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(Stroke. 2004;35:e94.)
© 2004 American Heart Association, Inc.

Letters to the Editor

CD105 (Endoglin), Apoptosis, and Stroke

Department of Pathology, Manchester University, United Kingdom

Mark Slevin Pat Kumar

Department of Biological Sciences, Manchester University, United Kingdom

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

To the Editor:

The recent paper by Zhu et al¹ in this journal provides an insight into the possible mechanism of hypoxia-induced upregulation of CD105 (endoglin). The following 3 points are relevant to their paper.

Suitability of Endothelial Cell Culture and Animals as Models for Human Stroke

Lately there has been a major debate regarding the relevance of cell culture/animal models for human stroke in general and for angiogenesis in particular. Some authors maintain that the failure of current therapies for stroke in humans based on the use of animal models is possibly owing to the fact that the pathobiology of human stroke is not mirrored by experimentally-induced stroke in animal models. If true, it would limit the value findings of Zhu et al,¹ which are based on the use of murine endothelial cell culture and an in vivo mouse model of focal cerebral ischemia. However, there is strong evidence to discount this possibility. First, CD105 has been found to be highly expressed in the penumbra region of human stroke.² Second, soluble CD105 levels in plasma have been found to be high in patients with stroke (our unpublished data, 2004). Furthermore, human vascular, like murine, endothelial cells showed an upregulation of CD105 expression when cultured under hypoxic conditions, although there were some notable differences in the 2 studies.^1,3

Hypoxia and Apoptosis

Li et al³ reported that hypoxia-induced upregulation of CD105 prevented vascular endothelial cells from undergoing TGF-ß–induced cell apoptosis. The overexpression of CD105 in hypoxic cells ameliorated cell apoptosis either with or without TGF-ß1, the conclusion being that CD105 functions via TGF-ß1 signaling plus another . . . [Full Text of this Article]

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