TY - JOUR
T1 - Adropin preserves the blood-brain barrier through a Notch1/Hes1 pathway after intracerebral hemorrhage in mice
AU - Yu, Lingyan
AU - Lu, Zhengyang
AU - Burchell, Sherrefa
AU - Nowrangi, Derek
AU - Manaenko, Anatol
AU - Li, Xue
AU - Xu, Yang
AU - Xu, Ningbo
AU - Tang, Jiping
AU - Dai, Haibin
AU - Zhang, John H.
N1 - Publisher Copyright:
© 2017 International Society for Neurochemistry
PY - 2017/12
Y1 - 2017/12
N2 - Adropin is expressed in the CNS and plays a crucial role in the development of stroke. However, little is currently known about the effects of adropin on the blood-brain barrier (BBB) function after intracerebral hemorrhage (ICH). In this study, the role of adropin in collagenase-induced ICH was investigated in mice. At 1-h post-ICH, mice were administered with recombinant human adropin by intranasal. Brain water +content, BBB permeability, and neurological function were measured at different time intervals. Proteins were quantified using western blot analysis, and the localizations of adropin and Notch1 were visualized via immunofluorescence staining. It is shown that adropin reduced brain water content and improved neurological functions. Adropin preserved the functionality of BBB by increasing N-cadherin expression and reducing extravasation of albumin. Moreover, in vivo knockdown of Notch1 and Hes1 both abolished the protective effects of adropin. Taken together, our data demonstrate that adropin constitutes a potential treatment value for ICH by preserving BBB and improving functional outcomes through the Notch1 signaling pathway.
AB - Adropin is expressed in the CNS and plays a crucial role in the development of stroke. However, little is currently known about the effects of adropin on the blood-brain barrier (BBB) function after intracerebral hemorrhage (ICH). In this study, the role of adropin in collagenase-induced ICH was investigated in mice. At 1-h post-ICH, mice were administered with recombinant human adropin by intranasal. Brain water +content, BBB permeability, and neurological function were measured at different time intervals. Proteins were quantified using western blot analysis, and the localizations of adropin and Notch1 were visualized via immunofluorescence staining. It is shown that adropin reduced brain water content and improved neurological functions. Adropin preserved the functionality of BBB by increasing N-cadherin expression and reducing extravasation of albumin. Moreover, in vivo knockdown of Notch1 and Hes1 both abolished the protective effects of adropin. Taken together, our data demonstrate that adropin constitutes a potential treatment value for ICH by preserving BBB and improving functional outcomes through the Notch1 signaling pathway.
KW - N-cadherin
KW - Notch1
KW - adropin
KW - blood-brain barrier
KW - intracerebral hemorrhage
KW - Humans
KW - Intercellular Signaling Peptides and Proteins
KW - Male
KW - Signal Transduction/physiology
KW - Peptides/metabolism
KW - Animals
KW - Blood-Brain Barrier/drug effects
KW - Cerebral Hemorrhage/metabolism
KW - Mice
KW - Receptor, Notch1/metabolism
KW - Transcription Factor HES-1/metabolism
KW - Blood Proteins/metabolism
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UR - https://www.mendeley.com/catalogue/8fc08396-346a-3fc8-a88c-be99cee7ad62/
U2 - 10.1111/jnc.14238
DO - 10.1111/jnc.14238
M3 - Article
C2 - 29030969
SN - 0022-3042
VL - 143
SP - 750
EP - 760
JO - Journal of Neurochemistry
JF - Journal of Neurochemistry
IS - 6
ER -