Identification of microRNAs involved in drought stress responses in early-maturing cotton by high-throughput sequencing.

Drought stress is one of the most important abiotic stresses. Cotton is classified as drought tolerant crop but the regulatory mechanism is unknown. MicroRNAs (miRNAs) have been implicated important roles in stress responses in many plants. However, the study of miRNAs in cotton responsive to drought stress is limited, especially in early-maturing cotton. In this study, we performed deep sequencing of small RNAs to identify known and novel miRNAs involved in the regulation of drought stress and understand the expression profile of miRNAs in early-maturing cotton. Three cotton small RNA libraries: non-stressed Shizao1 (early-maturing cotton variety) library (NSS), drought-stressed Shizao1 library (DSS) and non-stressed Jimian958 (medium-maturing cotton variety) library (NSJ) were constructed for deep sequencing. As a result, we identified a total of 64 known and 67 novel miRNAs in the 3 libraries and 88 of them were dramatically differentially expressed (greater than twofold) during drought stress. In addition, we found the expression of 41 miRNAs increased or reduced more than twofold in early-maturing cotton variety compared with that in medium-maturing cotton variety. Our results significantly increased the number of miRNAs in cotton and revealed for the first time the expression profile of miRNAs for early-maturing cotton.

Chitosan oligosaccharides protect rat primary hippocampal neurons from oligomeric ß-amyloid 1-42-induced neurotoxicity.

ß-Amyloid peptide (Aß), the major component of senile plaques in patients with Alzheimer's disease (AD), is believed to facilitate the progressive neurodegeneration that occurs in this disease. Mounting natural compounds are proved to be potential candidates for the prevention and treatment of AD. Chitosan oligosaccharides (COSs), the enzymatic hydrolysates of chitosan, have been reported to possess diverse biological activities. Here we investigated the effect of COSs on oligomeric Aß-mediated toxicity in rat primary hippocampal neurons. Pretreatment with COSs markedly inhibited cell death induced by Aß exposure as determined by cell viability assay and lactate dehydrogenase release assay. In parallel, the generation of reactive oxygen species and lipid peroxidation were attenuated by COSs. Furthermore, our results indicated that COSs remarkably prevented Aß-induced cell apoptosis as manifested by depressing the elevation of Bax/Bcl-2 ratio and caspase-3 activation, suggesting that the neuroprotective effect of COSs could be partially due to apoptosis regulation. In addition, pretreatment with COSs significantly blocked Aß-induced phosphorylation of c-Jun N-terminal kinase. Taken together, these findings may shed light on the role of COSs as a potential therapeutic agent for AD.