Activation of endothelial nitric oxide synthase following spinal cord injury in mice.
Endothelial nitric oxide synthase (eNOS) plays a neuroprotective role after cerebral ischemia through the production of NO, which enhances cerebral blood flow. However, precise details regarding activation of eNOS after spinal cord injury (SCI) largely remain to be elucidated. In the present study we investigated chronological alteration and cellular location of eNOS and phosphorylated (p)-eNOS at Ser(1177) following SCI in mice. Western blot analysis showed eNOS to be significantly phosphorylated at Ser(1177) from 1 to 2 days after mild SCI, with gradual decrease thereafter. Immunohistochemistry revealed the p-eNOS to be mainly expressed in the endothelial cells of microvessels within gray matter under these conditions. These findings suggest that mild SCI activates eNOS in the subacute stage, which increases spinal cord blood flow and may be involved in protective and repair responses.
Osuka
Koji
K
Department of Neurological Surgery, Aichi Medical University, 21 Karimata Yazako, Nagakute, Aichi-gun 480-1195, Japan.
Watanabe
Yasuo
Y
Takagi
Teruhide
T
Usuda
Nobuteru
N
Atsuzawa
Kimie
K
Yoshida
Jun
J
Takayasu
Masakazu
M
D000818:Animals; D004789:Enzyme Activation; D005260:Female; D051379:Mice; D008810:Mice, Inbred C57BL; D052248:Nitric Oxide Synthase Type I / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism*; D012694:Serine / Q000378:metabolism; D013119:Spinal Cord Injuries / Q000201:enzymology*; D013997:Time Factors
D012694:Serine; D052248:Nitric Oxide Synthase Type I; D052250:Nitric Oxide Synthase Type III