CoChat
Sign Up
Cited by 74Genetic and Kidney Cyst DiseasesIon Transport and Channel RegulationAcute Kidney Injury Research

Shear stress-induced alteration of epithelial organization in human renal tubular cells

Open access
Maggiorani, Damien, Dissard, Romain, Belloy, Marcy, Saulnier-Blache, Jean-Sébastien, Casemayou, Audrey, Ducasse, Laure, Grès, Sandra, Bellière, Julie +4 more·2015·PLOS ONE
DOI 10.1371/journal.pone.0131416PMC PMC4493045
Open this paper in CoChat — free accountOpen PDF

Abstract

Tubular epithelial cells in the kidney are continuously exposed to urinary fluid shear stress (FSS) generated by urine movement and recent in vitro studies suggest that changes of FSS could contribute to kidney injury. However it is unclear whether FSS alters the epithelial characteristics of the renal tubule. Here, we evaluated in vitro and in vivo the influence of FSS on epithelial characteristics of renal proximal tubular cells taking the organization of junctional complexes and the presence of the primary cilium as markers of epithelial phenotype. Human tubular cells (HK-2) were subjected to FSS (0.5 Pa) for 48 h. Control cells were maintained under static conditions. Markers of tight junctions (Claudin-2, ZO-1), Par polarity complex (Pard6), adherens junctions (E-Cadherin, β-Catenin) and the primary cilium (α-acetylated Tubulin) were analysed by quantitative PCR, Western blot or immunocytochemistry. In response to FSS, Claudin-2 disappeared and ZO-1 displayed punctuated and discontinuous staining in the plasma membrane. Expression of Pard6 was also decreased. Moreover, E-Cadherin abundance was decreased, while its major repressors Snail1 and Snail2 were overexpressed, and β-Catenin staining was disrupted along the cell periphery. Finally, FSS subjected-cells exhibited disappeared primary cilium. Results were confirmed in vivo in a uninephrectomy (8 months) mouse model where increased FSS induced by adaptive hyperfiltration in remnant kidney was accompanied by both decreased epithelial gene expression including ZO-1, E-cadherin and β-Catenin and disappearance of tubular cilia. In conclusion, these results show that proximal tubular cells lose an important number of their epithelial characteristics after long term exposure to FSS both in vitro and in vivo. Thus, the changes in urinary FSS associated with nephropathies should be considered as potential insults for tubular cells leading to disorganization of the tubular epithelium.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1371/journal.pone.0131416

Cites

1 of 1 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • The axial fluid shear stress experienced by proximal tubule cells in vivo is estimated to be in the range of 0.1 to 1 dyne/cm2.

    “the axial fluid shear stress experienced by proximal tubule cells in vivo is estimated to be in the range of 0.1 to 1 dyne/cm2”

    From Material-dependent oxygen transport governs ischemia-reperfusion injury and drug response in a kidney microphysiological system (2026) · cites this paper as Maggiorani et al., 2015

    The Materials and Methods section (HK-2 Cell Exposure to Shear Stress; page unavailable) estimates physiological shear stress at about 0.1 Pa, equivalent to 1 dyne/cm², in the initial portion of the proximal tubule. It does not give an in vivo estimate extending down to 0.1 dyne/cm²; the lower values elsewhere in the paper describe in vitro exposures. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Research works printed but not linked: 72

