KPC1 expression and essential role after acute spinal cord injury in adult rat |
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Authors: | Zhao Jian Zhang Shuangwei Wu Xiujie Huan Weipeng Liu Zhiqiang Wei Haixiang Shen Aiguo Teng Honglin |
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Institution: | (1) Orthopedic Department, Affiliated Hospital of Nantong University, and The Jiangsu Province Key Laboratory of Neuroregeneration, Nantong University, 226001 Nantong, People’s Republic of China;(2) Department of Spine Surgery, The First Affiliated Hospital of Wenzhou Medical College, 325000 Wenzhou, Zhejiang, People’s Republic of China; |
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Abstract: | KPC1 (Kip1 ubiquitylation-promoting complex 1) is the catalytic subunit of the ubiquitin ligase KPC, which regulates the degradation
of the cyclin-dependent kinase inhibitor p27kip1 at the G1 phase of the cell cycle. To elucidate the expression and role of KPC1 in nervous system lesion and repair, we performed
an acute spinal cord contusion injury (SCI) model in adult rats. Western blot analysis showed a significant up-regulation
of KPC1 and a concomitant down-regulation of p27kip1 following spinal injury. Immunohistochemistry and immunofluorescence revealed wide expression of KPC1 in the spinal cord,
including expression in neurons and astrocytes. After injury, KPC1 expression was increased predominantly in astrocytes, which
highly expressed PCNA, a marker for proliferating cells. Co-immunoprecipitation demonstrated increased interactions between
p27kip1 and KPC1 4 days after injury. To understand whether KPC1 plays a role in astrocyte proliferation, we applied LPS to induce
astrocyte proliferation in vitro. Western blot analysis demonstrated that p27kip1 expression was negatively correlated with KPC1 expression following LPS stimulation. Immunofluorescence analysis showed subcellular
localizations of p27kip1 and KPC1 were also changed following the stimulation of astrocytes with LPS. These results suggest that KPC1 is related to
the down-regulation of p27kip1; this event may be involved in the proliferation of astrocytes after SCI. |
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