Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0279530 (bone cancer)
 1,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tumor metastasis to bone can subsequently lead to bone cancer pain (BCP). Currently, BCP is difficult to conquer due to a poor understanding of the potential mechanisms. Several studies have indicated that astrocyte-specific connexin 43 (Cx43) was involved in the neuropathic pain, and Cx43 induced the release of chemokine CXCL12 in bone marrow stromal cells. However, whether spinal Cx43 mediates the production of CXCL12 to participate in the maintenance of BCP is still unknown. Here we showed that Walker 256 tumor cells inoculation into the tibia induced a significant mechanical allodynia, which was accompanied by upregulation of spinal p-Cx43 and CXCL12 expression levels from day 6 to day 18 after inoculation. Spinal Cx43 was mainly expressed in astrocytes, and intrathecal (43)Gap26 (a selective Cx43 blocker) markedly attenuated mechanical allodynia as well as reduced p-Cx43 and CXCL12 expression at day 18 after inoculation. Pre-intrathecal administration of CXCL12 almost abolished the attenuated mechanical allodynia by (43)Gap26. Furthermore, intrathecal injection of anti-CXCL12 neutralizing antibody could ameliorate mechanical allodynia with concomitant inhibition of upregulation of CXCL12 expression, but not influence on p-Cx43 expression. Our results indicate that Cx43 mediates CXCL12 production from spinal dorsal horn in astrocytes to maintain bone cancer pain in rats. These findings may improve our understanding of the underlying mechanisms of BCP and provide a novel target for the treatment of BCP.
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PMID:Connexin 43 Mediates CXCL12 Production from Spinal Dorsal Horn to Maintain Bone Cancer Pain in Rats. 2672 9

Brain plasticity is referred to the ability of the brain to change in structure and functional activities from microscopic aspects (synapses) in individual neurons to larger-scale aspects such as cortical remapping, neuronal remodeling, etc. in response to injury. Acupuncture has a positive effect in the treatment of cerebral diseases, thus leading to an increasing research on its underlying mechanisms in regulating brain plasticity. The present paper reviewed recent development of studies on acupuncture treatment of Alzheimer's disease, vascular dementia, cerebral ischemia, bone cancer pain, autism, etc. from 1) regulating synaptic plasticity (up-regulating the proportion of hippocampal synapses, increasing synaptic curvature, post-synaptic density, and numerical density, areal density, and lowering synaptic cleft); 2) increasing hippocampal post-synaptic potential slop, peak and peak area of population spikes to evoke long-term potentiation (LTP) by regulating the expression of glutamate N-methyl-D-aspartate (NMDA) and alpha amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) receptors, and growth associated protein (GAP-43); 3) down-regulating the expression of glial fibrillary acidic protein (GFAP) to suppress the activity of astrocytes in the ischemic cerebral area and hippocampus in cerebral ischemia rats, and in the spinal cord dorsal horns of bone cancer rats, etc. and promoting vimentin and connexin 43 expression; and 4) promoting neuronal remodeling, and repair and regeneration of the injured nerve in the central nervous system via regulating neuron-glia network, expression of nerve growth factor, brain derived neurotrophic factor, etc. The future studies should pay more attention to 1) the contribution of acupuncture intervention to the correlation between the initiation of the endogenous protective effect and the brain plasticity during the onset of nerve injury and repair of the injured nerve, and 2) standarization of stimulating quantity, manipulation and duration of acupuncture treatment, as well as the relationship between the stimulating quantity and efficacy.
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PMID:[Progress of Researches on Mechanisms of Acupuncture Therapy in Regulating Brain Plasticity]. 3036 66