Anti-CREG1 monoclonal antibody, clone 2C8

Neutrophils are vital components of defense mechanisms against invading pathogens and are closely linked with the individual antiviral capacity of pigs and other mammals. Neutrophilia is a well-known clinical characteristic of viral and bacterial infections. Using Affymetrix porcine genome microarrays, we investigated the gene expression profiles associated with neutrophil variation in porcine peripheral blood before and after polyriboinosinic-polyribocytidylic acid stimulation. Transcriptomic analysis showed 796 differentially expressed genes (DEGs) in extreme response (ER) pigs and 192 DEGs in moderate response (MR) pigs. Most DEGs were related to immune responses, included MXD1, CXCR4, CREG1, MyD88, CD14, TLR2, TLR4, IRF3 and IRF7. Gene ontology analysis indicated that the DEGs of both ER and MR pigs were involved in common biological processes, such as cell proliferation, growth regulation, immune response, inflammatory response and cell activation. The ER and MR groups also showed differences in DEGs involved in biological processes. DEGs involved in cell division and cell cycle were specifically found in the ER pigs, whereas DEGs involved in cell migration were specifically found in the MR pigs. The study provides a basic understanding of the molecular basis for the antiviral capacity of pigs and other mammals.

Cerebral ischemia/reperfusion (I/R) injury is associated with various cardiovascular and cerebrovascular diseases with high disability, morbidity, and mortality rates. MicroRNAs (miRNAs) are related to the pathogenesis of the above diseases. MiR-505-5p, a kind of such miRNAs, was found to be highly expressed in cerebral I/R injuries, but the mechanism of action of this miRNA in cerebral I/R injury was unclear. In our study, up-regulation of miR-505-5p was detected in cultured oxygen-glucose deprivation/reoxygenation (OGD/R)-subjected PC12 and HEC293 cells. Silencing of miR-505-5p in OGD/R-affected neuron-like cells not only decreased the OGD/R-injury (according to cell viability, SOD increase, and LDH and MDA decreases), but also reduced apoptosis (decreasing the cleaved caspase-3 and PARP protein levels). Interestingly, expression of CREG1 (Cellular Repressor of E1Astimulated Genes 1) was low in OGD/R-subjected neurons; it was verified as a possible target gene of miR-505-5p. CREG1 knockdown can reverse the effect of miR-505-5p silencing in OGD/R-induced neural injury. Taken together, the data obtained provide a new target for cerebral I/R injury treatment.