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Neurochem Int. 2019 Mar 29;128:14-20. doi: 10.1016/j.neuint.2019.03.019. [Epub ahead of print]

Increased REDD1 facilitates neuronal damage after subarachnoid hemorrhage.

Author information

1
Department of Laboratory Medicine, Affiliated Hospital of Nantong University, Nantong, China.
2
Department of Neurochemistry, Institute of Special Environmental Medicine, Co-Innovation Center of Neuroregeneration, Nantong University, Nantong, China.
3
Department of Neurosurgery, Affiliated Hospital of Nantong University, Nantong, China.
4
Department of Neurosurgery, Affiliated Hospital of Nantong University, Nantong, China. Electronic address: chenjian9079@163.com.
5
Department of Neurochemistry, Institute of Special Environmental Medicine, Co-Innovation Center of Neuroregeneration, Nantong University, Nantong, China. Electronic address: wuxmsu@ntu.edu.cn.

Abstract

Regulated in development and DNA damage responses 1 (REDD1) is a highly conserved stress-response protein and can be induced by hypoxia/ischemia and DNA damage. However, it is not known whether REDD1 involves in neuronal damage caused by subarachnoid hemorrhage (SAH) that is known as one of the most important causes of disability and death worldwide. Here, we first found that SAH markedly induced the increase of REDD1 (35.467 ng/ml) in cerebrospinal fluid (CSF) of patients at acute stage (within 24 h from bleeding) compared to that of control (0.644 ng/ml). And, REDD1 level was positively correlated with severity of brain injuries (Hunt-Hess grade of SAH), but it showed an obvious decline at recovery stage 6.201 ng/ml (before discharge from hospital) because of good recovery. Moreover, it was found that the expression of REDD1 was significantly induced by hemolysate in a dose-dependent way in neurons. Knockdown of REDD1 by lentivirus encoded REDD1-shRNA could inhibit the neuronal apoptosis and LDH leakage caused by hemolysate. Importantly, the level of REDD1 in peripheral blood of SAH patients was significantly higher (4.364 ng/ml) than that of healthy persons (1.317 ng/ml) and also was positively correlated with that in CSF. Taken together, our findings provide the novel and direct evidence that REDD1 could play a critical role of process of neuronal damage caused by SAH, suggesting a new molecular target to protect brain function from SAH injury.

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