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Preeclampsia is a severe multisystem disorder, and its pathophysiology is still not completely understood. Autophagy, a recycling process that maintains cellular homoeostasis during differentiation and development, is controversial regarding increased or decreased autophagic activity in preeclampsia. The aim of this study was to determine whether autophagy is increased in the placentas of women with preeclampsia by examining the protein levels of autophagy markers (Beclin 1 and SQSTM1/p62) and phosphorylation of cyclin E. For this purpose, placentas from preeclampsia (n=10) and control (n=10) pregnancies were included in this study. The protein expression of autophagy-related markers Beclin1, SQSTM1/p62 and phosphorylation status of cyclin E were detected by Western blot. Our data showed that the protein levels of both Beclin 1 and SQSTM1/p62 were significantly increased, while the phosphorylation level of cyclin E was significantly decreased in placentas with preeclampsia compared to those derived from controls. The results of this study suggest that the autophagic activity is perpetually increased in preeclampsia and cyclin E protein stabilisation might be involved in the induction of autophagy.

Behçet's disease (BD) is achronic inflammatory disorder characterized by recurrent oral and genital ulcers, uveitis and skin lesions. Although,the pathogenesis of BD remains poorly understood, excessive or dysregulatedcytokine production including IL-10 is associated with BD. Revealing the key molecular mechanism by which IL-10 expression is regulated is crucial to understanding the pathogenesis of BD. The aim of this study was to investigate whether Src family kinases (SFKs) are upstream mediators of STAT3/IL-10 pathway in peripheral blood mono nuclear cells(PBMCs) of active BD patients.Twenty active BD patients and twenty healthy subjects used as control were included in the study. PBMCs were isolated from total blood by density gradient centrifugation.Western blot and ELISA methods were applied to analyzelipopolysaccharide (LPS)-induced SFKs/STAT3/IL10 signaling pathway in BD.Inhibition of SFKs activity suppressed LPS-induced IL-10 production in PBMCs fromboth controls and active BD patients. Similarly, blockage of STAT3 activation abrogated LPS-induced IL-10 production. However, LPS-induced STAT3 activation required for IL-10 production was found to be dependent on SFKs activity as LPS-induced STAT3 phosphorylation was reduced by the inhibition of SFKs activity in PBMCs of active BD patients.SFKs activity is essential for LPS-induced STAT3/IL-10 pathway in PBMCs of active BD patients. Manipulation of the SFKs activity may offer a novel therapeutic approach for BD.