A vital role for myosin-9 in puromycin aminonucleoside-induced podocyte injury by affecting actin cytoskeleton

References

• Lal MA, Young KW, Andag U. Targeting the podocyte to treat glomerular kidney disease. Drug Discov Today 2015;20:1228–1234.
   PubMed Web of Science ®Google Scholar
• Motonishi S, Nangaku M, Wada T, Ishimoto Y, Ohse T, Matsusaka T, et al. Sirtuin1 maintains actin cytoskeleton by deacetylation of cortactin in injured podocytes. J Am Soc Nephrol 2015;26:1939–1959.
   Google Scholar
• Lal MA, Andersson AC, Katayama K, Xiao Z, Nukui M, Hultenby K, et al. Rhophilin-1 is a key regulator of the podocyte cytoskeleton and is essential for glomerular filtration. J Am Soc Nephrol 2015;26:647–662.
   PubMed Web of Science ®Google Scholar
• Hays T, D’Agati VD, Garellek JA, Warren T, Trubin ME, Hyink DP, et al. Glomerular MYH9 expression is reduced by HIV-1. AIDS 2012;26:797–803.
   PubMed Web of Science ®Google Scholar
• Seri M, Pecci A, Di Bari F, Cusano R, Savino M, Panza E, et al. MYH9-related disease: May–Hegglin anomaly, Sebastian syndrome, Fechtner syndrome, and Epstein syndrome are not distinct entities but represent a variable expression of a single illness. Medicine (Baltimore) 2003;82:203–215.
   PubMed Web of Science ®Google Scholar
• Sellers JR. Myosins: a diverse superfamily. Biochim Biophys Acta 2000;1496:3–22.
   PubMed Web of Science ®Google Scholar
• Berg JS, Powell BC, Cheney RE. A millennial myosin census. Mol Biol Cell 2001;12:780–794.
   PubMed Web of Science ®Google Scholar
• Hodge T, Cope MJ. A myosin family tree. J Cell Sci 2000;113Pt19:3353–3354.
   Google Scholar
• Muller T, Rumpel E, Hradetzky S, Bollig F, Wegner H, Blumenthal A, et al. Non-muscle myosin IIA is required for the development of the zebrafish glomerulus. Kidney Int 2011;80:1055–1063.
   PubMed Web of Science ®Google Scholar
• Miura K, Kurihara H, Horita S, Chikamoto H, Hattori M, Harita Y, et al. Podocyte expression of nonmuscle myosin heavy chain-IIA decreases in idiopathic nephrotic syndrome, especially in focal segmental glomerulosclerosis. Nephrol Dial Transplant 2013;28:2993–3003.
   PubMed Web of Science ®Google Scholar
• Pawluczyk IZ, Ghaderi Najafabadi M, Patel S, Desai P, Vashi D, Saleem MA, Topham PS. Sialic acid attenuates puromycin aminonucleoside-induced desialylation and oxidative stress in human podocytes. Exp Cell Res 2014;320:258–268.
   PubMed Web of Science ®Google Scholar
• Kinugasa S, Tojo A, Sakai T, Tsumura H, Takahashi M, Hirata Y, Fujita T. Selective albuminuria via podocyte albumin transport in puromycin nephrotic rats is attenuated by an inhibitor of NADPH oxidase. Kidney Int 2011;80:1328–1338.
   PubMed Web of Science ®Google Scholar
• Oh J, Beckmann J, Bloch J, Hettgen V, Mueller J, Li L, et al. Stimulation of the calcium-sensing receptor stabilizes the podocyte cytoskeleton, improves cell survival, and reduces toxin-induced glomerulosclerosis. Kidney Int 2011;80:483–492.
   PubMed Web of Science ®Google Scholar
• Suzuki K, Fukusumi Y, Yamazaki M, Kaneko H, Tsuruga K, Tanaka H, et al. Alteration in the podoplanin-ezrin-cytoskeleton linkage is an important initiation event of the podocyte injury in puromycin aminonucleoside nephropathy, a mimic of minimal change nephrotic syndrome. Cell Tissue Res 2015;362:201–213.
   PubMed Web of Science ®Google Scholar
• Mundel P, Reiser J, Kriz W. Induction of differentiation in cultured rat and human podocytes. J Am Soc Nephrol 1997;8:697–705.
   PubMed Web of Science ®Google Scholar
• Yuan Y, Xu X, Zhao C, Zhao M, Wang H, Zhang B, et al. The roles of oxidative stress, endoplasmic reticulum stress, and autophagy in aldosterone/mineralocorticoid receptor-induced podocyte injury. Lab Invest 2015;95:1374–1386.
   PubMed Web of Science ®Google Scholar
• Yuan Y, Huang S, Wang W, Wang Y, Zhang P, Zhu C, et al. Activation of peroxisome proliferator-activated receptor-γ coactivator 1α ameliorates mitochondrial dysfunction and protects podocytes from aldosterone-induced injury. Kidney Int 2012;82:771–789.
