Pathologic human vitreous stimulates development of tractional forces by porcine Muller cells

Academic Article


  • Purpose. To determine if human vitreous samples, removed by vitrectomy from patients with proliferative diseases, contain factors capable of stimulating tractional force generation by Muller cells, and to correlate levels of this activity with diagnostic categories. Methods. Human vitreous samples (n=30) were obtained during vitrectomy using a modified infusion solution containing small amounts of a fluorochrome to permit quantification of vitreous dilution. Cultures of Muller cells were established by sequential papain and DNase digestion of porcine retina. Muller cells, attached to collagen gels, were incubated in varying concentrations of vitreal protein and changes in gel thickness were monitored. Levels of contraction-stimulating activity were standardized against the cellular response to serum, yielding activity measurements in serum equivalent (SE) per ml of native vitreous. Results. Muller cells were stimulated by pathologi; vitreous to contract the gels to varying degrees. Activities varied over a wide range from 0-28.1 SE/ml with a mean of 3.53. Diagnostic groups with mean activities in the high range (2.0-8.0 SE/ml) included patients with proliferative vitreoretinopathy, vitreous hemorrhage, epimacular proliferation, traction retinal detachment, rhegmatogenous retina) detachment and full thickness retinal defects. Categories with mean activities in the moderate range (1.0-2.0 SE/ml) included patients with ischemia, pigmented cells in the vitreous and open-globe trauma. Samples from patients with proliferative diabetic retinopathy, neovascularization and uveitis had the lowest mean levels of activity (< 1,0 SE/ml). Conclusions. Muller cells are stimutated to develop tractional forces by soluble promoters present in pathologic vitreous. Levels of this activity can vary widely depending on the clinical features at the time of surgery.
  • Author List

  • Hardwick CW; Morris R; Feist R; White M; Witherspoon CD; Guidry C
  • Volume

  • 37
  • Issue

  • 3