Research Topics
Species | N DmitrievaSummaryAffiliation: National Institutes of Health Country: USA Publications
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Publications
Protection of renal inner medullary epithelial cells from apoptosis by hypertonic stress-induced p53 activationN Dmitrieva
NHLBI, National Institutes of Health, Bethesda, Maryland 20892 1603 and the Whitney Laboratory, University of Florida, St Augustine, Florida 32086 8623, USA
J Biol Chem 275:18243-7. 2000..We conclude that induction of active p53 in mIMCD3 cells by hypertonic stress contributes to cell survival...
Mre11 is expressed in mammalian mitochondria where it binds to mitochondrial DNANatalia I Dmitrieva
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA
Am J Physiol Regul Integr Comp Physiol 301:R632-40. 2011..Our results suggest a role for Mre11 in the maintenance of genome integrity in mitochondria in addition to its previously known role in maintenance of nuclear DNA...
Increased insensible water loss contributes to aging related dehydrationNatalia I Dmitrieva
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, United States of America
PLoS ONE 6:e20691. 2011..We propose that insensible water loss through skin and respiration increases with age, making a major contribution to aging related dehydration...
Knockout of Ku86 accelerates cellular senescence induced by high NaClNatalia I Dmitrieva
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA
Aging (Albany NY) 1:245-53. 2009..We conclude that Ku86 deficiency accelerates high NaCl(-) induced cellular senescence,particularly in the renal medulla where NaCl normally is high...
Analysis of DNA breaks, DNA damage response, and apoptosis produced by high NaClNatalia I Dmitrieva
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung and Blood Institute, National Institutes of Health, Dept of Health and Human Services, 9000 Rockville Pike, Bethesda, MD 20892 1603, USA
Am J Physiol Renal Physiol 295:F1678-88. 2008..We conclude that gammaH2AX induction and MRN activation in response to high NaCl are associated with apoptosis, not DNA repair...
High NaCl promotes cellular senescenceNatalia I Dmitrieva
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung and Blood Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland 20892, USA
Cell Cycle 6:3108-13. 2007..We conclude that high NaCl accelerates cellular senescence and aging, most likely secondary to the DNA breaks and oxidative damage that it causes...
The saltiness of the sea breaks DNA in marine invertebrates: possible implications for animal evolutionNatalia I Dmitrieva
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA
Cell Cycle 5:1320-3. 2006..We speculate that, since DNA breaks cause mutations, salinity might have important background effects on the rate and course of evolution...
Ku86 preserves chromatin integrity in cells adapted to high NaClNatalia I Dmitrieva
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, and Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
Proc Natl Acad Sci U S A 102:10730-5. 2005..We propose that Ku86 ameliorates the effects of high NaCl-induced DNA breaks in adapted cells by supporting alignment of the broken ends of the DNA and thus maintaining integrity of the fragmented chromatin...
DNA double-strand breaks induced by high NaCl occur predominantly in gene desertsNatalia I Dmitrieva
Systems Biology Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA
Proc Natl Acad Sci U S A 108:20796-801. 2011..We propose that the universal presence of NaCl around animal cells has directly influenced the evolution of the structure of their genomes...
High NaCl causes Mre11 to leave the nucleus, disrupting DNA damage signaling and repairNatalia I Dmitrieva
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bldg 10, Rm 6N260, Bethesda, MD 20892, USA
Am J Physiol Renal Physiol 285:F266-74. 2003....
Rapid activation of G2/M checkpoint after hypertonic stress in renal inner medullary epithelial (IME) cells is protective and requires p38 kinaseNatalia I Dmitrieva
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung and Blood Institute, and Gene Response Section, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
Proc Natl Acad Sci U S A 99:184-9. 2002..We propose that the rapid initiation of G(2) delay by p38 kinase after hypertonicity protects the cells by decreasing the level of DNA breaks caused by aberrant mitosis entry...
p53 Protects renal inner medullary cells from hypertonic stress by restricting DNA replicationN Dmitrieva
National Heart, Lung, and Blood Institute, National Institutes of Health, Bldg 10, Rm 6N260, Bethesda, MD 20892 1603, USA
Am J Physiol Renal Physiol 281:F522-30. 2001....
Cells adapted to high NaCl have many DNA breaks and impaired DNA repair both in cell culture and in vivoNatalia I Dmitrieva
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892 1603, USA
Proc Natl Acad Sci U S A 101:2317-22. 2004..Thus, both in cell culture and in vivo, although cells adapt to high NaCl, their DNA is damaged and its repair is inhibited...
Living with DNA breaks is an everyday reality for cells adapted to high NaClNatalia I Dmitrieva
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892 1603, USA
Cell Cycle 3:561-3. 2004....
