Sestrin2 Overexpression Attenuates Focal Cerebral Ischemic Injury in Rat by Increasing Nrf2/HO-1 Pathway-Mediated Angiogenesis

In this study the investigators examine the effects of Sesn2 on cerebral ischemia damage by increasing angiogenesis through the Nrf2/HO-1 signaling pathway. Healthy adult Sprague–Dawley (SD) rats were exposed to photochemical cerebral ischemia while AAV injection was used to overexpress Sesn2. At five days after photochemical embolization, the investigators observed a reduction in neurological problems, decreased infarct volume, and diminished neuronal injury in the Sesn2 overexpression samples compared to the controls. To further explore these defensive mechanisms, the investigators also silenced Nrf2. While Sesn2, Nrf2, HO-1, and VEGF were significantly increased following cerebral ischemia, overexpression of Sesn2 further increased their expression. After silencing Nrf2, the opposite effect was observed. These results imply that Sestrin2 may activate the Nrf2 / HO-1 pathway, leading to enhanced angiogenesis following photothrombotic cerebral ischemia.
Source: Neuroscience - Category: Neuroscience Source Type: research