  1. [1]Duan Y, Weinstein AM, Weinbaum S and Wang T. Shear stress-induced changes of membrane transporter localization and expression in mouse proximal tubule cells. Proc Natl Acad Sci U S A 2010, 107: 21860– 21865. 10.1073/pnas.1015751107 21106755 PMC3003103 · DOI
  2. [2]Jang KJ, Cho HS, Kang do H, Bae WG, Kwon TH and Suh KY. Fluid-shear-stress-induced translocation of aquaporin-2 and reorganization of actin cytoskeleton in renal tubular epithelial cells. Integr Biol (Camb) 2011, 3: 134– 141. 21079870
  3. [3]Carattino MD, Sheng S and Kleyman TR. Epithelial Na+ channels are activated by laminar shear stress. J Biol Chem 2004, 279: 4120– 4126. 14625286
  4. [4]Holtzclaw JD, Liu L, Grimm PR and Sansom SC. Shear stress-induced volume decrease in C11-MDCK cells by BK-alpha/beta4. Am J Physiol Renal Physiol 2010, 299: F507– 516. 10.1152/ajprenal.00222.2010 20576683 PMC2944292 · DOI
  5. [5]Raghavan V, Rbaibi Y, Pastor-Soler NM, Carattino MD and Weisz OA. Shear stress-dependent regulation of apical endocytosis in renal proximal tubule cells mediated by primary cilia. Proc Natl Acad Sci U S A 2014, 111: 8506– 8511. 10.1073/pnas.1402195111 24912170 PMC4060694 · DOI
  6. [6]Gonzalez J, Essig M, Klein J, Caubet C, Dissard R, Bascands JL et al [ Renal urinary shear stress: a novel actor in nephropathies]. Med Sci (Paris) 2013, 29: 279– 285. 23544382
  7. [7]Essig M, Terzi F, Burtin M and Friedlander G. Mechanical strains induced by tubular flow affect the phenotype of proximal tubular cells. Am J Physiol Renal Physiol 2001, 281: F751– 762. 11553522
  8. [8]Grabias BM and Konstantopoulos K. The physical basis of renal fibrosis: effects of altered hydrodynamic forces on kidney homeostasis. Am J Physiol Renal Physiol 2014, 306: F473– 485. 10.1152/ajprenal.00503.2013 24352503 · DOI
  9. [9]Rohatgi R and Flores D. Intratubular hydrodynamic forces influence tubulointerstitial fibrosis in the kidney. Curr Opin Nephrol Hypertens 2010, 19: 65– 71. 10.1097/MNH.0b013e32833327f3 19851105 PMC2887746 · DOI
  10. [10]Nauli SM, Alenghat FJ, Luo Y, Williams E, Vassilev P, Li X et al Polycystins 1 and 2 mediate mechanosensation in the primary cilium of kidney cells. Nat Genet 2003, 33: 129– 137. 12514735
  11. [11]Nauli SM, Rossetti S, Kolb RJ, Alenghat FJ, Consugar MB, Harris PC et al Loss of polycystin-1 in human cyst-lining epithelia leads to ciliary dysfunction. J Am Soc Nephrol 2006, 17: 1015– 1025. 16565258
  12. [12]Eddy AA. Plasminogen activator inhibitor-1 and the kidney. Am J Physiol Renal Physiol 2002, 283: F209– 220. 12110504
  13. [13]Kolb RJ, Woost PG and Hopfer U. Membrane trafficking of angiotensin receptor type-1 and mechanochemical signal transduction in proximal tubule cells. Hypertension 2004, 44: 352– 359. 15262908
  14. [14]Miravète M, Dissard R, Klein J, Gonzalez J, Caubet C, Pecher C et al Renal tubular fluid shear stress facilitates monocyte activation towards inflammatory macrophages. Am J Physiol Renal Physiol 2012, 302: F1409– F1417. 10.1152/ajprenal.00409.2011 22419690 · DOI
  15. [15]Miravète M, Klein J, Besse-Patin A, Gonzalez J, Pecher C, Bascands JL et al Renal tubular fluid shear stress promotes endothelial cell activation. Biochem Biophys Res Commun 2011, 407: 813– 817. 10.1016/j.bbrc.2011.03.105 21443862 · DOI
  16. [16]Wang S and Dong Z. Primary cilia and kidney injury: current research status and future perspectives. Am J Physiol Renal Physiol 2013, 305: F1085– 1098. 10.1152/ajprenal.00399.2013 23904226 PMC3798724 · DOI
  17. [17]Schneeberger EE and Lynch RD. The tight junction: a multifunctional complex. Am J Physiol Cell Physiol 2004, 286: C1213– 1228. 15151915
  18. [18]Szaszi K and Amoozadeh Y. New insights into functions, regulation, and pathological roles of tight junctions in kidney tubular epithelium. Int Rev Cell Mol Biol 2014, 308: 205– 271. 10.1016/B978-0-12-800097-7.00006-3 24411173 · DOI
  19. [19]Denker BM and Sabath E. The biology of epithelial cell tight junctions in the kidney. J Am Soc Nephrol 2011, 22: 622– 625. 10.1681/ASN.2010090922 21415157 · DOI
