Biomedical Research

NF-κB is implicated in microglia activation, and tends to stimulate Secondary Spinal Cord Injury (SCI). The method entails activation of NF-κB signaling pathway by TRAF6 via the function of polyubiquitination. It is renowned that deubiquitination of TRAF6 that is mediated via Deubiquitinating enzyme (DUB) can considerably impede NF-κB pathway activation. The ubiquitinspecific protease 22 (USP22) is a member of the deubiquitinase family. We, therefore, put forward that USP22 is involved in the activation of microglial as well as successive neuronal inflammation subsequent to SCI. We investigated the manifestation and the function of USP22 after SCI. The Western blot analysis indicated that expression of USP22 had been downregulated while the p-p65 expression had been upregulated in the spinal cord subsequent to SCI. Immunohistochemical along with staining of immunofluorescence demonstrated that USP22 had been manifested in microglia even though its expression declined subsequent to SCI. In vitro LPS-induced microglia activation demonstrated a declined USP22 expression as well as an improvement of p-p65 and TRAF6 expressions. Furthermore, silencing of USP22 in LPS-induced microglia activation supported the p-p65 and TRAF6 expression of in addition to TNF-α and IL-1β secretion. Summarily, this study details the initial proof that in microglial cells expression of USP22 declines subsequent to SCI in rats. USP22 expression’ downregulation may endorse activation of microglia as well as successive neuronal inflammation via NF- κB through attenuation of the deubiquitination of the TRAF6. The mechanism can be said to be of great importance in the secondary SCL’s pathophysiology.

Author(s): Weizhi Fang, Qixin Zheng
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