Nanoparticles are a class of newly emerging environmental pollutions. To date, few experiments have been conducted to investigate the effect nanoparticles may have on plant growth and development. It is important to study the effects nanoparticles have on plants because they are stationary organisms that cannot move away from environmental stresses like animals can, therefore they must overcome these stresses by molecular routes such as altering gene expression. microRNAs (miRNA) are a newly discovered, endogenous class of post-transcriptional gene regulators that function to alter gene expression by either targeting mRNAs for degradation or inhibiting mRNAs translating into proteins. miRNAs have been shown to mediate abiotic stress responses such as drought and salinity in plants by altering gene expression, however no study has been performed on the effect of nanoparticles on the miRNA expression profile; therefore our aim in this study was to classify if certain miRNAs play a role in plant response to Al2O3 nanoparticle stress. In this study, we exposed tobacco (Nicotiana tabacum) plants (an important cash crop as well as a model organism) to 0%, 0.1%, 0.5%, and 1% Al2O3 nanoparticles and found that as exposure to the nanoparticles increased, the average root length, the average biomass, and the leaf count of the seedlings significantly decreased. We also found that miR395, miR397, miR398, and miR399 showed an extreme increase in expression during exposure to 1% Al2O3 nanoparticles as compared to the other treatments and the control, therefore these miRNAs may play a key role in mediating plant stress responses to nanoparticle stress in the environment. The results of this study show that Al2O3 nanoparticles have a negative effect on the growth and development of tobacco seedlings and that miRNAs may play a role in the ability of plants to withstand stress to Al2O3 nanoparticles in the environment.

Dysfunction along the electron transport system contributes to cardiomyopathy in a number of mitochondrial diseases. Several pharmacological approaches are currently being tested for their ability to improve mitochondrial function, yet almost none of the leading candidates specifically target to mitochondria. In this study we determined the biological efficacy of a novel conjugate of idebenone and mitochondria-targeting peptide, SBT-61. Using a vertically-integrated approach we tested the ability of SBT-61 to improve functional recovery and bioenergetics in: perfused rat hearts subjected to ischemia-reperfusion, cultured cells exposed to hypoxia-reoxygenation injury, and isolated heart mitochondria where complexes I and/or III were inhibited. SBT-61 treatment preserved post-ischemic cardiac function as assessed by left ventricular developed pressure (40 ± 5 vs 24 ± 3 mmHg, P<0.0001), rate of contraction (1853 ± 236 vs. 1069 ± 109 mmHg/s, P<0.0001), rate of relaxation (-1349 ± 231 vs. -792 ± 52 mmHg/s, P<0.0001), and a 30% reduction in infarct size. In cells expressing an shRNA knockdown of glutathione reductase, treatment with SBT-61 normalized maximal mitochondrial respiration after hypoxia-reoxygenation. In isolated mitochondria with complexes I or III inhibited, SBT-61 stimulated respiration and was shown to directly reduce complex III and cytochrome c, indicating that SBT-61 can bypass defects in the electron transport system. These data highlight the cardioprotective potential of a mitochondria-targeted idebenone conjugate to stabilize mitochondrial bioenergetics.

No abstract