Endothelial cells residing in the coronary arteries can function as cardiac stem cells to produce new heart muscle tissue, Vanderbilt University investigators have discovered.
The findings, published in Cell Reports, offer insights into how the heart maintains itself and could lead to new strategies for repairing the heart when it fails after a heart attack.
The heart has long been considered to be an organ without regenerative potential. Recent findings, however, have demonstrated that new heart muscle cells are generated at a low rate, suggesting the presence of cardiac stem cells. The source of these cells was unknown.
The researchers postulated that the endothelial cells that line blood vessels might have the potential to generate new heart cells. They knew that endothelial cells give rise to other cell types, including blood cells, during development.
Using sophisticated technologies to track cells in a mouse model the team demonstrated that endothelial cells in the coronary arteries generate new cardiac muscle cells in healthy hearts. They found two populations of cardiac stem cells in the coronary arteries, a quiescent population in the media layer and a proliferative population in the adventitia (outer) layer.
The finding that coronary arteries house a cardiac stem cell ‘niche’ has interesting implications. Coronary artery disease, the No. 1 killer in the United States, would impact this niche. The study suggests that coronary artery disease could lead to heart failure not only by blocking the arteries and causing heart attacks, but also by affecting the way the heart is maintained and regenerated.
The current research follows a previous study in which the team demonstrated that after a heart attack, endothelial cells give rise to the fibroblasts that generate scar tissue. It looks like the same endothelial system generates myocytes (muscle cells) during homeostasis and then switches to generate scar tissue after a myocardial infarction. After injury, regeneration turns to fibrosis.
Understanding this switch could lead to new strategies for restoring regeneration and producing new heart muscle after a heart attack, during aging or in disease conditions such as diabetes and high blood pressure.
The researchers summise that if they can understand the molecular mechanisms that regulate the fate switch that happens after injury, perhaps they can use some sort of chemical or drug to restore regeneration and make muscle instead of scar. The team state that there is an opportunity here to improve treatment for people who come into the clinic after myocardial infarction.
Source: Vanderbilt University
Here is some info for the notesThe blood vessels are part of the ciltcrauory system and function to transport blood throughout the body. The most important types, arteries and veins, carry blood away from or towards the heart, respectively.TypesThere are various kinds of blood vessels:ArteriesAorta (the largest artery, carries blood out of the heart)Branches of the aorta, such as the carotid artery, the subclavian artery, the celiac trunk, the mesenteric arteries, the renal artery and the iliac artery.ArteriolesCapillaries (the smallest blood vessels)VenulesVeinsLarge collecting vessels, such as the subclavian vein, the jugular vein, the renal vein and the iliac vein.Venae cavae (the 2 largest veins, carry blood into the heart) AnatomyAll blood vessels have the same basic structure. The inner lining is the endothelium and is surrounded by subendothelial connective tissue. Around this there is a layer of vascular smooth muscle, which is highly developed in arteries. Finally, there is a further layer of connective tissue known as the adventitia, which contains nerves that supply the muscular layer, as well as nutrient capillaries in the larger blood vessels.PhysiologyBlood vessels do not actively engage in the transport of blood (they have no appreciable peristalsis), but arteries and veins to a degree can regulate their inner diameter by contraction of the muscular layer.This changes the blood flow to downstream organs, and is determined by the autonomic nervous system. Vasodilation and vasoconstriction are also used antagonistically as methods of thermoregulation.Oxygen (bound to hemoglobin in red blood cells) is the most critical nutrient carried by the bloodThe blood pressure in blood vessels is traditionally expressed in millimetres of mercury (1 mmHg = 133 Pa). In the arterial system, this is usually around 120 mmHg systolic (high pressure wave due to contraction of the heart) and 80 mmHg diastolic (low pressure wave). In contrast, pressures in the venous system are constant and rarely exceed 10 mmHg.Vasoconstriction is the constriction of blood vessels (narrowing, becoming smaller in cross-sectional area) by contracting the vascular smooth muscle in the vessel walls. It is regulated by vasoconstrictors (agents that cause vasoconstriction). These include paracrine factors (e.g. prostaglandins), a number of hormones (e.g. vasopressin and angiotensin) and neurotransmitters (e.g. epinephrine) from the nervous system.Vasodilation is a similar process mediated by antagonistically acting mediators. The most prominent vasodilator is nitric oxide (termed endothelium-derived relaxing factor for this reason).Permeability of the endothelium is pivotal in the release of nutrients to the tissue. It is also increased in inflammation in response to histamine, prostaglandins and interleukins, which leads to most of the symptoms of inflammation (swelling, redness and warmth).Role in diseaseBlood vessels play a role in virtually every medical condition. Cancer, for example, cannot progress unless the tumor causes angiogenesis (formation of new blood vessels) to supply the malignant cells’ metabolic demand. Atherosclerosis, the formation of lipid lumps (atheromas) in the blood vessel wall, is the prime cause of cardiovascular disease, the main cause of death in the Western world.Blood vessel permeability is increased in inflammation. Damage, due to trauma or spontaneously, may lead to haemorrhage. In contrast, occlusion of the blood vessel (e.g. by a ruptured atherosclerotic plaque, by an embolised blood clot or a foreign body) leads to downstream ischemia (insufficient blood supply) and necrosis (tissue breakdown).Vasculitis is inflammation of the vessel wall, due to autoimmune disease or infection.Capillaries consist of little more than a layer of endothelium and occasional connective tissue.References :