  20. [20]Meng W and Takeichi M. Adherens junction: molecular architecture and regulation. Cold Spring Harb Perspect Biol 2009, 1: a002899 10.1101/cshperspect.a002899 20457565 PMC2882120 · DOI
  21. [21]Takeichi M. Dynamic contacts: rearranging adherens junctions to drive epithelial remodelling. Nat Rev Mol Cell Biol 2014, 15: 397– 410. 10.1038/nrm3802 24824068 · DOI
  22. [22]Yoshida Y, Fogo A, Shiraga H, Glick AD and Ichikawa I. Serial micropuncture analysis of single nephron function in subtotal renal ablation. Kidney Int 1988, 33: 855– 867. 3386138
  23. [23]Hostetter TH, Olson JL, Rennke HG, Venkatachalam MA and Brenner BM. Hyperfiltration in remnant nephrons: a potentially adverse response to renal ablation. Am J Physiol 1981, 241: F85– 93. 7246778
  24. [24]Brenner BM. Hemodynamically mediated glomerular injury and the progressive nature of kidney disease. Kidney Int 1983, 23: 647– 655. 6336299
  25. [25]Huang B, Pi L, Chen C, Yuan F, Zhou Q, Teng J et al WT1 and Pax2 re-expression is required for epithelial-mesenchymal transition in 5/6 nephrectomized rats and cultured kidney tubular epithelial cells. Cells Tissues Organs 2012, 195: 296– 312. 10.1159/000327530 21778682 · DOI
  26. [26]Bolati D, Shimizu H and Niwa T. AST-120 ameliorates epithelial-to-mesenchymal transition and interstitial fibrosis in the kidneys of chronic kidney disease rats. J Ren Nutr 2012, 22: 176– 180. 10.1053/j.jrn.2011.10.015 22200438 · DOI
  27. [27]Blantz RC and Singh P. Glomerular and tubular function in the diabetic kidney. Adv Chronic Kidney Dis 2014, 21: 297– 303. 10.1053/j.ackd.2014.03.006 24780458 · DOI
  28. [28]Jerums G, Premaratne E, Panagiotopoulos S and MacIsaac RJ. The clinical significance of hyperfiltration in diabetes. Diabetologia 2010, 53: 2093– 2104. 10.1007/s00125-010-1794-9 20496053 · DOI
  29. [29]Magee GM, Bilous RW, Cardwell CR, Hunter SJ, Kee F and Fogarty DG. Is hyperfiltration associated with the future risk of developing diabetic nephropathy? A meta-analysis. Diabetologia 2009, 52: 691– 697. 10.1007/s00125-009-1268-0 19198800 · DOI
  30. [30]Molina-Jijon E, Rodriguez-Munoz R, Namorado Mdel C, Pedraza-Chaverri J and Reyes JL. Oxidative stress induces claudin-2 nitration in experimental type 1 diabetic nephropathy. Free Radic Biol Med 2014, 72: 162– 175. 10.1016/j.freeradbiomed.2014.03.040 24726862 · DOI
  31. [31]Ryan MJ, Johnson G, Kirk J, Fuerstenberg SM, Zager RA and Torok-Storb B. HK-2: an immortalized proximal tubule epithelial cell line from normal adult human kidney. Kidney Int 1994, 45: 48– 57. 8127021
  32. [32]Bonvalet JP and de Rouffignac C. Distribution of ferrocyanide along the proximal tubular lumen of the rat kidney: its implications upon hydrodynamics. J Physiol 1981, 318: 85– 98. 7320905 PMC1245479
  33. [33]Duan Y, Gotoh N, Yan Q, Du Z, Weinstein AM, Wang T et al Shear-induced reorganization of renal proximal tubule cell actin cytoskeleton and apical junctional complexes. Proc Natl Acad Sci U S A 2008, 105: 11418– 11423. 10.1073/pnas.0804954105 18685100 PMC2516248 · DOI · Paper page
  34. [34]Belliere J, Casemayou A, Ducasse L, Zakaroff-Girard A, Martins F, Iacovoni JS et al Specific Macrophage Subtypes Influence the Progression of Rhabdomyolysis-Induced Kidney Injury. J Am Soc Nephrol 2014. PMC4446873 25270069
  35. [35]Qi Z, Whitt I, Mehta A, Jin J, Zhao M, Harris RC et al Serial determination of glomerular filtration rate in conscious mice using FITC-inulin clearance. Am J Physiol Renal Physiol 2004, 286: F590– 596. 14600035
  36. [36]Lin D, Edwards AS, Fawcett JP, Mbamalu G, Scott JD and Pawson T. A mammalian PAR-3-PAR-6 complex implicated in Cdc42/Rac1 and aPKC signalling and cell polarity. Nat Cell Biol 2000, 2: 540– 547. 10934475
  37. [37]Suzuki A, Yamanaka T, Hirose T, Manabe N, Mizuno K, Shimizu M et al Atypical protein kinase C is involved in the evolutionarily conserved par protein complex and plays a critical role in establishing epithelia-specific junctional structures. J Cell Biol 2001, 152: 1183– 1196. 11257119 PMC2199212
  38. [38]Liu Y. Cellular and molecular mechanisms of renal fibrosis. Nat Rev Nephrol 2011, 7: 684– 696. 10.1038/nrneph.2011.149 22009250 PMC4520424 · DOI
