Into the Heart

Blocking Build Up in the Artery: Intimal Proliferation

The intimal layer of the artery lies just below the endothelium. Smooth muscle cells are responsible for maintaining vascular tone and normally lie in the medial layer of the artery.  During the atherosclerosis process smooth muscle cells from the media of the artery (along with foam cells) migrate and proliferate in the intimal layer of the artery.  Upon migration smooth muscle cells reproduce themselves (divide) and make (synthesize) connective tissue. Macrophages stimulate the migration, proliferation of smooth muscle cells and synthesis of connective tissue (collagen).

The process of smooth muscle cell migration, division and synthesis is referred to as intimal proliferation (buildup) and causes thickening and narrowing of the intima. Smooth muscle cells contribute to a substantial bulk of the atherosclerosis lesion which may protrude several millimeters above the surface of the intima.  As the fatty streak and fibrous plaque enlarge and bulge into the lumen, the sub endothelium becomes exposed to the blood at sites of endothelial retraction or tear, as a result platelets aggregate and mural thrombi form.

The growth of smooth muscle cells depends upon factors derived from the endothelium or platelets. Prostaglandins, thromboxanes, leukotrienes, angiotensin II, catecholamines and cytokines such as TNFa, interleukin and interferon also have a role in the proliferation and/or migration of smooth muscle cells.

Protein Kinase C (PKC) is involved in smooth muscle cell proliferation. Vitamin E, alpha tocopherol inhibits PKC activity by attenuating the generation of membrane derived diacylglycerol: a lipid that facilitates PKC translocation thus increasing its activity.

Mitogen activated protein kinase (MAPK) is also involved in smooth muscle proliferation. Both alpha tocopherol and gamma tocopherol  (vitamin E)  help inhibit MAPK activity.

The isoflavone compound genistein (soybeans/chickpeas) is a broad spectrum protein tyrosine kinase inhibitor.

As such, soy muffins with sunflower seeds (vitamin E) enhance arterial health.

Sources:
Genistein, A Protein Tyrosine Kinase Inhibitor inhibits Thrombane A2
American Society for Pharmacology and Experimental Therapeutics
Volume 39, Issue 4, pp. 475-480,

Genistein Acutely Stimulates Nitric Oxide Synthesis in Vascular Endothelial Cells by a Cyclic Adenosine 5 Monophasphate Dependent Mechanism
Endrocrinology Vol. 145, No 12

Vitamin E Prevents LDL Cholesterol Damage

Vitamin E prevents cell membrane damage by inhibiting peroxidation of membrane phospholipids and disrupting free radical chain reactions induced by formation of lipid peroxides. Peroxidation is the process by which fatty acids get oxidized (rancid).

The oxidation of LDL cholesterol is considered to be a trigger  for a number of cellular events which lead to the formation of atherosclerotic plaque. This includes the uptake of oxidized LDL- by monocytes which leads to foam cell formation, endothelial cell damage and stimulation of cytokine and growth factor release from cells in the artery wall. Vitamin E protects LDL cholesterol from oxidation, thereby limiting the initiation of plaque formation in the arteries.

The Daily Reference Intake of vitamin E for individuals over age fifty is 15 mg.
Vitamin E is found only in foods of plant origin and predominantly in plant oils. 
One fourth a cup of sunflower seeds, contains 17.0 mg vitamin E, one tablespoon of sunflower oil contains 7.0 mg, two tablespoons of peanut butter contains 3.3 mg, and two tablespoons of wheat germ contains 2.6 mg of vitamin E.

Vitamin E is a fat-soluble vitamin; its bioavailability depends on fat intake for stimulation of bile acids required for micelle formation. As such, sliced red grapes with a dallop of sour cream (fat content) and a tablespoon of sunflower seeds is a healthful snack.

Vitamin E occurs in food as tocopherols or tocotrienols. Alpha-tocopherol has the highest bioactivity. Vitamin E occurs naturally as d-alpha-tocopherol. The synthetic version is the dl-isomer has 25% less bioactivity than the d-isomer.  A vitamin supplement that lists "dl"-alpha-tocopherol in the ingredient is less expensive and less potent.

Vitamin E along with selenium, copper, and manganese are integral components of the cellular antioxidant defense system.