   PubMed Web of Science ®Google Scholar
• Reiser J, Oh J, Shirato I, Asanuma K, Hug A, Mundel TM, et al. Podocyte migration during nephrotic syndrome requires a coordinated interplay between cathepsin L and alpha3 integrin. J Biol Chem 2004;279:34827–34832.
   PubMed Web of Science ®Google Scholar
• Hsu HH, Hoffmann S, Di Marco GS, Endlich N, Peter-Katalinic J, Weide T, Pavenstadt H. Downregulation of the antioxidant protein peroxiredoxin 2 contributes to angiotensin II-mediated podocyte apoptosis. Kidney Int 2011;80:959–969.
   PubMed Web of Science ®Google Scholar
• Su M, Dhoopun AR, Yuan Y, Huang S, Zhu C, Ding G, et al. Mitochondrial dysfunction is an early event in aldosterone-induced podocyte injury. Am J Physiol Renal Physiol 2013;305:F520–F531.
   PubMed Web of Science ®Google Scholar
• Wiggins RC. The spectrum of podocytopathies: a unifying view of glomerular diseases. Kidney Int 2007;71:1205–1214.
   PubMed Web of Science ®Google Scholar
• Mathieson PW. Podocyte actin in health, disease and treatment. Nephrol Dial Transplant 2010;25:1772–1773.
   PubMed Web of Science ®Google Scholar
• Schiffer M, Teng B, Gu C, Shchedrina VA, Kasaikina M, Pham VA, et al. Pharmacological targeting of actin-dependent dynamin oligomerization ameliorates chronic kidney disease in diverse animal models. Nat Med 2015;21:601–609.
   PubMed Web of Science ®Google Scholar
• Welsh GI, Saleem MA. The podocyte cytoskeleton-key to a functioning glomerulus in health and disease. Nat Rev Nephrol 2012;8:14–21.
   Web of Science ®Google Scholar
• Dai R, Lin Y, Liu H, Rao J, Zhai Y, Zha X, et al. A vital role for Angptl3 in the PAN-induced podocyte loss by affecting detachment and apoptosis in vitro. BMC Nephrol 2015;16:38.
   PubMed Web of Science ®Google Scholar
• Liu Y, Liang W, Yang Y, Pan Y, Yang Q, Chen X, et al. IQGAP1 regulates actin cytoskeleton organization in podocytes through interaction with nephrin. Cell Signal 2015;27:867–877.
   PubMed Web of Science ®Google Scholar
• Li X, Zhang X, Li X, Ding F, Ding J. The role of survivin in podocyte injury induced by puromycin aminonucleoside. Int J Mol Sci 2014;15:6657–6673.
   PubMed Web of Science ®Google Scholar
• Oh T, Jung Seo H, Taek Lee K, Jo Kim H, Jun Kim H, Lee JH, et al. MYH9 nephropathy. Kidney Res Clin Pract 2015;34:53–56.
   PubMedGoogle Scholar
• Johnstone DB, Zhang J, George B, Leon C, Gachet C, Wong H, et al. Podocyte-specific deletion of Myh9 encoding nonmuscle myosin heavy chain 2A predisposes mice to glomerulopathy. Mol Cell Biol 2011;31:2162–2170.
   PubMed Web of Science ®Google Scholar
• Hays T, Ma’ayan A, Clark NR, Tan CM, Teixeira A, Teixeira A, et al. Proteomics analysis of the non-muscle myosin heavy chain IIa-enriched actin-myosin complex reveals multiple functions within the podocyte. PLoS One 2014;9:e100660.
   Google Scholar
• Johnstone DB, Ikizler O, Zhang J, Holzman LB. Background strain and the differential susceptibility of podocyte-specific deletion of Myh9 on murine models of experimental glomerulosclerosis and HIV nephropathy. PLoS One 2013;8:e67839.
   Google Scholar
• Liapis H, Romagnani P, Anders HJ. New insights into the pathology of podocyte loss: mitotic catastrophe. Am J Pathol 2013;183:1364–1374.
   PubMed Web of Science ®Google Scholar
• Reidy K, Susztak K. Epithelial–mesenchymal transition and podocyte loss in diabetic kidney disease. Am J Kidney Dis 2009;54:590–593.
   PubMed Web of Science ®Google Scholar
• Inoki K, Mori H, Wang J, Suzuki T, Hong S, Yoshida S, et al. mTORC1 activation in podocytes is a critical step in the development of diabetic nephropathy in mice. J Clin Invest 2011;121:2181–2196.
   PubMed Web of Science ®Google Scholar
• Datta N, Lindfors S, Miura N, Saleem MA, Lehtonen S. Overexpression of transcription factor FOXC2 in cultured human podocytes upregulates injury markers and increases motility. Exp Cell Res 2016;340:32–42.
   PubMed Web of Science ®Google Scholar
• Chen S, Meng XF, Zhang C. Role of NADPH oxidase-mediated reactive oxygen species in podocyte injury. Biomed Res Int 2013;2013:839761.
   PubMedGoogle Scholar