  39. [39]Park SW, Kim M, Brown KM, D'Agati VD and Lee HT. Inhibition of sphingosine 1-phosphate receptor 2 protects against renal ischemia-reperfusion injury. J Am Soc Nephrol 2012, 23: 266– 280. 10.1681/ASN.2011050503 22095950 PMC3269189 · DOI
  40. [40]Quaggin SE and Kapus A. Scar wars: mapping the fate of epithelial-mesenchymal-myofibroblast transition. Kidney Int 2011, 80: 41– 50. 10.1038/ki.2011.77 21430641 · DOI
  41. [41]Cattaneo I, Condorelli L, Terrinoni AR, Antiga L, Sangalli F and Remuzzi A. Shear stress reverses dome formation in confluent renal tubular cells. Cell Physiol Biochem 2011, 28: 673– 682. 10.1159/000335813 22178879 · DOI
  42. [42]Dankers PY, Boomker JM, Huizinga-van der Vlag A, Wisse E, Appel WP, Smedts FM et al Bioengineering of living renal membranes consisting of hierarchical, bioactive supramolecular meshes and human tubular cells. Biomaterials 2011, 32: 723– 733. 10.1016/j.biomaterials.2010.09.020 20943265 · DOI
  43. [43]Jang KJ, Mehr AP, Hamilton GA, McPartlin LA, Chung S, Suh KY et al Human kidney proximal tubule-on-a-chip for drug transport and nephrotoxicity assessment. Integr Biol (Camb) 2013, 5: 1119– 1129. 23644926
  44. [44]Jang KJ and Suh KY. A multi-layer microfluidic device for efficient culture and analysis of renal tubular cells. Lab Chip 2010, 10: 36– 42. 10.1039/b907515a 20024048 · DOI
  45. [45]Frohlich EM, Zhang X and Charest JL. The use of controlled surface topography and flow-induced shear stress to influence renal epithelial cell function. Integr Biol (Camb) 2012, 4: 75– 83. 22139064
  46. [46]Friedrich C, Endlich N, Kriz W and Endlich K. Podocytes are sensitive to fluid shear stress in vitro. Am J Physiol Renal Physiol 2006, 291: F856– 865. 16684926
  47. [47]Grabias BM and Konstantopoulos K. Epithelial-mesenchymal transition and fibrosis are mutually exclusive reponses in shear-activated proximal tubular epithelial cells. Faseb J 2012, 26: 4131– 4141. 10.1096/fj.12-207324 22744866 PMC3448778 · DOI
  48. [48]Luo DD, Fielding C, Phillips A and Fraser D. Interleukin-1 beta regulates proximal tubular cell transforming growth factor beta-1 signalling. Nephrol Dial Transplant 2009, 24: 2655– 2665. 10.1093/ndt/gfp208 19420104 · DOI
  49. [49]Bondeva T, Heinzig J, Franke S and Wolf G. Angiotensin II differentially regulates Morg1 expression in kidney cells. Am J Nephrol 2012, 35: 442– 455. 10.1159/000337922 22555025 · DOI
  50. [50]Dankers PY, Boomker JM, Meijer EW, Popa ER and van Luyn MJ. From kidney development to drug delivery and tissue engineering strategies in renal regenerative medicine. J Control Release 2011, 152: 177– 185. 10.1016/j.jconrel.2011.01.034 21334390 · DOI
  51. [51]Weinbaum S, Duan Y, Thi MM and You L. An Integrative Review of Mechanotransduction in Endothelial, Epithelial (Renal) and Dendritic Cells (Osteocytes). Cell Mol Bioeng 2011, 4: 510– 537. 23976901 PMC3748935
  52. [52]Carrisoza-Gaytan R, Liu Y, Flores D, Else C, Lee HG, Rhodes G et al Effects of biomechanical forces on signaling in the cortical collecting duct (CCD). Am J Physiol Renal Physiol 2014, 307: F195– 204. 10.1152/ajprenal.00634.2013 24872319 PMC4152160 · DOI
  53. [53]Hinnebusch BF, Ma Q, Henderson JW, Siddique A, Archer SY and Hodin RA. Enterocyte response to ischemia is dependent on differentiation state. J Gastrointest Surg 2002, 6: 403– 409. 12022993
  54. [54]Jansen JH, Weyts FA, Westbroek I, Jahr H, Chiba H, Pols HA et al Stretch-induced phosphorylation of ERK1/2 depends on differentiation stage of osteoblasts. J Cell Biochem 2004, 93: 542– 551. 15378606
  55. [55]Makino A, Prossnitz ER, Bunemann M, Wang JM, Yao W and Schmid-Schonbein GW. G protein-coupled receptors serve as mechanosensors for fluid shear stress in neutrophils. Am J Physiol Cell Physiol 2006, 290: C1633– 1639. 16436471
  56. [56]Krouwer VJ, Hekking LH, Langelaar-Makkinje M, Regan-Klapisz E and Post JA. Endothelial cell senescence is associated with disrupted cell-cell junctions and increased monolayer permeability. Vasc Cell 2012, 4: 12 10.1186/2045-824X-4-12 22929066 PMC3527188 · DOI
