We investigated the effect of large isoform of ribulose-1,5-bisphosphate carboxylase/oxygenase (RuBPCO) activase (RuBPCO-A) on photosynthesis and constructed two plant expression vectors and introduced them into rice cultivars (Oryza sativa f. japonica cv. Nipponbare) through Agrobacterium tumefaciens-mediated transformation. Plasmid pCBrbcSRca contained the cDNA of RuBPCO-A large isoform (rca) controlled by RuBPCO small subunit gene promoter (rbcS), and plasmid pCBUbi-antirca contained a reversed rca sequence driven by maize ubiquitin promoter. Transformants were screened by polymerase chain reaction (PCR), Southern and Western blot analysis. Compared to the control rice plants, RuBPCO activity was improved in the pCBrbcSRca rice plants, which is opposite to RuBPCO activity in the pCBUbi-antirca rice plants. Net photosynthetic rate, quantum yield of electron transport in photosystem 2, and steady state photochemical fluorescence quenching increased in the pCBrbcSRca plants, but decreased in the pCBUbi-antirca plants as compared to the controls. The pCBrbcSRca plants had heavier grains and accelerated development, while the pCBUbi-antirca plants showed reverse changes. Thus RuBPCO-A large isoform exerts considerable effect on photosynthesis and is a promising target for plant breeding to improve rice crop yield. and H. R. Wu ... [et al.].
Apolipoprotein J (clusterin) is a component of high-density lipoproteins, the high level of which is reversely correlated with the risk of coronary heart disease. In addition, it exerts anti-inflammatory and anti-apoptotic effects on endothelial cells and inhibits smooth muscle cell migration and proliferation, indicating that it may play a protective role in cardiovascular disease. However, the exact mechanisms by which this occurs remain unclear. This study aimed to clarify these underlying protective mechanisms by researching the inhibitory effects of apolipoprotein J via the NOD-like receptor protein 3 pathway on the inflammation induced by cholesterol crystals in THP‑1 macrophages. In culture, THP-1 macrophages were infected with adenoviral vectors containing apolipoprotein J genes and subsequently treated with cholesterol crystals. The inflammatory cytokines interleukin‑1β, interleukin 18 and tumour necrosis factor α were quantitatively measured with ELISA kits. NOD-like receptor protein 3, cysteinyl aspartate specific proteinase 1 and interleukin 1β were evaluated by Western blot and PCR analysis. As a result, apolipoprotein J expression was found to remarkably decrease the levels of inflammatory cytokines, including tumour necrosis factor α, interleukin 18 and interleukin 1β, secreted by THP‑1 macrophages. It was also found capable of inhibiting the levels of NOD-like receptor protein 3, cysteinyl aspartate-specific proteinase 1 and interleukin 1β both at the protein and mRNA levels. In the current study, we revealed that over-expression of apolipoprotein J attenuated the inflammation induced by cholesterol crystals through inhibition of the NOD-like receptor protein 3 inflammasome pathway.