1,245
Views
0
CrossRef citations to date
0
Altmetric
Clinical Study

Salt-induced phosphoproteomic changes in the subfornical organ in rats with chronic kidney disease

, , , , &
Article: 2171886 | Received 21 Sep 2022, Accepted 09 Jan 2023, Published online: 30 Jan 2023

References

  • GBD Chronic Kidney Disease Collaboration. Global, regional, and national burden of chronic kidney disease, 1990–2017: a systematic analysis for the Global Burden of Disease Study 2017. Lancet. 2020;395(10225):709–733.
  • Weir MR, Fink JC. Salt intake and progression of chronic kidney disease: an overlooked modifiable exposure? A commentary. Am J Kidney Dis. 2005;45(1):176–188.
  • Cole NI, Suckling RJ, Desilva V, et al. Serum sodium concentration and the progression of established chronic kidney disease. J Nephrol. 2019;32(2):259–264.
  • Heerspink L, Navis HJ, Ritz G. E. Salt intake in kidney disease–a missed therapeutic opportunity? Nephrol Dial Transplant. 2012;27(9):3435–3442.
  • Malta D, Petersen KS, Johnson C, et al. High sodium intake increases blood pressure and risk of kidney disease. From the science of salt: a regularly updated systematic review of salt and health outcomes. J Clin Hypertens 2016;20(12):1654–1665.
  • Stocker SD, Lang SM, Simmonds SS, et al. Cerebrospinal Fluid hypernatremia elevates sympathetic nerve activity and blood pressure via the rostral ventrolateral medulla. Hypertension. 2015;66(6):1184–1190.
  • Kinsman BJ, Browning KN, Stocker SD. NaCl and osmolarity produce different responses in organum vasculosum of the lamina terminalis neurons, sympathetic nerve activity and blood pressure. J Physiol. 2017;595(18):6187–6201.
  • Coble JP, Grobe JL, Johnson AK, et al. Mechanisms of brain renin angiotensin system-induced drinking and blood pressure: importance of the subfornical organ. Am J Physiol Regul Integr Comp Physiol. 2015;308(4):R238–R249.
  • Hiyama TY, Watanabe E, Ono K, et al. Na(x) channel involved in CNS sodium-level sensing. Nat Neurosci. 2002;5(6):511–512.
  • Noda M. The subfornical organ, a specialized sodium channel, and the sensing of sodium levels in the brain. Neuroscientist. 2006;12(1):80–91.
  • Noda M, Hiyama TY. Sodium-level-sensitive sodium channel and salt-intake behavior. Chem Senses. 2005;30(Suppl 1):i44–i45.
  • Watanabe E, Hiyama TY, Shimizu H, et al. Sodium-level-sensitive sodium channel Na(x) is expressed in glial laminate processes in the sensory circumventricular organs. Am J Physiol Regul Integr Comp Physiol. 2006;290(3):R568–R576.
  • Nomura K, Hiyama TY, Sakuta H, Matsuda T, Lin CH, Kobayashi K, et al. [Na(+)] increases in body fluids sensed by central Na(x) induce sympathetically mediated blood pressure elevations via H(+)-dependent activation of ASIC1a. Neuron. 2019;101(1):60–75.e66.
  • Leenen FH. The Central role of the brain aldosterone-“ouabain” pathway in salt-sensitive hypertension. Biochim Biophys Acta. 2010;1802(12):1132–1139.
  • Gabor A, Leenen FH. Central neuromodulatory pathways regulating sympathetic activity in hypertension. J Appl Physiol (1985). 2012;113(8):1294–1303.
  • Blaustein MP, Leenen FH, Chen L, et al. How NaCl raises blood pressure: a new paradigm for the pathogenesis of salt-dependent hypertension. Am J Physiol Heart Circ Physiol. 2012;302(5):H1031–H1049.
  • Leenen FHH, Wang HW, Hamlyn JM. Sodium pumps, ouabain and aldosterone in the brain: a neuromodulatory pathway underlying salt-sensitive hypertension and heart failure. Cell Calcium. 2020;86:102151.
  • Cao W, Li A, Wang L, et al. A salt-induced reno-cerebral reflex activates renin-angiotensin systems and promotes CKD progression. J Am Soc Nephrol. 2015;26(7):1619–1633.
  • Hunter T. Signaling–2000 and beyond. Cell. 2000;100(1):113–127.
  • Derouiche A, Cousin C, Mijakovic I. Protein phosphorylation from the perspective of systems biology. Curr Opin Biotechnol. 2012;23(4):585–590.
