Tenascin-C modulates alveolarization in bronchopulmonary dysplasia.

Bronchopulmonary dysplasia (BPD) is a chronic lung disease characterized by retarded alveolarization. Tenascin-C (TN-C), an extracellular matrix glycoprotein and soluble molecule, is involved in tissue morphogenesis. In the present study, we demonstrated that the level of TN-C in lung tissues was greater in a mouse model of BPD induced by 85% oxygen. TN-C deficiency, however, impaired alveolarization in the hyperoxia-induced BPD model. In contrast, a functional TN-C blocking antibody ameliorated alveolar dysplasia in BPD-like mice. Mechanistically, hyperoxia increased the soluble TN-C (sTN-C) released from respiratory epithelial cells. On one hand, low-dose sTN-C promoted lung epithelial cell proliferation and migration, which was mediated by ICAM-1. On the other hand, high-dose sTN-C hindered the proliferation and migration of epithelial cells. Overall, this study revealed that TN-C plays a dual role in lung alveolarization and that TN-C may be a target in BPD therapy.

Inhibition of hippocampal cyclin-dependent kinase 5 activity ameliorates learning and memory dysfunction in a mouse model of bronchopulmonary dysplasia.

AIMS: Oxygen therapy plays a vital role in the development of bronchopulmonary dysplasia (BPD), which is the independent risk factor for neurodevelopment deficits in premature infants. However, the effect of hippocampal cyclin-dependent kinase 5 (CDK5) on BPD-associated neurodevelopment deficits is not fully understood. METHODS: Mice were placed in a hyperoxia chamber from postnatal Day 1 to Day 7. Hematoxylin and eosin staining was used to evaluate the lung histomorphological characteristics. Learning and memory functions of mice were detected by Morris water maze. TUNEL staining was applied to measure the number of apoptotic cells. The expression of CDK5, apoptosis-related protein, and neuroplasticity-related proteins were analyzed by Western blot. Golgi staining was used to assess the structure of dendritic spines. RESULTS: Hyperoxia-induced BPD mice showed a long-term learning and memory dysfunction, more severe neuronal apoptosis, and a decline of synaptic plasticity. Inhibition of CDK5 overactivation ameliorated cognitive deficits, neuronal apoptosis, and synaptic plasticity disorders in BPD mice. CONCLUSIONS: This study first found a vital role of CDK5 in BPD-associated neurodevelopmental disorders. Inhibition of CDK5 overexpression could effectively improve cognitive dysfunctions in BPD mice, which indicated that hippocampal CDK5 may be a new target for prevention and treatment in learning and memory dysfunction of BPD.

Transcriptomic analyses identify albino-associated genes of a novel albino tea germplasm 'Huabai 1'.

Albinism in shoots of tea plants is a common phenotypic expression which gives the tea infusion a pleasant umami taste. A novel natural albino mutant tea germplasm containing high amino acids content was found and named as 'Huabai 1'. 'Huabai 1' has white jade tender shoots under low temperature and turns green with increased temperature. In order to understand the molecular mechanism of color change in leaf of 'Huabai 1', transcriptome analysis was performed to identify albino-associated differentially expressed genes (DEGs). A total of 483 DEGs were identified from white shoots of 'Huabai 1' compared to its green shoots. There were 15 DEGs identified to be involved in phenylpropanoid biosynthesis, which account for the majority of characterized DEGs. The metabolites related to phenylpropanoid biosynthesis revealed similar expression pattern of DEGs. Furthermore, metabolic pathways such as ubiquonone, tyrosine, and flavonoid biosynthesis associated with phenylpropanoid biosynthesis could also contribute to the color change in 'Huabai 1' tender shoots. Protein-protein interaction analysis revealed a hub protein NEDD8 (CSA009575) which interacted with many regulated genes in spliceosome, nitrogen metabolism, phenylpropanoid biosynthesis, and other pathways. In conclusion, the findings in this study indicate that the color change of 'Huabai 1' tender shoots is a combined effect of phenylpropanoid biosynthesis pathway and other metabolic pathways including flavonoid biosynthesis in tea plants. Chlorophyll biosynthesis-related genes LHCII and SGR may also play some roles in color change of 'Huabai 1'.

Association between tea consumption and osteoporosis: A meta-analysis.

BACKGROUND: Previous reports have suggested a potential association of tea consumption with the risk of osteoporosis. As such association is controversial, we conducted a meta-analysis to assess the relationship between tea consumption and osteoporosis. METHODS AND FINDINGS: We systematically searched PubMed, EMBASE and WanFang databases until March 30, 2016, using the keywords "tea and osteoporosis," without limits of language. Odds ratios (ORs) with 95% confidence intervals (95% CIs) were derived by using random-effects models throughout the analyses. We conducted the analysis of the statistical heterogeneity using Cochrane I. The funnel plot was used to speculate the publication bias, while the subgroup analysis and multiround elimination method were employed. RESULTS: Our study was based on 17 journal articles, including 2 prospective cohort studies, 4 case-control studies, and 11 cross-sectional studies. In the present study, the total OR of osteoporosis for the highest versus the lowest categories of tea consumption was 0.62 (95% CI, 0.46-0.83), with significant heterogeneity among studies (I = 94%, P < .01). There was, however, no publication bias of the meta-analysis about tea consumption and osteoporosis. Subgroup analysis showed that tea consumption could reduce the risk of osteoporosis in all examined subgroups. CONCLUSION: In the present study, it can be concluded from the results that tea consumption can reduce the risk of osteoporosis.