By a News Reporter-Staff News Editor at Gene Therapy Weekly -- Current study results on Biotechnology have been published. According to news originating from Taipei, Taiwan, by NewsRx correspondents, research stated, "Chronic inflammatory processes have been increasingly shown to be involved in the pathogenesis of diabetes and diabetic nephropathy. Recently, we demonstrated that a lectin-like domain of thrombomodulin (THBD), which is known as THBD domain 1 (THBDD1) and which acts independently of protein C activation, neutralised an inflammatory response in a mouse model of sepsis."
Our news journalists obtained a quote from the research from the Graduate Institute of Life Sciences, "Here, therapeutic effects of gene therapy with adeno-associated virus (AAV)-carried THBDD1 (AAV-THBDD1) were tested in a mouse model of type 2 diabetic nephropathy. To assess the therapeutic potential of THBDD1 and the mechanisms involved, we delivered AAV-THBDD1 (10(11) genome copies) into db/db mice and tested the effects of recombinant THBDD1 on conditionally immortalised podocytes. A single dose of AAV-THBDD1 improved albuminuria, renal interstitial inflammation and glomerular sclerosis, as well as renal function in db/db mice. These effects were closely associated with: (1) inhibited activation of the nuclear factor kappa B (NF-kappa B) pathway and the NACHT, LRR and PYD domains-containing protein 3 (NLRP3) inflammasome; (2) promotion of nuclear factor (erythroid-derived 2)-like 2 (NRF2) nuclear translocation; and (3) suppression of mitochondria-derived apoptosis in the kidney of treated mice."
According to the news editors, the research concluded: "AAV-THBDD1 gene therapy resulted in improvements in a model of diabetic nephropathy by suppressing the NF-kappa B-NLRP3 inflammasome-mediated inflammatory process, enhancing the NRF2 antioxidant pathway and inhibiting apoptosis in the kidney."
For more information on this research see: Thrombomodulin domain 1 ameliorates diabetic nephropathy in mice via anti-NF-kappa B/NLRP3 inflammasome-mediated inflammation, enhancement of NRF2 antioxidant activity and inhibition of apoptosis. Diabetologia, 2014;57(2):424-434. Diabetologia can be contacted at: Springer, 233 Spring St, New York, NY 10013, USA. (Springer - www.springer.com; Diabetologia - www.springerlink.com/content/0012-186x/)
The news correspondents report that additional information may be obtained from S.M. Yang, Natl Def Med Center, Grad Inst Life Sci, Taipei, Taiwan. Additional authors for this research include S.M. Ka, H.L. Wu, Y.C. Yeh, C.H. Kuo, K.F. Hua, G.Y. Shi, Y.J. Hung, F.C. Hsiao, S.S. Yang, Y.S. Shieh, S.H. Lin, C.W. Wei, J.S. Lee, C.Y. Yang and A. Chen (see also Biotechnology).
Keywords for this news article include: Asia, Antioxidants, Biotechnology, Taipei, Taiwan, Genetics, Apoptosis, NF-kappa B, Nephrology, Gene Therapy, Inflammation, Endocrinology, Bioengineering, Thrombomodulin, Nuclear Proteins, Diabetes Mellitus, Membrane Proteins, Protective Agents, Thrombin Receptors, DNA-Binding Proteins, Diabetic Nephropathy
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