Research reportIncreased expression of HERPUD1 involves in neuronal apoptosis after intracerebral hemorrhage

- Expression of HERPUD1 was obviously increased around the hematoma in rat ICH model.
- The expression of apoptosis markers including cytochrome c (cyt c) and active caspase-3 increased accompanied to HERPUD1 in vivo.
- HERPUD1 silence brought about up-regulation of cyt c and active caspase-3 coupled with increased cell apoptosis in vitro model.
- HERPUD1 might play a protective role in ICH-induced neuronal apoptosis in rat models.
- ER stress might play a part in the complicated and various mechanism of ICH.

Homocysteine-inducible endoplasmic reticulum stress-inducible ubiquitin-like domain member 1 protein (HERPUD1) is involved in endoplasmic reticulum stress response. Immense amounts of research showed HERPUD1 plays multiple roles in various models. In this work, we explored the role of HERPUD1 during the pathophysiological processes of intracerebral hemorrhage (ICH). Rat ICH model was established and verified by behavioral test. Western blot and immunohistochemistry revealed a significant up-regulation of HERPUD1 expression around the hematoma after ICH. Besides, the expression of cytochrome c (cyt c) and active caspase-3 increased accompanied to HERPUD1 expression. Double-labeled immunofluorescence indicated HERPUD1 mainly colocalized with neurons. Further study showed HERPUD1 silence brought about up-regulation of apoptosis markers including cyt c and active caspase-3 coupled with increased cell apoptosis in vitro model. All these findings suggested that HERPUD1 might play a protective role in ICH-induced neuronal apoptosis in rat models.