  • Zhou G, Li J, Zeng T, et al. The regulation effect of WNT-RAS signaling in hypothalamic paraventricular nucleus on renal fibrosis. J Nephrol. 2020;33(2):289–297.
  • Wiśniewski JR, Zougman A, Nagaraj N, et al. Universal sample preparation method for proteome analysis. Nat Methods. 2009;6(5):359–362.
  • Li L, Li J, Tan L, et al. Salt-induced phosphoproteomic changes in the hypothalamic paraventricular nucleus in rats with chronic renal failure. Brain Res. 2017;1669:1–10.
  • Benowitz LI, Routtenberg A. GAP-43: an intrinsic determinant of neuronal development and plasticity. Trends Neurosci. 1997;20(2):84–91.
  • He Q, Dent EW, Meiri KF. Modulation of actin filament behavior by GAP-43 (neuromodulin) is dependent on the phosphorylation status of serine 41, the protein kinase C site. J Neurosci. 1997;17(10):3515–3524.
  • Meiri KF, Saffell JL, Walsh FS, et al. Neurite outgrowth stimulated by neural cell adhesion molecules requires growth-associated protein-43 (GAP-43) function and is associated with GAP-43 phosphorylation in growth cones. J Neurosci. 1998;18(24):10429–10437.
  • Stetler RA, Gao Y, Signore AP, et al. HSP27: mechanisms of cellular protection against neuronal injury. Curr Mol Med. 2009;9(7):863–872.
  • Robinson AA, Dunn MJ, McCormack A, et al. Protective effect of phosphorylated Hsp27 in coronary arteries through actin stabilization. J Mol Cell Cardiol. 2010;49(3):370–379.
  • Meier M, King GL, Clermont A, et al. Angiotensin at(1) receptor stimulates heat shock protein 27 phosphorylation in vitro and in vivo. Hypertension. 2001;38(6):1260–1265.
  • Bei Y, Xu T, Lv D, et al. Exercise-induced circulating extracellular vesicles protect against cardiac ischemia-reperfusion injury. Basic Res Cardiol. 2017;112(4):38.
  • Stetler RA, Gao Y, Zhang L, et al. Phosphorylation of HSP27 By protein kinase D is essential for mediating neuroprotection against ischemic neuronal injury. J Neurosci. 2012;32(8):2667–2682.
  • Rasmussen AH, Rasmussen HB, Silahtaroglu A. The DLGAP family: neuronal expression, function and role in brain disorders. Mol Brain. 2017;10(1):43.
  • Agarwal M, Johnston MV, Stafstrom CE. SYNGAP1 mutations: clinical, genetic, and pathophysiological features. Int J Dev Neurosci. 2019;78:65–76.
  • Li J, Wilkinson B, Clementel VA, et al. Long-term potentiation modulates synaptic phosphorylation networks and reshapes the structure of the postsynaptic interactome. Sci Signal. 2016;9(440):rs8.
  • Hamed SA. Neurologic conditions and disorders of uremic syndrome of chronic kidney disease: presentations, causes, and treatment strategies. Expert Rev Clin Pharmacol. 2019;12(1):61–90.
  • Bloom GS, Luca FC, Vallee RB. Widespread cellular distribution of MAP-1A (microtubule-associated protein 1A) in the mitotic spindle and on interphase microtubules. J Cell Biol. 1984;98(1):331–340.
  • Maccioni RB, Cambiazo V. Role of microtubule-associated proteins in the control of microtubule assembly. Physiol Rev. 1995;75(4):835–864.
  • Nixon RA, Fischer I, Lewis SE. Synthesis, axonal transport, and turnover of the high molecular weight microtubule-associated protein MAP 1A in mouse retinal ganglion cells: tubulin and MAP 1A display distinct transport kinetics. J Cell Biol. 1990;110(2):437–448.
  • Gao HL, Yu XJ, Liu KL, et al. PVN Blockade of p44/42 MAPK pathway attenuates salt-induced hypertension through modulating neurotransmitters and attenuating oxidative stress. Sci Rep. 2017;7:43038.
  • DiMicco JA, Abshire VM, Shekhar A, Wilbe JH Jr. Role of GABAergic mechanisms in the central regulation of arterial pressure. Eur Heart J. 1987;8(Suppl B):133–138.
  • Zhang W, Mifflin S. Plasticity of GABAergic mechanisms within the nucleus of the solitary tract in hypertension. Hypertension. 2010;55(2):201–206.