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Li Y.,Xiamen University | Shi G.,Xiamen University | Wang D.,Molecular Biology Research Center | Wang Y.,Chengdu Medical College
Current Pharmaceutical Biotechnology

Psoriatic arthritis (PsA) is an inflammatory arthritis, characterized by mild arthralgia to severe joint deformities. Long term management of these diseases with nonsteroidal anti-inflammatory drugs (NSAIDs) and disease-modifying antirheumatic drugs (DMARDs) is limited due to lack of efficacy and potential organ toxicity. Recently, the approval of injectable biologics, such as T cell inhibitors and TNF-α antagonist, has changed the treatment of moderate-to- severe psoriasis and PsA. Unlike NSAIDs and DMARDs, TNF-α antagonists not only provide unambiguous benefits for the skin and joints, but also prevent the progression of structural damage in peripheral joints. Biological agents in the treatment of PsA have broad prospects. More and more biological agents are being developed for the treatment of PsA. In the current review, we will discuss the progress of biological agents on PsA. © 2014 Bentham Science Publishers. Source

Wang D.,Molecular Biology Research Center | Li Y.,Xiamen University | Liu Y.,Xiamen University | Shi G.,Xiamen University
Current Pharmaceutical Biotechnology

The use of biologic agents has revolutionized the management of rheumatoid arthritis (RA) in the past two decades. These biologic agents directly target molecules and cells involved in the pathogenesis of RA. Biologic agents indeed lead to a better prognosis and clinical remission in patients with RA, especially in patients who are not well-controlled with traditional disease-modifying anti-rheumatic drugs (DMARDs). Currently, five TNF inhibitors (infliximab, etanercept, adalimumab, golimumab and certolizumab pegol), an IL-6 receptor antagonist (tocilizumab), an IL-1 receptor antagonist (anakinra), a B cell depleting agent (rituximab) and a T cell co-stimulation inhibitor (abatacept) have been approved for the treatment of RA. With the increased understanding of the pathogenic mechanisms of RA and advantages in manufacturing biotechnology of pharmaceutical companies, a series of novel biologic therapeutic approaches are being developed. In the present paper, we will summarize the biologic agents currently available to treat RA, and the prospective biologic therapies that might be used in the management of RA in future. © 2014 Bentham Science Publishers. Source

Azizmohammadi S.,Tehran University of Medical Sciences | Safari A.,Tehran University of Medical Sciences | Seifoleslami M.,Tehran University of Medical Sciences | Rabati R.G.,Molecular Biology Research Center | And 2 more authors.
Tumor Biology

In this study, we evaluate the clinical significance of the PRSS3 and Wiskott–Aldrich syndrome protein family verprolin-homologous protein 1 (WAVE1) in patients with epithelial ovarian cancer (EOC) by immunohistochemistry. In current study, all adjacent non-cancerous tissues showed absent or low expression of PRSS3. The expression of PRSS3 was significantly increased in the EOCs than adjacent non-cancerous tissues. Moreover, the expression of WAVE1 was significantly observed in all EOC tissues when compared with normal tissues. Furthermore, WAVE1 expression was absent in 35 (89.74 %) adjacent non-cancerous tissues. Our findings showed that high expression of PRSS3 was markedly linked to FIGO stage (P = 0.02), advanced grade (P = 0.017), and lymph node metastases (P = 0.001), but no relationship was determined with other clinicopathological parameters. Furthermore, high expression of WAVE1 was significantly correlated with FIGO stage (P = 0.001), grade of tumor (P = 0.011), and residual tumor size (P = 0.041), but no significant associations were found between WAVE1 expression and age, lymph node metastasis, and histological subtypes (all P > 0.05). In conclusion, our study showed that increased expression of PRSS3 and WAVE1 may be involved in development of EOC. © 2015 International Society of Oncology and BioMarkers (ISOBM) Source

Wang D.,Molecular Biology Research Center | Zhang Y.,Luzhou Medical College | He Y.,Xiamen University | Li Y.,Xiamen University | And 2 more authors.
Immunology and Cell Biology

We have previously reported that Gαq, the α subunit of the Gq protein, had important roles in dendritic cell migration, B-cell survival and autoimmunity. In this study, we showed that the deficiency of Gαq led to enhanced T-cell survival. Cultured Gnaq-/- T cells exhibited survival advantages both in medium alone and in the presence of anti-CD3 stimulation. Gnaq-/- T cells still exhibited a survival advantage when they were cultured in the presence of interleukin (IL)-2 or IL-7. Gnaq-/- T cells were more resistant to activation-induced cell death (AICD) in vitro. The survival advantage of Gnaq-/- T cells was further confirmed by transferring T cells into syngeneic hosts in vivo. Gαq deficiency might promote T-cell survival by upregulated Bcl-x L expression and downregulated Fas and FasL expressions. Furthermore, upon T-cell receptor (TCR) ligation, Akt activity was increased in Gnaq-/- T cells in comparison with wild-type (WT) T cells. The survival advantage of Gnaq-/- T cells was significantly attenuated after adding Akt inhibitor. Taken together, our data demonstrated a negative role of Gαq in regulating T-cell survival. © 2014 Australasian Society for Immunology Inc. Source

Liu Y.,Xiamen University | Wang D.,Molecular Biology Research Center | Li F.,Chongqing Medical University | Shi G.,Xiamen University
Immunology and Cell Biology

Gαq, the α-subunit of Gq protein, is ubiquitously expressed in mammalian cells. It initially attracted attention for its physiological significance in cardiovascular system. In recent years, studies have also indicated the important roles of Gαq in regulating immunity, supplying us a new insight into the mechanism of immune regulation. T helper type 17 (Th17) cells are potent inducers of tissue inflammation. Many studies have shown that Th17 cells are major effector cells in the pathogenesis of many experimental autoimmune diseases and human inflammatory conditions such as rheumatoid arthritis (RA). One of our previous studies has shown that Gαq negatively controls the disease activity of RA. However, how Gαq controls the pathogenesis of autoimmune disease is not clear. Whether this effect is via the regulation of Th17 differentiation is still not known. We aimed to find out the role of Gαq in control of Th17 differentiation. We investigated the relationship between Gαq and Th17 in RA patients. We then investigated the mechanism of how Gαq regulated Th17 differentiation by using Gnaq-/- mice. We observed that the expression of Gαq was negatively associated with interleukin-17A expression in RA patients, indicating that Gαq negatively controlled the differentiation of Th17 cells. By using Gnaq-/- mice, we demonstrated that Gαq inhibited the differentiation of Th17 cell via regulating the activity of extracellular signal-regulated kinase-1/2 to control the expression of STAT3 (signal transducer and activator of transcription 3) and RORα (RAR-related orphan receptor-α). These data suggest the possibility of targeting Gαq to develop a novel therapeutic regimen for autoimmune disease. Source

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