  57. [57]Venkatesh D, Fredette N, Rostama B, Tang Y, Vary CP, Liaw L et al RhoA-mediated signaling in Notch-induced senescence-like growth arrest and endothelial barrier dysfunction. Arterioscler Thromb Vasc Biol 2011, 31: 876– 882. 10.1161/ATVBAHA.110.221945 21273559 PMC3252819 · DOI
  58. [59]Verzola D, Gandolfo MT, Gaetani G, Ferraris A, Mangerini R, Ferrario F et al Accelerated senescence in the kidneys of patients with type 2 diabetic nephropathy. Am J Physiol Renal Physiol 2008, 295: F1563– 1573. 10.1152/ajprenal.90302.2008 18768588 · DOI · Paper page
  59. [60]Martin JA, Klingelhutz AJ, Moussavi-Harami F and Buckwalter JA. Effects of oxidative damage and telomerase activity on human articular cartilage chondrocyte senescence. J Gerontol A Biol Sci Med Sci 2004, 59: 324– 337. 15071075
  60. [61]Warboys CM, de Luca A, Amini N, Luong L, Duckles H, Hsiao S et al Disturbed flow promotes endothelial senescence via a p53-dependent pathway. Arterioscler Thromb Vasc Biol 2014, 34: 985– 995. 10.1161/ATVBAHA.114.303415 24651677 · DOI · Paper page
  61. [62]Ardura JA, Rayego-Mateos S, Ramila D, Ruiz-Ortega M and Esbrit P. Parathyroid hormone-related protein promotes epithelial-mesenchymal transition. J Am Soc Nephrol 2010, 21: 237– 248. 10.1681/ASN.2009050462 19959711 PMC2834553 · DOI
  62. [63]Smith JP, Pozzi A, Dhawan P, Singh AB and Harris RC. Soluble HB-EGF induces epithelial-to-mesenchymal transition in inner medullary collecting duct cells by upregulating Snail-2. Am J Physiol Renal Physiol 2009, 296: F957– 965. 10.1152/ajprenal.90490.2008 19244405 PMC2681361 · DOI
  63. [64]Docherty NG, O'Sullivan OE, Healy DA, Murphy M, O'Neill A J, Fitzpatrick JM et al TGF-beta1-induced EMT can occur independently of its proapoptotic effects and is aided by EGF receptor activation. Am J Physiol Renal Physiol 2006, 290: F1202– 1212. 16368739
  64. [65]Norvell SM, Alvarez M, Bidwell JP and Pavalko FM. Fluid shear stress induces beta-catenin signaling in osteoblasts. Calcif Tissue Int 2004, 75: 396– 404. 15592796
  65. [66]Xiao C, Ogle SA, Schumacher MA, Schilling N, Tokhunts RA, Orr-Asman MA et al Hedgehog signaling regulates E-cadherin expression for the maintenance of the actin cytoskeleton and tight junctions. Am J Physiol Gastrointest Liver Physiol 2010, 299: G1252– 1265. 10.1152/ajpgi.00512.2009 20847300 PMC3006246 · DOI
  66. [67]Kim MK, Maeng YI, Sung WJ, Oh HK, Park JB, Yoon GS et al The differential expression of TGF-beta1, ILK and wnt signaling inducing epithelial to mesenchymal transition in human renal fibrogenesis: an immunohistochemical study. Int J Clin Exp Pathol 2013, 6: 1747– 1758. PMC3759481 24040439
  67. [68]Abed A, Toubas J, Kavvadas P, Authier F, Cathelin D, Alfieri C et al Targeting connexin 43 protects against the progression of experimental chronic kidney disease in mice. Kidney Int 2014. 24850151
  68. [69]Vongwiwatana A, Tasanarong A, Rayner DC, Melk A and Halloran PF. Epithelial to mesenchymal transition during late deterioration of human kidney transplants: the role of tubular cells in fibrogenesis. Am J Transplant 2005, 5: 1367– 1374. 15888043
  69. [70]Verghese E, Weidenfeld R, Bertram JF, Ricardo SD and Deane JA. Renal cilia display length alterations following tubular injury and are present early in epithelial repair. Nephrol Dial Transplant 2008, 23: 834– 841. 17962379
  70. [71]Rozycki M, Lodyga M, Lam J, Miranda MZ, Fatyol K, Speight P et al The fate of the primary cilium during myofibroblast transition. Mol Biol Cell 2014, 25: 643– 657. 10.1091/mbc.E13-07-0429 24403605 PMC3937090 · DOI
  71. [72]Sharma A, Mucino MJ and Ronco C. Renal functional reserve and renal recovery after acute kidney injury. Nephron Clin Pract 2014, 127: 94– 100. 10.1159/000363721 25343829 · DOI
  72. [73]Yang GK, Har RL, Lytvyn Y, Yip P and Cherney DZ. Renal hyperfiltration is associated with glucose-dependent changes in fractional excretion of sodium in patients with uncomplicated type 1 diabetes. Diabetes Care 2014, 37: 2774– 2781. 10.2337/dc14-0798 25011944 · DOI

