This week’s Round-up looks to the future, as nanoparticles and stem cell-derived cardiac muscle cells get a closer look. More good news for lovers of yogurt, and a smelly but effective treatment for atherosclerosis as well.
Using stem cells extracted from the patient’s own blood and skin cells, this Japanese research team completed the first-in-human transplant of cardiac muscle cells derived from pluripotent stem cells. The team achieved this by “reprogramming” them, reverting them to their embryonic-like pluripotent initial state. “I hope that (the transplant) will become a medical technology that will save as many people as possible, as I’ve seen many lives that I couldn’t save,” Yoshiki Sawa, a professor in the Osaka University cardiovascular surgery unit, said in a press report.
Like something from a sci-fi horror novel, this team of researcher examined the role that nanoparticles that eat dead cells and stabilize atherosclerotic plaque may be able to play in the future of atherosclerosis treatment. “We found we could stimulate the macrophages to selectively eat dead and dying cells – these inflammatory cells are precursor cells to atherosclerosis – that are part of the cause of heart attacks,” one of the authors said in press release. “We could deliver a small molecule inside the macrophages to tell them to begin eating again.” The authors noted that after a single-cell RNA sequencing analysis, they observed that the prophagocytic nanotubes decreased inflammatory gene expression linked to cytokine and chemokine pathways in lesional macrophages, thereby treating the cell from the inside out.
In this large analysis of more than 120,000 individuals, the authors reported multivariable-adjusted hazard ratios (95% CI for all) for mortality were reduced in regular (more than four servings per week) consumers of yogurt, and there was an inverse relationship between regular consumption and cancer mortality as well as cardiovascular-related mortality in women. “In our study, regular yogurt consumption was related to lower mortality risk among women,” the authors wrote. “Given that no clear dose–response relation was apparent, this result must be interpreted with caution.”
This research teamlooked human microphages and compared them to dying cells in a dish. They observed that macrophages reclaim arginine and other amino acids when they “eat” dead cells, and then use an enzyme to convert arginine to putrescine. The putrescine, in return, activates a protein (Rac1) that causes the macrophage to eat more dead cells, suggesting to the authors that the problem of atherosclerosis may be, in part, a problem of putrescine. The findings, according to the accompanying press release, suggest that the compound could be use to potentially treat conditions with chronic inflammation, such as Alzheimer’s disease.