CD105 (endoglin), apoptosis, and stroke

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. 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 …