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The aim of this study is to investigate the effect of microtubule depolymerization by colchicine on hyperalgesia mediated by transient receptor potential vanilloid 4 (TRPV4) in a neuropathic pain model of chronic compression of the dorsal root ganglion (DRG) (hereafter termed CCD) in rat. Intrathecal administration of microtubule-depolymerizing agent, colchicine, attenuated the activated effect of 4alpha-phorbol 12, 13-didecanoate (4alpha-PDD, TRPV4 specific agonist) on mechanical and thermal hyperalgesia in CCD rats. This observation is in agreement with our in vitro experiments with DRG cells that showed a significant attenuation of 4alpha-PDD-activated Ca(2+)-influx and substance P (SP) release with the colchicine treatment. We conclude that microtubule depolymerization by colchicine can regulate pain sensitivity by depressing the hyperalgesia mediated by TRPV4.

Objective: This study aimed to investigate the incidence and clinical characteristics of chronic subdural haematoma (CSDH) evolving from traumatic subdual hydroma (TSH). Methods: The clinical characteristics of 44 patients with CSDH evolving from TSH were analysed retrospectively and the relevant literature was reviewed. Results: In 22.6% of patients, TSH evolved into CSDH. The time required for this evolution was 14–100 days after injury. All patients were cured with haematoma drainage. Conclusions: TSH is one possible origin of CSDH. The clinical characteristics of TSH evolving into CSDH include polarization of patient age and chronic small effusion. The injuries usually occur during deceleration and are accompanied by mild cerebral damage.

Transient receptor potential vanilloid 4 (TRPV4) is a Ca(2+)-permeable, non-selective cation channel that is involved in the transmission of pain signals mediated by dorsal root ganglion (DRG). Annexin A2 belongs to a class of membrane-binding proteins that plays an important role in the regulation of ion channels. Nevertheless, little is known about the interaction between them in DRG. In this paper, we evaluated the functional interaction of TRPV4 with annexin A2 in DRG. We have used immunocytochemistry and co-immunoprecipitation assays to investigate the interaction between annexin A2 and TRPV4 in DRG. The role of annexin A2 in the regulation of TRPV4 activity in DRG was further verified by measurement of intracellular free calcium concentrations ([Ca(2+)](i)) and substance P (SP) release. First, annexin A2 was showed partial co-localization with TRPV4 in DRG neurons. Then, annexin A2 and TRPV4 were co-precipitated with each other in DRG lysates. Furthermore, the downregulation of annexin A2 using specific small interfering RNA significantly inhibited Ca(2+) influx and SP mediated by TRPV4. Our results provide evidence that annexin A2 is associated with TRPV4 and regulates TRPV4-mediated Ca(2+) influx and SP release in DRG neurons. The objective of this work is to determine the influence of annexin A2 on TRPV4 in DRG neurons, which may be the basis for treatment of pain relief.

Prodigiosin (PG), a member of a family of natural red pigments produced by a variety of bacteria, was first discovered in Serratia marcescens. PG has been reported to have an apoptosis-inducing effect in many cancers, such as lymphoma, colon cancer and nasopharyngeal carcinoma. For this study, we used three glioblastoma (GBM) cell lines (LN229, U251 and A172) to explore the effect of prodigiosin on GBM cells. A CCK8 assay was used to evaluate cell viability. We determinedthe cell cycle distribution by flow cytometry and measured proliferation by an EdU incorporation assay. The expression of different molecules was investigated by western blotting and RT-PCR. We further confirmed our results by plasmid transfection and lentiviral transduction. The LN229 xenograft model was used to study the effect of prodigiosin in vivo. We confirmed that prodigiosin played an anticancer role in several GBM cell lines through the KIAA1524/PP2A/Akt signalling pathway. Prodigiosin inhibited the protein expression of KIAA1524 by suppressing its transcription, which led to activation of PP2A. Afterward, PP2A inhibited the phosphorylation of Akt, thereby inducing increased expression of p53/p21. Furthermore, it was verified that prodigiosin inhibited the KIAA1524/PP2A/Akt axis in vivo in the LN229 xenograft model. These data improve the understanding of the anticancer effects of prodigiosin and further highlight the potential of prodigiosin for the development of anti-glioma drugs.