The Developmental Delay of Seedlings With Cotyledons Only Confers Stress Tolerance to Suaeda aralocaspica (Chenopodiaceae) by Unique Performance on Morphology, Physiology, and Gene Expression.

Cotyledons play an important role in seedling establishment, although they may just exist for a short time and become senescent upon the emergence of euphylla. So far, the detailed function of cotyledons has not been well understood. Suaeda aralocaspica is an annual halophyte distributed in cold deserts; its cotyledons could exist for a longer time, even last until maturity, and they must exert a unique function in seedling development. Therefore, in this study, we conducted a series of experiments to investigate the morphological and physiological performances of cotyledons under salt stress at different developmental stages. The results showed that the cotyledons kept growing slowly to maintain the normal physiological activities of seedlings by balancing phytohormone levels, accumulating osmoprotectants and antioxidants, and scavenging reactive oxygen species (ROS). Salt stress activated the expression of osmoprotectant-related genes and enhanced the accumulation of related primary metabolites. Furthermore, differentially expressed transcriptional profiles of the cotyledons were also analyzed by cDNA-AFLP to gain an understanding of cotyledons in response to development and salt stress, and the results revealed a progressive increase in the expression level of development-related genes, which accounted for a majority of the total tested TDFs. Meanwhile, key photosynthetic and important salt stress-related genes also actively responded. All these performances suggest that "big cotyledons" are experiencing a delayed but active developmental process, by which S. aralocaspica may survive the harsh condition of the seedling stage.

Impaired autophagy contributes to adverse cardiac remodeling in acute myocardial infarction.

OBJECTIVE: Autophagy is activated in ischemic heart diseases, but its dynamics and functional roles remain unclear and controversial. In this study, we investigated the dynamics and role of autophagy and the mechanism(s), if any, during postinfarction cardiac remodeling. METHODS AND RESULTS: Acute myocardial infarction (AMI) was induced by ligating left anterior descending (LAD) coronary artery. Autophagy was found to be induced sharply 12-24 hours after surgery by testing LC3 modification and Electron microscopy. P62 degradation in the infarct border zone was increased from day 0.5 to day 3, and however, decreased from day 5 until day 21 after LAD ligation. These results indicated that autophagy was induced in the acute phase of AMI, and however, impaired in the latter phase of AMI. To investigate the significance of the impaired autophagy in the latter phase of AMI, we treated the mice with Rapamycin (an autophagy enhancer, 2.0 mg/kg/day) or 3-methyladenine (3MA, an autophagy inhibitor, 15 mg/kg/day) one day after LAD ligation until the end of experiment. The results showed that Rapamycin attenuated, while 3MA exacerbated, postinfarction cardiac remodeling and dysfunction respectively. In addition, Rapamycin protected the H9C2 cells against oxygen glucose deprivation in vitro. Specifically, we found that Rapamycin attenuated NFκB activation after LAD ligation. And the inflammatory response in the acute stage of AMI was significantly restrained with Rapamycin treatment. In vitro, inhibition of NFκB restored autophagy in a negative reflex. CONCLUSION: Sustained myocardial ischemia impairs cardiomyocyte autophagy, which is an essential mechanism that protects against adverse cardiac remodeling. Augmenting autophagy could be a therapeutic strategy for acute myocardial infarction.