Section A
“Selective Connexin43 Inhibition Prevents Isoproterenol-Induced Arrhythmias and Lethality in Muscular Dystrophy Mice” is a research paper that was conducted by Dr. Fraidenraich and his colleagues. Duchenne muscular dystrophy (DMD) is a severe form of muscular dystrophy that is life threatening and associated with muscle degeneration. It affects many newborn males, meaning that it is caused by an X-linked mutation. This mutation leads to the absence of a very important protein called, “dystrophin,” which plays a role in stabilizing the myocyte sarcolemma. DMD has also been associated with heart failure and inflammation, although the role of dystrphin in the heart is not understood as well as its role in the skeletal muscles. It has …show more content…
This includes, Human Samples, Animals, Electrocardiography, Statistics, Western Blotting, and Immunofluorescence. These were all very well developed and analyzed with thoroughness throughout the entire paper. Dr. Fraidenraich and his colleagues wanted to assess the changes in expression and localization of Cx43 in the hearts of several DMD models. To do this, they conducted immunofluorescence (IF) staining on WT, mdx, and mdx:utr mice at 2, 4, 8, and 12 months of age. mdx:utr mice were analyzed for 4 months, since they only survive 3-4 months. They found that Cx43 localizes tightly to the intercalated discs, which is important to form and maintain electrical signal conduction of cardiomyocytes. They did not see any changes in tissues in the hearts of mdx mice at 2, 4, or 8 months, although localization of Cx43 was greatly lateralized. Another thing to note is that Cx43 has a very short half-life. Knowing this, they wanted to observe what effect that β-adrenergic as on the patterns of protein expression. The same types of mice, WT, mdx, and mdx:utr mice, were challeneged by Iso at a 5mg/kg IP, and their hearts were viewed for any changes that occurred on Cx43 after about an hour. What they found was that there was an increase in Cx43 lateralization in the hearts of mdx and mdx:utr, but relatively no change in the heart of the WT mice. Another thing that Dr. Fraidenraich and his colleagues did was a western …show more content…
Never before has anyone else specifically targeted Cx43, the most abundant protein expressed in cardiomyocytes. Selectively targeting this protein in DMD models prevents arrhythmogenesis and significantly improves pathlogy. By using selective Cx43 peptide mimetics in Iso, such as Gap19 and Gap26, Dr. Fraidenraich and his colleagues found a way to prevent arrhythmias. By targeting Cx43, there was an increase in survival, so this was clearly beneficial and would be beneficial if applied in a clinical setting. I think it was especially interesting that they used immunofluorescence for detection of proteins, and did not just rely solely on western blotting. This was a very eye-opening research paper and I hope it is carried out in a real-world situation in the near future to help all those with
“Selective Connexin43 Inhibition Prevents Isoproterenol-Induced Arrhythmias and Lethality in Muscular Dystrophy Mice” is a research paper that was conducted by Dr. Fraidenraich and his colleagues. Duchenne muscular dystrophy (DMD) is a severe form of muscular dystrophy that is life threatening and associated with muscle degeneration. It affects many newborn males, meaning that it is caused by an X-linked mutation. This mutation leads to the absence of a very important protein called, “dystrophin,” which plays a role in stabilizing the myocyte sarcolemma. DMD has also been associated with heart failure and inflammation, although the role of dystrphin in the heart is not understood as well as its role in the skeletal muscles. It has …show more content…
This includes, Human Samples, Animals, Electrocardiography, Statistics, Western Blotting, and Immunofluorescence. These were all very well developed and analyzed with thoroughness throughout the entire paper. Dr. Fraidenraich and his colleagues wanted to assess the changes in expression and localization of Cx43 in the hearts of several DMD models. To do this, they conducted immunofluorescence (IF) staining on WT, mdx, and mdx:utr mice at 2, 4, 8, and 12 months of age. mdx:utr mice were analyzed for 4 months, since they only survive 3-4 months. They found that Cx43 localizes tightly to the intercalated discs, which is important to form and maintain electrical signal conduction of cardiomyocytes. They did not see any changes in tissues in the hearts of mdx mice at 2, 4, or 8 months, although localization of Cx43 was greatly lateralized. Another thing to note is that Cx43 has a very short half-life. Knowing this, they wanted to observe what effect that β-adrenergic as on the patterns of protein expression. The same types of mice, WT, mdx, and mdx:utr mice, were challeneged by Iso at a 5mg/kg IP, and their hearts were viewed for any changes that occurred on Cx43 after about an hour. What they found was that there was an increase in Cx43 lateralization in the hearts of mdx and mdx:utr, but relatively no change in the heart of the WT mice. Another thing that Dr. Fraidenraich and his colleagues did was a western …show more content…
Never before has anyone else specifically targeted Cx43, the most abundant protein expressed in cardiomyocytes. Selectively targeting this protein in DMD models prevents arrhythmogenesis and significantly improves pathlogy. By using selective Cx43 peptide mimetics in Iso, such as Gap19 and Gap26, Dr. Fraidenraich and his colleagues found a way to prevent arrhythmias. By targeting Cx43, there was an increase in survival, so this was clearly beneficial and would be beneficial if applied in a clinical setting. I think it was especially interesting that they used immunofluorescence for detection of proteins, and did not just rely solely on western blotting. This was a very eye-opening research paper and I hope it is carried out in a real-world situation in the near future to help all those with