LivingNew ways to reduce blood vessel damage in diabetes

New ways to reduce blood vessel damage in diabetes

Enzymes are soluble proteins responsible for regulating chemical reactions in the body. One of the first symptoms of diabetes is the separation of the endothelium, the layers of tissues that line the inside of the blood vessels or the heart, and the power plants that generate them. This is the first step in the distraction of the vasculature, the set of blood vessels. A new scientific study has found evidence that this breakdown occurs as a result of decompensation of enzymes.

The study carried out by the Georgia School of Medicine and published in ‘ Cell Reports’ indicates that the levels of the PDIA1 enzyme decrease in cases of diabetes. This enzyme is responsible for endothelial cell homeostasis, ensuring that conditions inside the cells are stable and blood vessels can be produced and repaired. On the other hand, the activity of the enzyme Drp1 , a key regulator in cell fission, is increased.

This imbalance causes endothelial cells and their power plants to separate, creating a vicious cycle in which the mitochondria generate too many reactive oxygen species ( ROS ). According to Dr. Masuko Ushio-Fukai , a vascular biologist at the Vascular Center for Biology at Augusta University, the fracture of power plants causes more Drp1 to oxidize and activate, generating even more reactive oxygen species. ” Fission induces fragmentation, which generates more ROS and contributes to the oxidation of Drp1 ,” says Ushio-Fukai.

Consequence of enzyme imbalance

The ‘biological glue’ that holds the endothelial cells together separates, causing previously connected cells to do so as well and promoting the appearance of inflammatory cells such as macrophages , generating even more disorders. The discoveries provide new targets for treatments for senescence or aging problems associated with endothelial cells, such as diabetes or cardiovascular disease. One potential form of intervention will be to restore the balance between PDIA1 and Drp1 and slow down the high oxidative level typical of diabetes.

Although some reactive oxygen species are necessary for the proper development of bodily functions, high levels are associated with the aging of the entire body. In endothelial cells, the mitochondria produce ROS , rather than the cellular fuel ATP, to feed the mitochondria themselves so that they can produce the energy necessary to fuel cell activity. The energy provided by ROS is enough to hold the cells of our blood vessels together but not enough to feed the muscles of the heart.

The study points out that this imbalance causes other detrimental health effects, noting that the mitochondria literally fall apart instead of following the natural process of fission and fusion. This anomaly generates a higher production of ROS, which feeds back the problem.

After eliminating the PDIA1 enzyme from the endothelial cells, it was found that the blood vessels showed greater aging than they corresponded to, with less cell growth and proliferation. This behavior demonstrated that the enzyme was necessary for the maintenance of functional endothelial cells. PDIA1 appears to have a direct role in regulating Drp1 fission and has the ability to rescue cells from excessive mitochondrial fragmentation by releasing more PDIA1 directly into cells and their mitochondria .

Another of the results obtained during the study was related to wound healing , a common problem in cases of diabetes. Using mice with type 2 diabetes, PDIA1 from healthy mice were injected into endothelial cell tissues. This caused a normalization in protein levels and an improvement in wound healing in the mice with diabetes.

The next step, according to Dr. Ushio-Fukai, includes developing a clinical Drp1 inhibitor and a PDIA1 delivery system that enables the use of biological packages called exosomes, which cells use to communicate and exchange substances.

Reference: Young-Mee Kim & Masuko Ushio-Fukai. ‘Redox regulation of mithochondrial fission protein Drp1 by protein disulfide isomerase limits endothelial senescense’. Cell Reports (2018) DOI: 10.1016 / j.celrep.2018.05.054

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