This Article Full Text Full Text (PDF) All Versions of this Article: 38/7/2036    most recent STROKEAHA.107.489856v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Dietrich, H. H. Search for Related Content PubMed PubMed Citation Articles by Dietrich, H. H. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Hazardous Substances DB CHOLESTEROL Related Collections Animal models of human disease Risk Factors Genetically altered mice Brain Circulation and Metabolism Risk Factors for Stroke Endothelium/vascular type/nitric oxide Other Vascular biology Related Article

(Stroke. 2007;38:2036.)
© 2007 American Heart Association, Inc.

Editorials

Apolipoprotein E in Hypercholesteremia and Beyond

Hans H. Dietrich, PhD

From the Department of Neurological Surgery, Washington University Medical School, St. Louis, Mo.

Correspondence to Hans H. Dietrich, Department of Neurological Surgery, Washington University Medical School, 660 South Euclid Avenue, St. Louis, MO 63110. E-mail dietrich_h@wustl.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

See related article, pages 2136–2141.

Apolipoprotein E (ApoE) is a protein related to the receptor-mediated removal of lipids from the blood stream. When ApoE-deficient mice were introduced,^1,2 these animals displayed hypercholesteremia and increased atherosclerosis, providing a new tool to study hypercholesteremia-related pathological mechanisms and have been used extensively ever since. With respect to the cerebral circulation, it is interesting to note that not until 1998 did the first study on ApoE deficiency and cerebral ischemia appear³ and only 5 more studies, mostly related to stroke and inflammation, followed to this date in this field.

Kitayama et al are interested to study the effect of hypercholesteremia on pial arteriolar vasomotor responses. They used hemizygous (ApoE^+/–) animals as their control (rather than homozygotes) and ApoE-deficient mice (ApoE^–/–) that were fed normal or high-fat diets. The first observation is that the hemizygous control animals have similar cholesterol levels as homozygous mice, indicating that one functioning allel of ApoE may be sufficient to keep blood cholesterol at normal levels. After demonstrating that especially severe hypercholesteremia adversely affects pial arteriolar dilation, the group continues to show that scavenging oxygen radicals with Tempol or inhibiting NADPH oxidase with Apocynin can restore vessel dilation to Acetylcholine at the lower concentration tested. But at the higher concentration used, Acetylcholine did not achieve dilation comparable to control animals. This seems to indicate that another factor besides oxygen radicals affects the vascular dilation to Acetylcholine in severely hypercholesteremic arterioles. If there is another factor and what this . . . [Full Text of this Article]

Related Article:

Cerebral Vascular Dysfunction During Hypercholesterolemia

Jiro Kitayama, Frank M. Faraci, Steven R. Lentz, and Donald D. Heistad
Stroke 2007 38: 2136-2141. [Abstract] [Full Text] [PDF]