Microplitis bicoloratus bracovirus (MbBV) is a polydnavirus found in the parasitic wasp M. bicoloratus. Although MbBV is a known inducer of apoptosis in host hemocytes, the mechanism by which this occurs remains elusive. In this study, we found that expression of cyclophilin A (CypA) was significantly upregulated in Spodoptera litura hemocytes at 6day post-parasitization. Similar results were reported in High Five cells (Hi5 cells) infected by MbBV, suggesting that the upregulation of CypA is linked to MbBV infection in insect cells. cDNA encoding CypA was cloned from parasitized hemocytes of S. litura, and bioinformatic analyses showed that S. litura CypA belongs to the cyclophilin family of proteins. Overexpression of S. litura CypA in Hi5 cells revealed that the protein promotes MbBV-induced apoptosis in vitro. Conversely, suppression of the expression and activity of CypA protein significantly rescued the apoptotic phenotype observed in MbBV-infected Hi5 cells, suggesting that it plays a key role in this process. MbBV infection also promoted the cytoplasmic-nuclear translocation of CypA in Hi5 cells. Taken together, these results suggest that MbBV infection upregulates the expression of CypA, which is required for MbBV-mediated apoptosis. Our findings Arch. Insect Biochem. Physiol. 2019;100:e21534.wileyonlinelibrary.com/journal/arch
Angiotensin II (Ang II) is a principal molecule of the renin-angiotensin system, which promotes hypertrophy and fibrosis. It has been demonstrated that Ang II upregulates the expression of cyclophilin A (CypA), which is a potential myocardial hypertrophy factor. However, the mechanisms by which Ang II induces the expression of CypA in cardiomyocytes remain unclear. In the present study, reactive oxygen species (ROS) were detected by fluorescence microscopy, and western blot analysis and ELISA were used to measure CypA expression. It was identified that Ang II enhanced the production of ROS in rat cardiomyocytes. ROS, in turn, promoted CypA expression and secretion. Notably, the action of Ang II was primarily dependent on the angiotensin type 2 receptor (AT2R), not the type 1 receptor. These results provided an insight into the role of the AT2R signaling pathway in Ang II-induced myocardial hypertrophy.
Microplitis bicoloratus bracovirus (MbBV) induces apoptosis in hemocytes of the host (Spodoptera litura) via the cyclophilin A (CypA)‐mediated signaling pathway. However, the mechanisms underlying CypA‐mediated signaling during apoptosis remain largely unknown. Therefore, in this study, we investigated how CypA and apoptosis‐inducing factor (AIF) interact during MbBV‐mediated apoptosis. Our findings showed that MbBV induces apoptosis through the CypA‐AIF axis of insect immune suppression. In MbBV‐infected Spli221 cells, both the expression of the cypa gene and the release of AIF from the mitochondria increased the number of apoptotic cells. CypA and AIF underwent concurrent cytoplasm‐nuclear translocation. Conversely, blocking of AIF release from mitochondria not only inhibited the CypA‐AIF interaction but also inhibited the cytoplasmic‐nuclear translocation of AIF and CypA. Importantly, the survival of the apoptotic phenotype was significantly rescued in MbBV‐infected Spli221 cells. In addition, we found that the cyclosporine A‐mediated inhibition of CypA did not prevent the formation of the CypA and AIF complex; rather, this only suppressed genomic DNA fragmentation. In vitro experiments revealed direct molecular interactions between recombinant CypA and AIF. Taken together, our results demonstrate that the CypA‐AIF interaction plays an important role in MbBV‐induced innate immune suppression. This study will help to clarify aspects of insect immunological mechanisms and will be relevant to biological pest control.
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