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Archive - Oct 1, 2020

Exosome Treatment Improves Recovery from Heart Attacks in Pig Model

Science has long known that recovery from experimental heart attacks is improved by injection of a mixture of heart muscle cells, endothelial cells, and smooth muscle cells, yet results have been limited by poor engraftment and retention, and researchers worry about potential tumorigenesis and heart arrhythmia. Now, research in pigs shows that using the exosomes naturally produced from that mixture of heart muscle cells, endothelial cells, and smooth muscle cells--which were all derived from human induced pluripotent stem cells (hiPSCs)--yields regenerative benefits equivalent to the injected human induced pluripotent stem cell-cardiac cells, or hiPSC-CCs. Exosomes are sub-cellular, cell-released, membrane-bound extracellular vesicles (EVs) that can contain biologically active proteins, RNAs, and microRNAs. Exosomes are well known to participate in cell-to-cell communication, and they are actively studied as potential clinical therapies. “The hiPSC-CC exosomes are acellular and, consequently, may enable physicians to exploit the cardioprotective and reparative properties of hiPSC-derived cells while avoiding the complexities associated with tumorigenic risks, cell storage, transportation, and immune rejection,” said Ling Gao, PhD, and Jianyi “Jay” Zhang (photo), MD, PhD, University of Alabama at Birmingham (UAB), corresponding authors of the study, published online on September 16, 2020 in Science Translational Medicine. “Thus, exosomes secreted by hiPSC-derived cardiac cells improved myocardial recovery without increasing the frequency of arrhythmogenic complications and may provide an acellular therapeutic option for myocardial injury.” The article is titled “Exosomes Secreted by hiPSC-Derived Cardiac Cells Improve Recovery From Myocardial Infarction In Swine.” At UAB, Dr.

Scientists Trace 13.5% of Severe COVID-19 to Auto-Antibodies Against Type I Interferons or Mutations in Type I Interferon Genes

More than 10 percent of people who develop severe COVID-19 have misguided antibodies that attack not the virus, but the immune system itself, new research shows. Another 3.5 percent, at least, carry a specific kind of genetic mutation. In both groups, the upshot is basically the same: The patients lack type I interferons, a set of 17 proteins crucial for protecting cells and the body from viruses. Whether the proteins have been neutralized by so-called auto-antibodies, or were not produced in sufficient amounts in the first place due to a faulty gene, their missing-in-action appears to be a common theme among a subgroup of COVID-19 sufferers whose disease has thus far been a mystery. Published online on September 24, 2020 in two papers in Science, the findings help explain why some people develop a disease much more severe than others in their age group—including, for example, individuals who required admission to the ICU despite being in their 20s and free of underlying conditions. The findings may also provide the first molecular explanation for why more men than women die from the disease. The two open-access Science articles are “Auto-Antibodies Against Type I IFNs in Patients with Life-Threatening COVID-19” (https://science.sciencemag.org/content/early/2020/09/23/science.abd4585) and “Inborn Errors of Type I IFN Immunity in Patients with Life-Threatening COVID-19” (https://science.sciencemag.org/content/early/2020/09/29/science.abd4570). “These findings provide compelling evidence that the disruption of type I interferon is often the cause of life-threatening COVID-19,” says Jean-Laurent Casanova, MD, PhD, Head of the St.