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Oral mucosa stem cells alleviates spinal cord injury-induced neurogenic bladder symptoms in rats

Authors
Cho, Young-SamKo, Il-GyuKim, Sung-EunLee, Sung-MinShin, Mal-SoonKim, Chang-JuKim, Sang-HoonJin, Jun-JangKim, Khae-Hawn
Issue Date
13-May-2014
Publisher
BIOMED CENTRAL LTD
Keywords
Spinal cord injury; Oral mucosa stem cells; Cystometry; Apoptosis; Nerve growth factor; c-Fos
Citation
JOURNAL OF BIOMEDICAL SCIENCE, v.21
Journal Title
JOURNAL OF BIOMEDICAL SCIENCE
Volume
21
URI
https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/12632
DOI
10.1186/1423-0127-21-43
ISSN
1021-7770
Abstract
Background: Spinal cord injury (SCI) deteriorates various physical functions, in particular, bladder problems occur as a result of damage to the spinal cord. Stem cell therapy for SCI has been focused as the new strategy to treat the injuries and to restore the lost functions. The oral mucosa cells are considered as the stem cells-like progenitor cells. In the present study, we investigated the effects of oral mucosa stem cells on the SCI-induced neurogenic bladder in relation with apoptotic neuronal cell death and cell proliferation. Results: The contraction pressure and the contraction time in the urinary bladder were increased after induction of SCI, in contrast, transplantation of the oral mucosa stem cells decreased the contraction pressure and the contraction time in the SCI-induced rats. Induction of SCI initiated apoptosis in the spinal cord tissues, whereas treatment with the oral mucosa stem cells suppressed the SCI-induced apoptosis. Disrupted spinal cord by SCI was improved by transplantation of the oral mucosa stem cells, and new tissues were increased around the damaged tissues. In addition, transplantation of the oral mucosa stem cells suppressed SCI-induced neuronal activation in the voiding centers. Conclusions: Transplantation of oral mucosa stem cells ameliorates the SCI-induced neurogenic bladder symptoms by inhibiting apoptosis and by enhancing cell proliferation. As the results, SCI-induced neuronal activation in the neuronal voiding centers was suppressed, showing the normalization of voiding function.
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