Editorials

Endothelial cell activation

BMJ 1998; 316 doi: https://doi.org/10.1136/bmj.316.7141.1328 (Published 02 May 1998) Cite this as: BMJ 1998;316:1328

A central pathophysiological process

  1. Beverley J Hunt, Consultant,
  2. Karen M Jurd, Honorary lecturer
  1. Departments of Haematology and Rheumatology, Guy's and St Thomas's Trust, London SE1 7EH
  2. Department of Haematology, Guy's and St Thomas's Trust, London SE1 7EH

    The endothelium is now recognised as not simply being an inert lining to blood vessels, as thought in the 1960s, but a highly specialised, metabolically active interface between blood and the underlying tissues—maintaining vascular tone, thromboresistance, and a selective permeability to cells and proteins. Moreover, under the stimulation of agents such as interleukin 1, the endothelium undergoes changes which allow it to participate in the inflammatory response; this is known as endothelial cell activation.

    The term was coined in the 1960s by Willms-Kretschmer.1 He noted that in delayed hypersensitivity reactions the endothelium became plump and leaky and displayed increased quantities of biosynthetic organelles such as endoplasmic reticulum.1 He used the term activated to imply a change in function as well as morphology. In the 1980s an avalanche of papers showed that the newly discovered cytokines, interleukin 1 and tumour necrosis factor, changed surface molecules and thus the functions of cultured endothelial cells. To emphasise that these changes did not represent injury or dysfunction, Pober reintroduced the term …

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