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The suppressor of cytokine signaling (SOCS) plays a negative role in the cytokine signaling pathway, preventing excessive signaling from interfering with the metabolic homeostasis of the body. By regulating the Janus kinase-signal transducer and activator of transcription pathway through negative feedback, SOCS have a significant impact on the regulation of both innate and adaptive immunity against pathogens, thus playing a crucial role in the immune response, growth, and development of the body. In this study, the cDNA sequences of SOCS1, 2, 3a, 3b, 4, 5b, 6, 7, 8, 9, and CISH genes of spotted seabass (Lateolabrax maculatus), an important marine economic fish in China, were cloned using RT-PCR, nested PCR, and RACE techniques. Multiple sequence alignment showed that the SOCS family members shared highly conserved functional structural domains, including the SRC homology 2 domain (SH2 domain) and the SOCS-box domain. The phylogenetic analysis showed that SOCS1, 2, 3a, 3b, 8, and CISH belonged to the type II subfamily of SOCS genes, while SOCS4, 5b, 6, 7, and SOCS9 belonged to the type I subfamily. Furthermore, gene organization and syntenic analysis confirmed the phylogenetic analysis and protein annotation of the SOCS gene family in spotted seabass. Constitutive expression of spotted seabass SOCS genes was observed in various tissues of healthy fish, with varying expression levels. Following the lipopolysaccharide and Edwardsiella tarda challenge, the expression profiles of spotted seabass SOCS genes were differently regulated in the gill, head kidney, intestine, and spleen. These findings provide a basis for future research on the functional properties of SOCS genes in spotted seabass. [ABSTRACT FROM AUTHOR]

Background: This study aims to investigate the independent and combined effects of progesterone and suppressor of cytokine signaling (SOCS)-3 DNA methylation on type 2 diabetes mellitus (T2DM) among men and postmenopausal women in rural China. Methods: A case–control study with 914 participants (329 T2DM, 585 controls) was conducted. Serum progesterone was detected with liquid chromatography-tandem mass spectrometry. DNA methylation of SOCS3 was determined by MethylTarget™. Linear regression was applied to evaluate the associations of progesterone and SOCS3 methylation with marks of glucose metabolism. Logistic regression was employed to investigate the independent and combined effects of progesterone and SOCS3 methylation with T2DM in men and postmenopausal women. Results: After multiple adjustment, progesterone was positively associated with T2DM in both men (odds ratio (OR) (95% confidence interval (CI)): 2.77 (1.79, 4.29)) and postmenopausal women (OR (95% CI): 1.85 (1.26, 2.72)). Methylation level of Chr17:76,356,190 or Chr17:76,356,199 (SOCS3) was negatively associated with T2DM in both men (OR (95% CI): 0.58 (0.39, 0.86) or 0.27 (0.14, 0.51)) and postmenopausal women (OR (95% CI): 0.43 (0.29, 0.65) or 0.53 (0.28, 0.99)). Subjects with high progesterone and low Chr17:76,356,190 or Chr17:76,356,199 methylation were more susceptible to have a higher prevalence of T2DM (men: OR (95% CI): 5.20 (2.49, 10.85) or 5.62 (2.74, 11.54); postmenopausal women: OR (95% CI): 3.66 (1.85, 7.26) or 3.27 (1.66, 6.45)). Conclusions: The independent and combined effects of progesterone and SOCS3 methylation on T2DM were found among men and postmenopausal women, suggesting that ensuring low levels of progesterone and high methylation of SOCS3 could reduce the prevalence of T2DM. Trial registration The Chinese Clinical Trial registration: The Henan Rural Cohort Study, ChiCTR-OOC-15006699. Registered 06 July 2015, http://www.chictr.org.cn/showproj.aspx?proj=11375 [ABSTRACT FROM AUTHOR]

Recently, populations of Chinese spiny frogs (Quasipaa spinosa), an important amphibian species in China, have decreased, mainly due to a disease caused by the gram-negative bacteria Proteus mirabilis. To elucidate the immune response of the frogs, this study aimed to identify novel candidate genes functionally associated with P. mirabilis infection-induced "rotting skin" disease. Chinese spiny frogs were infected with P. mirabilis , and the skin transcriptome was sequenced using the MGISEQ-2000 platform. A total of 233,965 unigenes were obtained by sequencing, of which 27.23 % were known genes. Screening of differentially expressed genes (DEGs) indicated 210 unigenes differentially expressed after P. mirabilis infection, of which 132 unigenes were up-regulated, and 78 unigenes were down-regulated. Using Kyoto Encyclopedia of Genes and Genomes enrichment analysis, DEGs were identified as enriched in signal pathways, such as oxidative phosphorylation, apoptosis, and the Janus kinase-signal transducer and activator of transcription pathway. Of the DEGs, there was a significant upregulation of the colony stimulating factor 2 receptor beta common subunit , interleukin 2 receptor subunit gamma , cathelicidin antimicrobial peptide , interleukin-17 receptor E , receptor-interacting serine/threonine-protein kinase 3 , and pulmonary surfactant-associated protein D immune genes following P. mirabilis infection. Conversely, scavenger receptor cysteine-rich domain-containing group B protein , tumor protein p53 inducible nuclear protein 2 , suppressor of cytokine signaling 2 , and metalloreductase STEAP3 were significantly downregulated. In conclusion, the first skin transcriptome database of Chinese spiny frogs was established, and several immune genes were identified to elucidate the pathogenic mechanism of "skin rot" in Chinese spiny frogs and other cultured frogs. [Display omitted] • Skin transcriptomes were obtained from Chinese spiny frogs with Proteus mirabilis. • 210 genes were differentially expressed between the P. mirabilis infected group and the control group. • Among the DEGs, many immune-related genes were closely associated with P. mirabilis infection. [ABSTRACT FROM AUTHOR]

