Cardiovascular disease affects the bone marrow


Immune cells are formed from blood stem cells that live in the bone marrow. Since the immune system cares about everything, the bone marrow reacts to a variety of signals that come to it from all tissues and organs. Blood stem cells (or hematopoietic cells) sit in special places (or niches) with their microenvironment. The service cells that provide this microenvironment affect how intensively stem cells divide, how quickly they will specialize in specific cells of the immune system, and which cells will be obtained from them. Molecular signals that enter the bone marrow act on the service cells. It is known that the nervous system influences the work of hematopoietic niches, that signals from the intestinal microflora come to them, that the service cells of the bone marrow are sensitive to the state of the pancreas – that is, for example, diabetes strongly affects the intensity with which ready immune cells leave their bone marrow niches and enter the bloodstream.

Employees Massachusetts Central Hospital studied how the bone marrow is affected by cardiovascular disease. Researchers write in Nature Cardiovascular Researchthat in people with high blood pressure, with atherosclerosis and those who have recently had a heart attack, hematopoiesis increases – that is, especially many new blood cells appear in the bone marrow. And to a greater extent this applies to myeloid immune cells. The most numerous of them are leukocytes, neutrophils, which are the first to meet various infections and trigger inflammation.

Experiments with mice prone to high blood pressure, atherosclerosis and heart attack showed the same: the bone marrow in these mice produced especially many myeloid immune cells. Moreover, they changed the blood vessels supplying the bone marrow with blood – the vessels themselves became larger, the vascular walls became thicker and at the same time more permeable. As the walls of the vessels became more permeable, more immune cells, formed in the bone marrow niches, went through them into the bloodstream. This, in turn, spurred the division of stem cells and the emergence of new mature immune cells.

The researchers were able to partially decipher the molecular mechanism that causes blood vessels to grow and become more permeable. After myocardial infarction, a lot of VEGF-A protein appears in the blood – vasculoendothelial growth factor A, or vascular endothelial growth factor A. As the name suggests, it stimulates vascular growth, and it has a special receptor through which it acts on cells. If this receptor is blocked, then the vessels in the bone marrow after a heart attack will not grow, and there will be no jump in myeloid immune cells. In addition, with a heart attack and atherosclerosis in the blood, the level of the signaling immune protein interleukin-6 and a complex proteoglycan called versican increase – both of them act on the bone marrow to stimulate hematopoiesis. True, it is not yet clear where exactly all these molecular factors that affect the bone marrow in cardiovascular diseases come from.

The fact that cardiovascular diseases are associated with immunity has been known for a long time, but it was still believed that the connection here is one-way, that some immune abnormalities that take place in the bone marrow only add the likelihood of high blood pressure, atherosclerosis, etc. However, , as we can see, cardiovascular disorders affect in response to what happens in the bone marrow. Although it would be strange if it were otherwise – after all, as we said at the beginning, immunity cares about everything, and it catches a variety of molecular signals, no matter where they come from. How much the new data will help in the treatment of atherosclerosis, high blood pressure and the consequences of a heart attack is not yet clear. On the one hand, even now you can think of some drugs that would prevent cardiovascular drugs from interfering with the life of the bone marrow, on the other hand, the study was carried out here mostly on mice, so, as usual, you need to wait for human confirmation mouse results.


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