Anti-SOCS6 (full length) polyclonal antibody

Periodontitis refers to the inflammation of gums and the surrounding structures and caused by a bacterial infection. The infection occurs owing to poor oral hygiene and could destroy the bone and the gum over time if left untreated. The present study identified the involvement of a key long noncoding RNA (lncRNA), i.e. FGD5-AS1, in the pathogenesis of periodontitis by assessing its expression in the gingival tissues of patients diagnosed with chronic periodontitis (CP). Overexpression of FGD5-AS1 in primary human periodontal ligament cells (PDLCs) significantly reduced the lipopolysaccharide (LPS)-induced periodontitis, whereas its suppression aggravated this injury. Moreover, the miR-142-3p was markedly expressed in the gingival samples of patients diagnosed with CP and LPS-induced PDLCs. We found that the FGD5-AS1-mediated reduction in the inflammation was mediated through downside regulation of miR-142-3p, as evident from the upregulation of SOCS6, a target gene of miR-142-3p. Furthermore, the association between FGD5-AS1 and NF-kappa B pathway was detected. FGD5-AS1 was found to protect against LPS-stimulated PDLC injury through restraining the NF-kappa B signals. Based on these findings, we conclude that up-regulation of lncRNA FGD5-AS1 could protect against periodontitis via regulating the miR-142-3p/SOCS6/NF-kappa B signals. Therefore, the FGD5-AS1/miR-142-3p/SOCS6 axis may act as an important indicator in explaining the pathogenesis of periodontitis.

Suppressors of Cytokine Signaling (SOCS) Family Proteins are rapidly induced by interferon alpha 2a (IFN alpha) treatment. SOCS1 and SOCS3 mRNA is barely detectable in most cultured cells but upon IFN alpha stimulation transcript levels increase rapidly. Peak SOCS3 mRNA levels are reached three hours after IFN alpha induction followed by rapid degradation within a few hours. These results suggest post-transcriptional regulation of SOCS3 mRNA expression. In addition to various protein coding genes, also the levels of certain micro RNAs (miRNA) are upregulated by IFN alpha. Interestingly, the 3' UTR of SOCS1, SOCS3 and SOCS6 share conserved binding sites for IFN alpha inducible miRNAs. Here we propose a model in which the SOCS dependent negative feedback pathway of type I interferons may be controlled by RNA interference.