Journal Article

PreJuSER-15795

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png Glomerular podocytes: A study of mechanical properties and mechano-chemical signaling

Eekhoff, A. ; Bonakdar, N. ; Alonso, J. L. ; Hoffmann, B.FZJ* ; Goldmann, W. H.FZJ*

2011
Academic Press Orlando, Fla.

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Please use a persistent id in citations: doi:10.1016/j.bbrc.2011.02.022

Abstract: Kidney glomeruli function as filters, allowing the passage of small solutes and waste products into the urinary tract, while retaining essential proteins and macromolecules in the blood stream. These structures are under constant mechanical stress due to fluid pressure, driving filtration across the barrier. We mechanically stimulated adherent wildtype podocytes using the methods of magnetic tweezer and twisting as well as cell stretching. Attaching collagen IV-coated or poly-l-lysine-coated magnetic beads to cell receptors allowed for the determination of cellular stiffness. Angiotensin II-treated podocytes showed slightly higher stiffness than untreated cells, the cell fluidity (i.e. internal dynamics) remained similar, and showed an increase with force. The bead detachment (a measure of the binding strength) was higher in angiotensin II-treated compared to untreated podocytes. Magnetic twisting confirmed that angiotensin II treatment of podocytes increases and CDTA treatment decreases cell stiffness. However, treatment with both angiotensin II and CDTA increased the cell stiffness only slightly compared to solely CDTA-treated cells. Exposing podocytes to cyclic, uniaxial stretch showed an earlier onset of ERK(1/2) phosphorylation compared to MEF (control) cells. These results indicate that angiotensin II might free intracellularly stored calcium and affects actomyosin contraction, and that mechanical stimulation influences cell signaling.

Keyword(s): Angiotensin II: pharmacology (MeSH) ; Angiotensin II: physiology (MeSH) ; Animals (MeSH) ; Cell Adhesion (MeSH) ; Cytoskeleton: physiology (MeSH) ; Kidney Glomerulus: cytology (MeSH) ; Mechanical Processes (MeSH) ; Mechanotransduction, Cellular (MeSH) ; Mice (MeSH) ; Mitogen-Activated Protein Kinase 1: metabolism (MeSH) ; Mitogen-Activated Protein Kinase 3: metabolism (MeSH) ; Podocytes: drug effects (MeSH) ; Podocytes: physiology (MeSH) ; Angiotensin II ; Mitogen-Activated Protein Kinase 1 ; Mitogen-Activated Protein Kinase 3 ; J ; Podocytes (auto) ; Cell mechanics and signaling (auto) ; Magnetic tweezer (auto) ; Magnetic twisting cytometry (auto) ; Cell stretcher (auto) ; Actin cytoskeleton (auto) ; AT1 receptor (auto) ; Angiotensin II (auto) ; Calcium (auto)

Note: We thank Drs. Ben Fabry, Rudolf Merkel, Gerold Diez, James Smith, and Anna Klemm for helpful comments, Tim Feichtmeier for the cyclic stretch experiments on human umbilical cord fibroblasts, Andrea Zang for helping with OMTC, and Wolfgang Rubner for building a new cell stretcher. This work was supported by grants from Bayerisch-Franzosisches Hochschulzentrum, Deutscher Akademischer Austausch Dienst, Bavaria California Technology Center, and Deutsche Forschungsgemeinschaft.

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Contributing Institute(s):

1. Biomechanik (ICS-7)

Research Program(s):

1. BioSoft: Makromolekulare Systeme und biologische Informationsverarbeitung (P45)

Appears in the scientific report 2011

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