title: Sera from patients with scleroderma inhibit fibroblast micromotions monitored electrically.
abstract: OBJECTIVE
  To investigate scleroderma fibroblast behavior, and the effect of different human sera on fibroblast behavior, we established a model using the newly developed electrical biosensor, electrical cell-substrate impedance sensing (ECIS).
  
  
  METHODS
  Cellular locomotion, defined as cellular micromotion, measured by ECIS indicates the dynamic vertical motion of a given group of cells. The junctional resistance (Rb) between adjacent cells and the average height (h) between basal cell surface and substratum derived from ECIS were quantified for dermal fibroblasts obtained from patients with scleroderma and normal controls. The cellular micromotions of both scleroderma and normal control fibroblasts were compared in the presence of different human sera, including those from patients with scleroderma, systemic lupus erythematosus (SLE), and Sjögren's syndrome (SS) and from normal individuals.
  
  
  RESULTS
  The Rb and h levels for scleroderma and normal fibroblasts were 2.7 omega.cm2, 150 nm and 0.8 omega.cm2, 303 nm respectively. The micromotions of scleroderma fibroblasts were more active than those of normal fibroblasts. Sera from patients with scleroderma can inhibit the micromotions of normal fibroblasts but not those of scleroderma fibroblasts, while sera from patients with SLE and SS have no inhibitory effect on either normal or scleroderma fibroblast micromotions.
  
  
  CONCLUSIONS
  We have demonstrated the previously unrecognized characteristics of dermal fibroblasts and sera derived from patients with scleroderma. It is possible that in vivo activities cause scleroderma fibroblasts to display active cellular micromotions, while sera from patients with scleroderma inhibit the micromotions of normal fibroblasts. The use of ECIS technology has also provided a new approach to the study of scleroderma.
authors.affiliation: Department of Internal Medicine, Chung Shan Medical and Dental College, Taichung, Taiwan, Republic of China.
authors.forename: C N
authors.initials: CN
authors.lastname: Huang
authors.forename: C M
authors.initials: CM
authors.lastname: Lo
authors.forename: T C
authors.initials: TC
authors.lastname: Hsu
authors.forename: G J
authors.initials: GJ
authors.lastname: Tsay
mesh_terms: D000368:Aged; D001798:Blood Proteins / Q000494:pharmacology*; D002448:Cell Adhesion / Q000502:physiology; D002455:Cell Division / Q000502:physiology; D002465:Cell Movement / Q000187:drug effects* / Q000502:physiology; D048429:Cell Size / Q000502:physiology; D002478:Cells, Cultured; D017097:Electric Impedance; D005260:Female; D005347:Fibroblasts / Q000166:cytology* / Q000187:drug effects*; D006801:Humans; D007365:Intercellular Junctions / Q000502:physiology; D008297:Male; D008875:Middle Aged; D012595:Scleroderma, Systemic / Q000097:blood* / Q000473:pathology*
chemical_list: D001798:Blood Proteins