It is widely accepted that type II iodothyronine deiodinase (D2) is mostly present in the brain, where it maintains the homeostasis of thyroid hormone (TH) levels. Although intensive studies have been performed on activity and mRNA levels of the deiodinases, very little is known about their expression at the protein level due to the lack of specific antisera. The current study reports the production of a specific D2 polyclonal antiserum and its use in the comparison of D2 protein distribution with that of type I (D1) and type III (D3) deiodinase protein in the choroid plexus at the blood-brain barrier level. Immunocytochemistry showed very high D2 protein expression in the choroid plexus, especially in the epithelial cells, whereas the D1 and D3 proteins were absent. Furthermore, dexamethasone treatment led to an up-regulation of the D2 protein in the choroid plexus. The expression of D2 protein in the choroid plexus led to a novel insight into the working mechanism of the uptake and transport of thyroid hormones along the blood-brain barrier in birds. It is hypothesized that D2 allows the prohormone thyroxine (T 4 ) to be converted into the active 3,5,3 -triiodothyronine (T 3 ). Within the choroidal epithelial cells. T 3 is subsequently bound to its carrier protein, transthyretin (TTR), to allow transport through the cerebrospinal fluid. Neurons can thus not only be provided with a sufficient T 3 level via the aid of the astrocytes, as was hypothesized previously based on in situ hybridization data, but also by means of T 4 deiodination by D2, directly at the blood-brain barrier level.
Infections caused by SARE-CoV-2 are complicated with the concurrent pathologies, to name hypertension, diabetes mellitus and cardiovascular diseases. High level of glucose in blood weakens the immunity and increase the SARS-CoV-2 replication. Diabetes mellitus aggravates the COVID-19 outcome. The intrusion of SARS-CoV-2 into a host-cell occurs by means of its association with the angiotensin-converting enzyme-2 (ACE 2). Stimulating immune responses the COVID-19 infection causes the cytokine storm, and may result in the lethal outcome in the diabetics.Recent laboratory studies demonstrated that the type1 and type2 diabetes mellitus is the main consequence in 14% of the patients after corona infection. Thus, in 2% of 14% diabetes started progressing due to the corona virus. In the other, diabetes debut occurred as the direct and negative consequence of the disease. Hyperglycemia results in the formation of protein molecules known as the advanced glycation end products (AGEs). The AGEs and their receptors (RAGE) are of high significance in the host-cell’s virus invasion. Consequently, more strict glucose control is necessary for optimal outcome and reduction in mortality. The better control for the COVID-19 course can be provided by the targeted effect on the RAGE axis. The review helps elucidate the molecular mechanism underlying the exacerbation of pathophysiology in the diabetic COVID-19 patients.
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