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• W2045685154 abstract "It is well known that platelet-derived growth factor-B (PDGF-B), a member of the neurotrophic factor family, is involved in normal physiological conditions, pathological changes, and neuroregulation following lesions. But the roles of endogenous PDGF-B in neuroregulation following spinal cord injury are far from being well known, especially in primates. This study explored the role of PDGF-B in the spinal cord and motor cortex in rhesus monkeys subjected to cord hemisection. Evaluation of the hindlimb motor function and the cortical somatosensory evoked potentials (CSEP) demonstrated a significant partial recovery from 30 days post-operation (dpo) to 90 dpo. Immunostaining revealed PDGF-B expression in neurons and scattered macrophages in the spinal cord. The number of PDGF-B immunoreactive neurons in the ventral horn of the spinal cord decreased significantly at the injury site at 14 dpo, followed by a rapid increase that surpassed the numbers in the control group at 30 dpo, and remained at these levels until 90 dpo. The protein levels of PDGF-B and platelet-derived growth factor receptor-beta (PDGFR-beta) as assessed by Western blot, as well as the mRNA levels of PDGF-B as assessed by RT-PCR demonstrated a tendency similar to that seen with immunohistochemistry. PDGF-B antibody administration effectively decreased locomotor function in the hindlimbs, especially on the injured side. No PDGF-B immunoreactive cells were detected in the motor cortex. Taken together, the present findings indicate that intrinsic PDGF-B expressed in the spinal cord may play an essential role in neuroregulation in primates following cord hemisection." @default.
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• W2045685154 date "2009-02-01" @default.
• W2045685154 modified "2023-10-10" @default.
• W2045685154 title "Roles of Platelet-Derived Growth Factor-B Expression in the Ventral Horn and Motor Cortex in the Spinal Cord–Hemisected Rhesus Monkey" @default.
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• W2045685154 doi "https://doi.org/10.1089/neu.2007.0374" @default.
• W2045685154 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/19236168" @default.
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