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Immunological Investigations
A Journal of Molecular and Cellular Immunology
Volume 47, 2018 - Issue 3
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Research Article

Role of TGF-β activated kinase-1 inhibitor on the interaction between macrophages and mesangial cells on the condition of high glucose

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References

  • Ajibade AA , Wang HY , Wang RF. (2013). Cell type-specific function of TAK1 in innate immune signaling. Trends Immunol No 34(7), 307–316, doi:10.1016/j.it.2013.03.007.
  • Allam G , Nasr A , Im T , et al. (2017). Association between cytokine genes polymorphisms and type 1 diabetes: a case-control study on Saudi population. Immunol Invest 1–12. doi:10.1080/08820139.2017.1416398.
  • Cheng CI , Chen PH , Lin YC , Kao YH. (2015). High glucose activates Raw264.7 macrophages through RhoA kinase-mediated signaling pathway. Cell Signal 27(2), 283–292, doi:10.1016/j.cellsig.2014.11.012.
  • Cheng T , Peng XC , Li FF , et al. (2010). Transforming growth factor-beta activated kinase 1 signaling pathways regulate TNF-alpha production by titanium alloy particles in RAW 264.7 cells. J Biomed Mater Res A 93(4), 1493–1499, doi:10.1002/jbm.a.32618.
  • Fedulov AV , Ses TP , Gavrisheva NA , et al. (2005). Serum TGF-beta 1 and TNF-alpha levels and cardiac fibrosis in experimental chronic renal failure. Immunol Invest 34, 143–152. doi:10.1081/IMM-200055807.
  • Fogo AB. (1999). Mesangial matrix modulation and glomerulosclerosis. Exp Nephrol 1999(7), 147–159.
  • Ha H , Mi Ra Y , Yoon Jin C , et al. (2002). Role of high glucose–induced nuclear factor– B activation in monocyte chemoattractant protein-1 expression by mesangial cells. J Am Soc Nephrol 13, 894–902.
  • Hickey FB , Martin F . (2013). Diabetic kidney disease and immune modulation. Curr Opin Pharmacol No 13(4), 602–612, doi:10.1016/j.coph.2013.05.002.
  • Lei C-T , Tang H , Chen Y , et al. (2017). MDM2 contributes to high glucose-induced glomerular mesangial cell proliferation and extracellular matrix accumulation via Notch1. Scientific Reports, 7, 1. doi:10.1038/s41598-017-10927-5.
  • Lu Y , Zhang Y , Li L , et al. (2014). TAB1: a target of triptolide in macrophages. Chem Biol, 21(2), 246–256, doi:10.1016/j.chembiol.2013.12.009.
  • Ma FY , Tesch GH , Ozols E , et al. (2011). TGF-beta1-activated kinase-1 regulates inflammation and fibrosis in the obstructed kidney. Am J Physiol Renal Physiol 300(6), F1410–21, doi:10.1152/ajprenal.00018.2011.
  • Mihaly SR , Ninomiya-Tsuji J , Morioka S . (2014). TAK1 control of cell death. Cell Death Differ, 21(11), 1667–1676, doi:10.1038/cdd.2014.123.
  • Min D , Lyons JG , Bonner J , et al. (2009). Mesangial cell-derived factors alter monocyte activation and function through inflammatory pathways: possible pathogenic role in diabetic nephropathy. Am J Physiol Renal Physiol, 297(5), F1229–37, doi:10.1152/ajprenal.00074.2009.
  • Navarro-Gonzalez JF , Mora-Fernandez C . (2008). The role of inflammatory cytokines in diabetic nephropathy. J Am Soc Nephrol, 19(3), 433–442, doi:10.1681/asn.2007091048.
  • Nguyen DV , Shaw LC , Grant MB . (2012). Inflammation in the pathogenesis of microvascular complications in diabetes. Front Endocrinol (Lausanne), 3, 170. doi:10.3389/fendo.2012.00170.
  • Ono K , Ohtomo T , Ninomiya-Tsuji J , Tsuchiya M . (2003). A dominant negative TAK1 inhibits cellular fibrotic responses induced by TGF-β. Biochem Biophys Res Commun, 307(2), 332–337, doi:10.1016/s0006-291x(03)01207-5.
  • Pichler R , Afkarian M , Dieter BP , Tuttle KR . (2017). Immunity and inflammation in diabetic kidney disease: translating mechanisms to biomarkers and treatment targets. Am J Physiol Renal Physiol, 312(4), F716–f731, doi:10.1152/ajprenal.00314.2016.
  • Sakurai H . (2012). Targeting of TAK1 in inflammatory disorders and cancer. Trends Pharmacol Sci, 33(10), 522–530, doi:10.1016/j.tips.2012.06.007.
  • Seok SJ , Lee ES , Kim GT , et al. (2013). Blockade of CCL2/CCR2 signalling ameliorates diabetic nephropathy in db/db mice. Nephrol Dial Transplant, 28(7), 1700–1710, doi:10.1093/ndt/gfs555.
  • Shoukry A , Bdeer Sel A , El-Sokkary RH . (2015). Urinary monocyte chemoattractant protein-1 and vitamin D-binding protein as biomarkers for early detection of diabetic nephropathy in type 2 diabetes mellitus. Mol Cell Biochem, 408(1–2), 25–35, doi:10.1007/s11010-015-2479-y.
  • Sun YM , Su Y , Li J , Wang LF . (2013). Recent advances in understanding the biochemical and molecular mechanism of diabetic nephropathy. Biochem Biophys Res Commun, 433(4), 359–361, doi:10.1016/j.bbrc.2013.02.120.
  • Takaesu G , Surabhi RM , Park K-J , et al. (2003). TAK1 is critical for IκB kinase-mediated activation of the NF-κB pathway. J Mol Biol, 326(1), 105–115, doi:10.1016/s0022-2836(02)01404-3.
  • Tesch GH . (2010). Macrophages and diabetic nephropathy. Semin Nephrol 30(3), 290–301, doi:10.1016/j.semnephrol.2010.03.007.
  • Tuttle KR . (2005). Linking metabolism and immunology: diabetic nephropathy is an inflammatory disease. J Am Soc Nephrol, 16(6), 1537–1538, doi:10.1681/asn.2005040393.
  • Wu CC , Sytwu HK , Lin YF . (2012). Cytokines in diabetic nephropathy. Adv Clin Chem, 56, 55–74.
  • Yang X , Wang Y , Gao G . (2015). High glucose induces rat mesangial cells proliferation and MCP-1 expression via ROS-mediated activation of NF-κB pathway, which is inhibited by eleutheroside E. J Recept Signal Transduct, 36(2), 152–157, doi:10.3109/10799893.2015.1061002.
  • Ying W , Cheruku PS , Bazer FW , et al. (2013). Investigation of macrophage polarization using bone marrow derived macrophages. J Vis Exp, 76. doi:10.3791/50323.
  • Zhang L , Pang S , Deng B , et al. (2012). High glucose induces renal mesangial cell proliferation and fibronectin expression through JNK/NF-kappaB/NADPH oxidase/ROS pathway, which is inhibited by resveratrol. Int J Biochem Cell Biol, 44(4), 629–638, doi:10.1016/j.biocel.2012.01.001.
  • Zheng Z , Zheng F . (2016). Immune cells and inflammation in diabetic nephropathy. J Diabetes Res, 2016, 1841690. doi:10.1155/2016/1841690.

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