Pathophysiologic disease modeling for the complex regional pain syndrome by tibial fracture in laboratory animals

摘要

Through this study, we observed that the PIP between SQSTM1 and tau play an essential role in enhancing tau protein clearance. Thus, the enhancement of this PIP is thought to be a therapeutic strategy in brain disorders revealing a failure in tau protein degra- dation. Axon guidance molecules have been shown to play a role in guiding developing vascular network formation. Previous stud- ies revealed that the secreted Semaphorin 3E (Sema 3E) and its receptor Plexin-D1 pair, which is one of the traditional axon guid- ance cues is involved in the peripheral vascular remodeling as well as a normal vascular formation during development. However, it remains still unclear whether the Sema3E-Plexin-D1 signaling is implicated in the revascularization in the brain after ischemic insult. Given the importance of functional revascularization after ischemic stroke, it is critical to understand how brain vascular net- work is established adequately after such damage. To determine the role of Sema3E-PlexinD1 signaling in the post-stroke recovery, we performed a transient middle cerebral artery occlusion using genet- ically modified mouse models. Here we show that ischemic damage induced rapid Sema3e expression in the penumbral neurons, and a few days later, consecutive Plexin-D1 increase in the remodeling vessel. Surprisingly, ablation of Sema3e or Plxnd1 showed severe ischemic brain damage and delayed recovery accompanied by less and aberrant vasculature. Moreover, we also observed the BBB.