RGD Reference Report - Transplantation of olfactory ensheathing cells promotes the recovery of neurological functions in rats with traumatic brain injury associated with downregulation of Bad. - Rat Genome Database

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Transplantation of olfactory ensheathing cells promotes the recovery of neurological functions in rats with traumatic brain injury associated with downregulation of Bad.

Authors: Wang, You-Cui  Xia, Qing-Jie  Ba, Ying-Chun  Wang, Ting-Yong  LiN, Na  Zou, Yu  Shang, Fei-Fei  Zhou, Xin-Fu  Wang, Ting-Hua  Fu, Xue-Mei  Qi, Jian-Guo 
Citation: Wang YC, etal., Cytotherapy. 2014 Jul;16(7):1000-10. doi: 10.1016/j.jcyt.2013.12.009. Epub 2014 Feb 28.
RGD ID: 13782254
Pubmed: PMID:24582457   (View Abstract at PubMed)
DOI: DOI:10.1016/j.jcyt.2013.12.009   (Journal Full-text)


BACKGROUND AIMS: The neuroprotective effects of olfactory ensheathing cells (OECs) after transplantation have largely been known in the injured nervous system. However, the underlying mechanisms still must be further elucidated. We explored the effects of OEC transplantation on the recovery of neurophysiologic function and the related anti-apoptosis mechanism in acute traumatic brain injury.
METHODS: The OECs from neonatal Sprague-Dawley rats were isolated, identified and labeled and then were immediately transplanted into the regions surrounding the injured brain site that is resulted from free-weight drop injury.
RESULTS: Nerve growth factor and it's recepor, p75 was expressed in cultured OECs. Transplanted OECs survived, migrated around the injury site and significantly improved the neurological severe scores compared with the control group (P < 0.05). OEC transplantation significantly increased the number of GAP-43-immunopositive fibers and synaptophysin-positive vesicles (P < 0.05) but significantly decreased the number of apoptotic cells (P < 0.05). On the molecular level, the expression of Bad in the OEC transplantation group was significantly downregulated (P < 0.05).
CONCLUSIONS: OEC transplantation could effectively improve neurological deficits in TBI rats; the underlying mechanism may be related with their effects on neuroprotection and regeneration induction, which is associated with the downregulation of the apoptotic molecule Bad.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
traumatic brain injury treatmentISOBad (Rattus norvegicus)13782254; 13782254 RGD 
traumatic brain injury treatmentIEP 13782254 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Bad  (BCL2-associated agonist of cell death)

Genes (Mus musculus)
Bad  (BCL2-associated agonist of cell death)

Genes (Homo sapiens)
BAD  (BCL2 associated agonist of cell death)


Additional Information