The suppressor of cytokine signaling (SOCS) family members play crucial roles in regulating immune signal pathways by acting as inhibitors of cytokine receptor signaling. In this study, 10 SOCS genes were identified in soiny mullet (Liza haematocheila), an economically important aquaculture mugilid species in China and other Asian countries. Sequence comparison showed that the sequence identity between mullet SOCSs and their counterparts from other vertebrates ranged from 38.2% to 92.5%. All mullet SOCS genes were constitutively expressed in tissues examined, but their expression patterns were different. Further, following Streptococcus dysgalactiae infection, all mullet SOCS genes exhibited distinct expression patterns in tissues. These results suggest that SOCSs are involved in immune response to bacterial infection and provide the basis for understanding the complex cytokine regulatory network of teleosts. • Ten members of SOCSs family are obtained from soiny mullet. • This paper is the first report on SOCSs of Mugiliformes. • This paper investigates the expression of SOCSs under gram positive bacterial infection. [ABSTRACT FROM AUTHOR]

The aim is to analyze the relationship and significance of the FOS, FOSB, Suppressors of cytokine signaling (SOCS), and hypoxia-inducible factor 1 (HIF1) gene loci and their polymorphisms with periodontitis and osteopenia in the Chinese population. In this case-control study, data on questionnaires, periodontal examination, bone mineral density, and FOS, FOSB, SOCS3, and HIF1 gene loci and their polymorphisms were obtained from 474 participants. The data were analyzed using the analysis of variance, Kruskal-Wallis test, χ 2 test, and logistic regression. The incidence of osteopenia was significantly increased in patients with periodontitis compared to controls (58.6 vs. 34.4%, P < 0.001). Accordingly, the risk was increased 2.21-fold compared with controls (95% CI 2.09-4.95). Osteopenia patients had a significantly higher risk of periodontitis than patients with normal bone density (OR = 3.22, 95% CI 2.09-4.94). There were significant positive associations between FOSB and SOCS3 polymorphisms and periodontitis and osteopenia susceptibility. Individuals carrying the G/G genotype of the FOSB gene rs708905 locus had an increased risk of periodontitis (OR = 5.06, 95% CI 2.36-10.86) and osteopenia (OR = 3.26, 95% CI 1.34-7.96). Compared with the C/C genotype, the A/A genotype of the FOSB rs8105114 locus was associated with a significantly higher risk of periodontitis (OR = 2.14, 95% CI 1.02-4.53) and osteopenia (OR = 2.85, 95% CI 1.12-7.22). Compared with the A/A genotype, the risk of periodontitis in the G/G genotype of the SOCS3 rs7207782 locus was increased 3.10-fold (P < 0.001), and the risk of osteopenia was increased 2.01-fold (P = 0.023). There was a bidirectional relationship between periodontitis and osteopenia. The rs708905 G/G and rs8105114 A/A genotypes of FOSB and the rs7207782 G/G genotype of SOCS3 were risk factors for both periodontitis and osteopenia in the Chinese population, which could increase knowledge about disease‑specific and cross‑disease genetic pattern., (© 2022. The Author(s), under exclusive licence to The Society of The Nippon Dental University.)

Duck Tembusu virus (DTMUV), an emerging infectious pathogen, has caused severe disease in ducks and huge economic losses to the poultry industry in China since 2009. Despite considerable advances in understanding the effects of microRNAs on host antiviral immune responses, it remains unclear how miRNAs regulate DTMUV replication in duck embryo fibroblast (DEF) cells. This study aims to clarify the role of host microRNA-148a-5p (miR-148a-5p) in regulating DTMUV replication by targeting SOCS1. First, we found that during DTMUV infection, the expression of miR-148a-5p in DEFs was downregulated in a time-dependent and dose-dependent manner, while the expression of SOCS1 was significantly upregulated. In addition, we found that when miR-148a-5p mimics were transfected into DEFs, viral RNA copies, viral E protein expression levels and viral titres, which represent viral replication and proliferation, were significantly downregulated, while the opposite result was observed when miR-148a-5p inhibitor was transfected into DEFs. Next, we found that SOCS1 was the target gene of miR-148a-5p through software analysis. Therefore, we further confirmed that SOCS1 was the target of miR-148a-5p and that miR-148a-5p could negatively regulate the expression of SOCS1 at the mRNA and protein levels. Furthermore, our results indicated that overexpression of SOCS1 promoted DTMUV replication, while knockdown of SOCS1 inhibited DTMUV replication. Finally, we found that in DTMUV-infected DEFs, the overexpression of SOCS1 inhibited the production of IFN-α and IFN-β, while knocking down SOCS1 produced the opposite result. This indicates that during DTMUV infection, the virus promotes the expression of SOCS1 by downregulating the expression of miR-148a-5p, while the upregulation of SOCS1 suppresses the production of type I interferon and promotes virus replication. Taken together, these findings provide new insights into virus-host interactions during DTMUV infection and provide potential new antiviral treatment strategies for DTMUV infection. • In this study, we first verified the expression kinetics of miR-148a-5p and SOCS1 in DEF cells infected with DTMUV. • Next, we explored the direct effect of miR-148a-5p on DTMUV replication for the first time. • Futhermore, we found that miR-148a-5p negatively regulated SOCS1 mRNA and protein expression levels. Finally, we found that SOCS1 promoted viral replication by inhibiting the production of type I interferon. [ABSTRACT FROM AUTHOR]