J Korean Ophthalmol Soc.  1999 Nov;40(11):2975-2986.

The Effects of Nitric Oxide Synthesis and Cellular Metabolic Activity by Glucose, Interleukine-1beta, and Transforming Growth Factor-beta1 in Human Umbilical Vascular Endothelial Cells

• Lee JS
• Oum BS
• Park CH
• Kim YS

Abstract

The authors studied the effects of NO synthesis, cellular metabolic activity, and cellular morphology in the human umbilical vascular endothelial cells[HUVECs] by the concentration of glucose and cytokines such as interleukine[IL]-1 and transfoming growth factor[TGF]-beta1. A high concentration of glucose slightly increased NO synthesis, and a higher concentration of TGF-beta1 decreases NO synthesis in a concentration-dependent manner. Especially, the effect on NO synthesis of glucose or cytokine was distinctly revealed in a culture medium with fetus bovine serum. In cellular viability, there was no significant difference among glucose, IL-1, TGF-beta1 and both IL-1 and TGF-beta1 combined, when compared to the control. The typical cells as well as cells stimulated by IL-1 have relatively round spindle shape, but the cells stimulated by TGF-beta1 have a more elongated spindle shape. In ultrastructual findings, normal cells had slightly dilatated rough endoplasmic reticulum, mitochondria, and golgi complex. However, the cells stimulated by TGF-beta1 showed an atypical ultrastructual evidence of some bundles of microfilaments and dense plaque-like materials in the cytoplasm. As glucose or various kinds of cytokines can induce NO synthesis and cellular differentiation, it is very important that the control of glucose or cytokine in vascular diseases can inhibit the synthesis of free radicals and cellular differentiation of vascular endothelial cells. Furthermore, it is desirable to study the role of cellular differentiation in vascular endothelial cells stimulated by TGF-beta1.

Keyword

Cytokine; Glucose; Interleukin-1; Nitric oxide; Transforming growth factor-beta1

MeSH Terms

Actin Cytoskeleton
Cytokines
Cytoplasm
Endoplasmic Reticulum, Rough
Endothelial Cells*
Fetus
Free Radicals
Glucose*
Golgi Apparatus
Humans*
Interleukin-1
Mitochondria
Nitric Oxide*
Transforming Growth Factor beta1
Vascular Diseases
Cytokines
Free Radicals
Glucose
Interleukin-1
Nitric Oxide
Transforming Growth Factor beta1