Potassium regulates calcification of arteries

Foods rich in potassium like banana and avocado may protect against pathogenic vascular calcification.
Reduced dietary potassium promotes elevated aortic stiffness in a mouse model, as compared with normal-potassium-fed mice.

Arterial stiffness in humans is predictive of heart disease and death from heart disease, increased dietary potassium levels lessened vascular calcification and aortic stiffness. The different levels of dietary potassium were monitored by different blood levels of potassium in the three groups of mice.

When researchers looked at arterial cross-sections in cultures that were exposed to three different concentrations of potassium, based on normal physiological levels of potassium in the blood, they found a direct effect for the potassium on arterial calcification within arterial rings.

Arterial rings in low-potassium had markedly enhanced calcification, while high-potassium inhibited aortic calcification. In cell culture, low potassium levels in the culture media markedly enhanced calcification of vascular smooth muscle cells.

They discovered that the low-potassium conditions promoted the expression of several gene markers that are hallmarks of bone cells, but decreased the expression of vascular smooth muscle cell markers, suggesting the transformation of the vascular smooth muscle cells into bone-like cells under low-potassium conditions. They found that low-potassium increased intracellular calcium in the vascular smooth muscle cells, through a potassium transport channel called the inward rectifier potassium channel.
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Steroid hormone and age related bone loss

A group of steroid hormones could provide new insight into the bone loss and deterioration that occurs with aging, protein histone deacetylase 3, HDAC3, turns off the genes that encourage the stem cells in our bone marrow to make and store fat instead of making bone. As HDAC3 levels decrease naturally with age, bones become less dense and easily breakable.

 Looking at a group of steroid hormones known as glucocorticoids, which our bodies naturally have in circulation as a response to different stresses to help quiet the immune response, when these hormones enter bone cells, osteoblasts that make bone bind to a receptor that activates the expression of genes related to fat storage.

To get that effect of bone loss and increased marrow fat when you lose HDAC3, glucocorticoids must be present. Releasing glucocorticoids in response to various stimuli is a natural thing that body does, circulating glucocorticoid levels increase with age.

As with a lot of chemicals in the body, too much and not enough of something can be bad. While glucocorticoids occur naturally in the body, they are also used in various immune-suppressive therapies, many of which have osteoporosis as a side effect.

Researchers studied mice without receptors for the steroid hormones. The mice were placed on a calorie-restricted diet to stimulate the aging process which also has been shown to result in lower bone density and increased marrow fat. Extreme caloric restriction, such as with anorexia nervosa, can also lead to weak and brittle bones.

When looking at the bone cells in a culture dish, the receptor deficient mice show less lipid storage than regular mouse models of aging. They also showed more bone matrix, which is the cause of bone formation. Examination of tibia and femur in a living animal showed the receptor deficient mice actually had more marrow fat and lower bone mass.
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Bone marrow protein may be used for stem cell transplant

Bone marrow contains hematopoetic stem cells, the precursors to every blood cell type. These cells become after bone marrow transplants, bone marrow injury and during systemic infection, creating new blood cells, including immune cells.

Del-1 is a protein that plays a role in gum disease, it regulate the production of blood cells. Targeting it could be an effective way to improve stem cell transplants for both donors and recipients. Modulate levels of Del-1 in patients with certain blood cancers can enhance immune cell production.

Because the hematopoetic stem cell niche is so important for the creation of bone marrow and blood cells and because Del-1 is a soluble protein and is easily manipulated, it could be a target in many potential applications.

The researchers' investigations revealed that Del-1 was expressed by at least three cell types in the bone marrow that support hematopoetic stem cells: endothelial cells, CAR cells and osteoblasts.

Using mice deficient in Del-1, they found that the protein promotes proliferation and differentiation of hematopoetic stem cells, sending more of these progenitor cells down a path toward becoming myeloid cells, such as macrophages and neutrophils, rather than lymphocytes, such as T cells and B cells.

In bone marrow transplant experiments, researchers discovered that the presence of Del-1 in recipient
bone marrow is required for the transplanted stem cells to engraft in the recipient and to facilitate the process of myelopoesis, the production of myeloid cells.

When the researchers mimicked a systemic infection in mice, animals deficient in Del-1 were slower to begin making myeloid cells again compared to those with normal Del-1 levels.

The scientists see potential applications in bone marrow and stem cell transplants, for both donors and recipients. In donors, blocking the interaction between Del-1 and hematopoetic stem cells could enhance the mobilization of those progenitors into the bloodstream. This could be helpful for increasing donor cell numbers for transplantation.

Transplant recipients, on the other hand, may need enhanced Del-1 interaction to ensure the transplanted cells engraft and begin making new blood cells more rapidly. People undergoing chemotherapy who develop febrile neutropenia, associated with low levels of white blood cells, might benefit from the role of Del-1 in supporting the production of immune-related blood cells such as neutrophils.
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