Cloning, characterization and expression analysis of porcine microRNAs

Background: MicroRNAs (miRNAs) are small ~22-nt regulatory RNAs that can silence target genes, by blocking their protein production or degrading the mRNAs. Pig is an important animal in the agriculture industry because of its utility in the meat production. Besides, pig has tremendous biomedical importance as a model organism because of its closer proximity to humans than the mouse model. Several hundreds of miRNAs have been identified from mammals, humans, mice and rats, but little is known about the miRNA component in the pig genome. Here, we adopted an experimental approach to identify conserved and unique miRNAs and characterize their expression patterns in diverse tissues of pig.Results: By sequencing a small RNA library generated using pooled RNA from the pig heart, liver and thymus; we identified a total of 120 conserved miRNA homologs in pig. Expression analysis of conserved miRNAs in 14 different tissue types revealed heart-specific expression of miR-499 and miR-208 and liver-specific expression of miR-122. Additionally, miR-1 and miR-133 in the heart, miR-181a and miR-142-3p in the thymus, miR-194 in the liver, and miR-143 in the stomach showed the highest levels of expression. miR-22, miR-26b, miR-29c and miR-30c showed ubiquitous expression in diverse tissues. The expression patterns of pig-specific miRNAs also varied among the tissues examined.Conclusion: Identification of 120 miRNAs and determination of the spatial expression patterns of a sub-set of these in the pig is a valuable resource for molecular biologists, breeders, and biomedical investigators interested in post-transcriptional gene regulation in pig and in related mammals, including humans.Peer reviewedBiochemistry and Molecular BiologyAnimal Scienc

A long-term outcome of therapeutic angiogenesis by transplantation of peripheral blood stem cells in critical limb ischemia after interventional revascularization

A 61-year-old male patient with atherosclerotic critical limb ischemia in the left leg underwent stent insertion into the left superficial femoral artery. Stenting procedures improved Rutherford grade from III-5 to II-4. Granulocyte colony-stimulating factor stimulated the production of white blood cells over four-fold and mononuclear cells (MNCs) 1.5-fold in the whole blood. Transplantation of 7.9×10 9 autologous MNCs into the left femoral artery rapidly decreased the leg pain intensity, with further improvement of Rutherford grades from II-4 to 0-0 without any side effects. In the four-year follow-up, significant improvement was found in terms of ankle brachial index, from nondetectable to 0.67, and peak systolic velocity, from 14.8 to 36.1 cm/s. Limb salvage and decreased resting pain were the notable outcomes of the treatment

Alterations of Mitochondrial Network by Cigarette Smoking and E-Cigarette Vaping

Toxins present in cigarette and e-cigarette smoke constitute a significant cause of illnesses and are known to have fatal health impacts. Specific mechanisms by which toxins present in smoke impair cell repair are still being researched and are of prime interest for developing more effective treatments. Current literature suggests toxins present in cigarette smoke and aerosolized e-vapor trigger abnormal intercellular responses, damage mitochondrial function, and consequently disrupt the homeostasis of the organelle’s biochemical processes by increasing reactive oxidative species. Increased oxidative stress sets off a cascade of molecular events, disrupting optimal mitochondrial morphology and homeostasis. Furthermore, smoking-induced oxidative stress may also amalgamate with other health factors to contribute to various pathophysiological processes. An increasing number of studies show that toxins may affect mitochondria even through exposure to secondhand or thirdhand smoke. This review assesses the impact of toxins present in tobacco smoke and e-vapor on mitochondrial health, networking, and critical structural processes, including mitochondria fission, fusion, hyper-fusion, fragmentation, and mitophagy. The efforts are focused on discussing current evidence linking toxins present in first, second, and thirdhand smoke to mitochondrial dysfunction