Cited by

Sorted by citations

Authors
Maggiorani, D., Dissard, R., Belloy, M., Saulnier-Blache, J.-S., Casemayou, A., Ducasse, L., Grès, S., Bellière, J., Caubet, C., Bascands, J.-L., Schanstra, J. P., & Buffin-Meyer, B.
Affiliations
Université Toulouse III - Paul Sabatier (FR)
ORCID
Venue
PLOS ONE
Publisher
Public Library of Science (PLoS)
Published
2015-07-06
Volume
10
Issue
7
Pages
e0131416
ISSN
1932-6203 (ISSN-L)
DOI
10.1371/journal.pone.0131416
PMC
PMC4493045
OpenAlex
W821765141
Cited by
74
References
1
Citations by year
2026: 6 · 2025: 2 · 2024: 5 · 2023: 6 · 2022: 8 · 2021: 4 · 2020: 10 · 2019: 13 · 2018: 10 · 2017: 7 · 2016: 1 · 2015: 1
FWCI
3.93
Type
journal article
Language
en
Open access
Licence
Locations
  • PLoS ONE (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
  • Figshare (submittedVersion, cc-by)
Funders
Institut National de la Santé et de la Recherche Médicale (U1048-I2MC, INSERM U1048, U1048)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic and Kidney Cyst Diseases
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion Transport and Channel Regulation
  • Health Sciences › Medicine › Nephrology › Acute Kidney Injury Research
Keywords
fluid shear stress, renal tubular epithelium, proximal tubular epithelial cells, HK-2 cells, tight junctions, claudin-2, ZO-1, adherens junctions, E-cadherin, β-catenin, SNAI1, Snail2, primary cilia, epithelial phenotype, remnant kidney, unilateral nephrectomy, kidney injury, kidney disease
MeSH terms
Animals, Cilia, Epithelial Cells, Humans, Kidney, Kidney Tubules, Stress, Mechanical, Tubulin, Cadherins, Tight Junctions, Adaptor Proteins, Signal Transducing, beta Catenin, Mice, Claudin-2, Zonula Occludens-1 Protein

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review