[논문]Dual effects of carbon monoxide on pericytes and neurogenesis in traumatic brain injury

Choi, Yoon Kyung; Maki, Takakuni; Mandeville, Emiri T; Koh, Seong-Ho; Hayakawa, Kazuhide; Arai, Ken; Kim, Young-Myeong; Whalen, Michael J; Xing, Changhong; Wang, Xiaoying; Kim, Kyu-Won; Lo, Eng H

doi:10.1038/nm.4188

Dual effects of carbon monoxide on pericytes and neurogenesis in traumatic brain injury

Nature medicine, v.22 no.11, 2016년, pp.1335 - 1341

Choi, Yoon Kyung (Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, USA.) , Maki, Takakuni (Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, USA.) , Mandeville, Emiri T (Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, USA.) , Koh, Seong-Ho (Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, USA.) , Hayakawa, Kazuhide (Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, USA.) , Arai, Ken (Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, USA.) , Kim, Young-Myeong (Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, USA.) , Whalen, Michael J (Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, USA.) , Xing, Changhong (Department of Neurology, Hanyang University College of Medicine, Seoul, Republic of Korea.) , Wang, Xiaoying (Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, USA.) , Kim, Kyu-Won (Department of Neurology, Massachusetts Gene) , Lo, Eng H

Abstract ▼ AI-Helper

At low levels, carbon monoxide (CO) has physiological roles as a second messenger and neuromodulator(1,2). Here we assess the effects of CO in a mouse model of traumatic brain injury (TBI). Treatment with CO-releasing molecule (CORM)-3 reduced pericyte death and ameliorated the progression of neurological deficits. In contrast, although treatment with the radical scavenger N-tert-butyl-a-phenylnitrone (PBN) also reduced pericyte death, neurological outcomes were not rescued. As compared to vehicle-treated control and PBN-treated mice, CORM-3-treated mice showed higher levels of phosphorylated neural nitric oxide synthase within neural stem cells (NSCs). Inhibition of nitric oxide synthase diminished the CORM-3-mediated increase in the number of cells that stained positive for both the neuronal marker NeuN and 5-bromo-2'-deoxyuridine (BrdU; a marker for proliferating cells) in vivo, consequently interfering with neurological recovery after TBI. Because NSCs seemed to be in close proximity to pericytes, we asked whether cross-talk between pericytes and NSCs was induced by CORM-3, thereby promoting neurogenesis. In pericyte cultures that were undergoing oxygen and glucose deprivation, conditioned cell culture medium collected after CORM-3 treatment enhanced the in vitro differentiation of NSCs into mature neurons. Taken together, these findings suggest that CO treatment may provide a therapeutic approach for TBI by preventing pericyte death, rescuing cross-talk with NSCs and promoting neurogenesis.

참고문헌 (18)

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Dual effects of carbon monoxide on pericytes and neurogenesis in traumatic brain injury

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Dual effects of carbon monoxide on pericytes and neurogenesis in traumatic brain injury

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