to M. oryzae through the regulation of PA accumulation and the expression of the ethylene (ETH) signaling genes. Taken together, these results suggest that Osa-miR11117 is targeting OsPAO4 to regulate blast resistance by adjusting PA metabolism and ETH signaling pathways.

Retraction Notice to: Kcnq1ot1/miR-381-3p/ETS2 Axis Regulates Inflammation in Mouse Models of Acute Respiratory Distress Syndrome.

[This retracts the article DOI: 10.1016/j.omtn.2019.10.036.].

Vitamin B6, vitamin B12 and methionine and risk of pancreatic cancer: a meta-analysis.

BACKGROUND: Nutrients involved in one-carbon metabolism may play a key role in pancreatic carcinogenesis. The aim of this study was to examine the association between pancreatic cancer risk and intake or blood levels of vitamins B6, B12 and methionine via meta-analysis. METHODS: A systematic search was performed in PubMed, Web of Knowledge and Chinese National Knowledge Infrastructure (CNKI) up to April 2020 to identify relevant studies. Risk estimates and their 95% confidence intervals (CIs) were retrieved from the studies and combined by a random-effect model. RESULTS: A total of 18 studies were included in this meta-analysis on the association of vitamin B6, B12 and methionine with pancreatic cancer risk. The combined risk estimate (95% CI) of pancreatic cancer for the highest vs lowest category of vitamin B6 intake and blood pyridoxal 5'-phosphate (PLP, active form of vitamin B6) levels was 0.63 (0.48-0.79) and 0.65 (0.52-0.79), respectively. The results indicated a non-linear dose-response relationship between vitamin B6 intake and pancreatic risk. Linear dose-response relationship was found, and the risk of pancreatic cancer decreased by 9% for every 10 nmol/L increment in blood PLP levels. No significant association were found between pancreatic cancer risk and vitamin B12 intake, blood vitamin B12 levels, methionine intake and blood methionine levels. CONCLUSION: Our study suggests that high intake of vitamin B6 and high concentration of blood PLP levels may be protective against the development of pancreatic cancer. Further research are warranted to confirm the results.

Kcnq1ot1/miR-381-3p/ETS2 Axis Regulates Inflammation in Mouse Models of Acute Respiratory Distress Syndrome.

Inflammatory mediators play a key role in the pathogenesis of acute respiratory distress syndrome (ARDS). In this study, we aimed to explore the involvement of the Kcnq1 opposite strand/antisense transcript 1 (Kcnq1ot1)/miR-381-3p/E26 transformation-specific proto-oncogene 2 (ETS2) axis in inflammation of lipopolysaccharide (LPS)-induced ARDS. Microarray analysis revealed ETS2 as an upregulated gene in ARDS. Then, a LPS-induced ARDS mouse model was constructed, with a series of gain- or loss-of-function experiments conducted to evaluate the lung function and neutrophil extracellular trap (NET) formation in lung tissue and determine the neutrophil number, myeloperoxidase (MPO) activity, and inflammatory factor levels in bronchoalveolar lavage fluid (BALF). As the results revealed, downregulated expression of ETS2 resulted in improved lung function, decreased NETs, MPO activity, and levels of interleukin (IL)-6 and tumor necrosis factor alpha (TNF-α), as well as increased IL-10 level. Then, the assays of dual-luciferase reporter, RNA-binding protein immunoprecipitation (RIP), and RNA pull-down were performed to validate that Kcnq1ot1 promoted ETS2 expression by competitively binding to miR-381-3p. Meanwhile, it was also found that Kcnq1ot1 silencing reversed the promotive effect of EST2 on ARDS. Our results provide evidence that Kcnq1ot1 silencing may reduce the inflammatory response in LPS-induced ARDS via inhibition of miR-381-30-dependent ETS2, thereby presenting new molecular understanding for the development of ARDS.

Epimedin C Protects H2O2-Induced Peroxidation Injury by Enhancing the Function of Endothelial Progenitor HUVEC Populations.

Endothelial cell injury and apoptosis induced by oxidative stress serve important roles in many vascular diseases. The repair of endothelial cell vascular injury relies on the function of local endothelial progenitor cells (EPCs). Our previous study indicated that epimedin C, a major flavonoid derived from Herba epimedii (yin yang huo), could promote vascularization by inducing endothelial-like differentiation of mesenchymal stem cells C3H/10T1/2 both in vivo and in vitro. In view of the significant cardiovascular protective effects of Herba epimedii, we detected a protective effect of epimedin C on hydrogen peroxide (H2O2)-induced peroxidation injury in human umbilical vein endothelial cells (HUVECs) and the role of EPC in this process. The results show that epimedin C increased the expression of the stem cell marker, CD34 and PROM1, and subsequently enhanced the expression and function of vascular endothelial growth factor and matrix metalloproteinase (MMP)-2 in local vascular endothelial cells. In conclusion, epimedin C protects H2O2-induced peroxidation injury by enhancing the function of endothelial progenitor HUVEC populations.

[G894T mutation of the endothelial nitric oxide synthase gene in Chinese Han nationality].

OBJECTIVE: To investigate the distribution of G894T mutation of the endothelial nitric oxide synthase (eNOS) gene in Chinese Han nationality. METHODS: G894T mutation of the eNOS gene of 108 unrelated healthy individuals was studied by means of polymerase chain reaction/restriction fragment length polymorphism (PCR-RFLP) analysis. RESULT: All subjects were genotyped for eNOS gene; the frequencies of the GG, GT and TT genotypes were 0.9095, 0.0883 and 0.0021, respectively. In the Han nationality, the frequency of the GT, TT genotypes was lower than that in Japanese and Caucasian of UK (P< 0.05). CONCLUSION: These results suggest that there are significant differences in G894T mutation of eNOS gene between the Chinese Han nationality and other ethnic populations.

[The G894T mutation of the endothelial nitric oxide synthase gene is associated with coronary atherosclerotic heart disease in Chinese].

OBJECTIVE: To investigate the association of the endothelial nitric oxide synthase (eNOS) gene polymorphism with coronary atherosclerotic heart disease (CHD) in Chinese Han nationality. METHODS: For 106 patients with CHD and 108 unrelated health individuals, the G894T mutation at exon 7 of the endothelial nitric oxide synthase gene was studied by using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis. RESULTS: (1) Among the normal subjects of Chinese Han nationality, the frequencies of the eNOS/GG, GT and TT genotypes were 0.9095, 0.0883 and 0.0021, respectively. The G and T allele frequencies were 0.9537 and 0.0463. (2) The authors assumed the effects of the T allele to be dominant (GT and TT combined vs GG). The GT+TT genotype frequencies in CHD and myocardial infarction (MI) subgroup were 0.2219 and 0.2387, respectively. The frequencies of eNOS/GT+TT genotypes in CHD patients, as well as MI subgroup were significantly higher than that of the normal subjects (P<0.05), respectively. The frequencies of T allele in CHD, MI subgroup were significantly higher than that in the normal subjects (P<0.01), respectively. (3) This mutation was not related to the number of affected vessels in the 58 patients who had angiographically documented artery narrowing (P>0.05). CONCLUSION: The G894T mutation of the endothelial nitric oxide synthase gene may be a marker for genetical predisposition of CHD in Chinese Han population.