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Bisen Shivantika,Verma Shailendra Kumar,Mukhopadhyay Chandra Sekhar,Singh Nikhlesh K. 생화학분자생물학회 2024 Experimental and molecular medicine Vol.56 No.-
Human interleukin-33 (IL-33) is a 270 amino acid protein that belongs to the IL-1 cytokine family and plays an important role in various inflammatory disorders. Neutrophil proteases (Cathepsin G and Elastase) and mast cell proteases (tryptase and chymase) regulate the activity of IL-33 by processing full-length IL-33 into its mature form. There is little evidence on the role of these mature forms of IL-33 in retinal endothelial cell signaling and pathological retinal angiogenesis. Here, we cloned, expressed, and purified the various mature forms of human IL-33 and then evaluated the effects of IL-3395-270, IL-3399-270, IL-33109-270, and IL-33112-270 on angiogenesis in human retinal microvascular endothelial cells (HRMVECs). We observed that IL-3395-270, IL-3399-270, IL-33109-270, and IL-33112-270 significantly induced HRMVEC migration, tube formation and sprouting angiogenesis. However, only IL-3399-270 could induce HRMVEC proliferation. We used a murine model of oxygen-induced retinopathy (OIR) to assess the role of these mature forms of IL-33 in pathological retinal neovascularization. Our 3′-mRNA sequencing and signaling studies indicated that IL-3399-270 and IL-33109-270 were more potent at inducing endothelial cell activation and angiogenesis than the other mature forms. We found that genetic deletion of IL-33 significantly reduced OIR-induced retinal neovascularization in the mouse retina and that intraperitoneal administration of mature forms of IL-33, mainly IL-3399–270 and IL-33109–270, significantly restored ischemia-induced angiogenic sprouting and tuft formation in the hypoxic retinas of IL-33–/– mice. Thus, our study results suggest that blockade or inhibition of IL-33 cleavage by neutrophil proteases could help mitigate pathological angiogenesis in proliferative retinopathies.
Shukla Saurabh,Tripathi Anil Kumar,Verma Shailendra Prasad,Awasthi Nidhi 대한혈액학회 2020 Blood Research Vol.55 No.4
Background Aplastic anemia (AA), an unusual hematological disease, is characterized by hypoplasia of the bone marrow and failure to form blood cells of all three lineages resulting in pancytopenia. This study aimed to investigate TNF--308 and IFN--874 gene polymorphisms and their respective plasma protein levels in patients with AA and healthy controls. Methods Two hundred and forty individuals were included in this study; the case group comprised 120 AA patients, while 120 healthy individuals served as controls. Genotyping was performed using the PCR-restriction length fragment polymorphism method and TNF--308 and IFN--874 plasma levels were evaluated using an ELISA kit. Results There was a significantly higher prevalence of the IFN--874 genotype in patients with AA than in healthy controls, while the TNF--308 genotype was associated with lower risk of developing AA. Furthermore, the levels of both TNF--308 and IFN--874 were higher in the plasma of AA patients. Conclusion Our findings suggest that the IFN--874 genotype may be a greater risk factor in the causation of AA, whereas the TNF--308 genotype has a protective role in the North Indian population.