Cell cycle-dependent expression of thyroid hormone receptor-beta is a mechanism for variable hormone sensitivityPadma Maruvada
Molecular Regulation and Neuroendocrinology Section, Clinical Endocrinology Branch, National Institute of Diabetes, Digestive, and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
Mol Biol Cell 15:1895-903. 2004..These novel observations of cell cycle-dependent expression of TR suggest that differential hormone sensitivity can occur during the cell cycle and may contribute to cell cycle progression during normal development and oncogenesis...
Pax2 expression occurs in renal medullary epithelial cells in vivo and in cell culture, is osmoregulated, and promotes osmotic toleranceQi Cai
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD 20892 1603, USA
Proc Natl Acad Sci U S A 102:503-8. 2005....
Hypertonic stress responseNatalia I Dmitrieva
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung and Blood Institute, National Institutes of Health, Department of Health and Human Services, 10 Center Drive, Building 10, Room 6N260, Bethesda, MD 20892-1603, USA
Mutat Res 569:65-74. 2005..How high NaCl causes the DNA breaks and how the cells survive them is conjectural at this point. We discuss possible answers to these questions, based on current knowledge about induction and processing of DNA breaks...
Effects of expression of p53 and Gadd45 on osmotic tolerance of renal inner medullary cellsQi Cai
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892 1603, USA
Am J Physiol Renal Physiol 291:F341-9. 2006....
Ataxia telangiectasia-mutated, a DNA damage-inducible kinase, contributes to high NaCl-induced nuclear localization of transcription factor TonEBP/OREBPZheng Zhang
Laboratory of Kidney and Electrolyte Metabolism, National Heart Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA
Am J Physiol Renal Physiol 289:F506-11. 2005..In conclusion, activation of ATM contributes to high NaCl-induced nuclear translocation of TonEBP/OREBP...
Mediator of DNA damage checkpoint 1 (MDC1) contributes to high NaCl-induced activation of the osmoprotective transcription factor TonEBP/OREBPMargarita Kunin
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung and Blood Institute, Bethesda, Maryland, United States of America
PLoS ONE 5:e12108. 2010..Hypertonicity, such as induced by high NaCl, increases the activity of the transcription factor TonEBP/OREBP whose target genes increase osmoprotective organic osmolytes and heat shock proteins...
High urea and NaCl carbonylate proteins in renal cells in culture and in vivo, and high urea causes 8-oxoguanine lesions in their DNAZheng Zhang
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, Bethesda, MD 20892, USA
Proc Natl Acad Sci U S A 101:9491-6. 2004..iii) In mIMCD3 cells a normal plasma concentration of urea causes carbonylation, and carbonylation increases over the uremic range of urea concentration, indicating that urea can contribute directly to the carbonylation found in uremia...
Proliferation and osmotic tolerance of renal inner medullary epithelial cells in vivo and in cell cultureZheng Zhang
Laboratory of Kidney and Electrolyte Metabolism, National Heart Lung and Blood Institute, Bethesda, Maryland 20892, USA
Am J Physiol Renal Physiol 283:F302-8. 2002..We conclude that immortalization and continued DNA replication account for part of the previously observed difference in osmotic tolerance between IM cells in vivo and in cell culture but that other factors must also be involved...
Cellular response to hyperosmotic stressesMaurice B Burg
National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892 1603, USA
Physiol Rev 87:1441-74. 2007....
DNA damage and osmotic regulation in the kidneyNatalia I Dmitrieva
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, Department of Health and Human Services, Bethesda, MD 20892-1603, USA
Am J Physiol Renal Physiol 289:F2-7. 2005..Furthermore, we consider that the persistent DNA damage may be a sensor of hypertonicity that activates ATM kinase to provide a signal that contributes to protective osmotic regulation...
Toxicity of acetaminophen, salicylic acid, and caffeine for first-passage rat renal inner medullary collecting duct cellsQi Cai
Laboratory of Kidney and Electrolytes Metabolism, National Heart, Lung, and Blood Institute Department of Health and Human Services, National Institutes of Health, Bethesda, MD 20892-1603, USA
J Pharmacol Exp Ther 306:35-42. 2003....
MKP-1 inhibits high NaCl-induced activation of p38 but does not inhibit the activation of TonEBP/OREBP: opposite roles of p38alpha and p38deltaXiaoming Zhou
Division of Nephrology, Department of Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA
Proc Natl Acad Sci U S A 105:5620-5. 2008....
Osmotic stress and DNA damageNatalia I Dmitrieva
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA
Methods Enzymol 428:241-52. 2007..This chapter also discusses how specifics of the protocols influence the conclusions about types of DNA damage and what the limitations of these methods are for detecting different types of DNA damage...
