Vascular Endothelium - Tissue Functioning and Remodeling in the Circulatory and Ventilatory Systems - page 545

on protein synthesis, and sustained (duration hours to days). It recruits monocytes
and T lymphocytes. Moreover, intervention of innate immunocytes stimulates
lymphocytes of adaptive immunity. Activated T lymphocytes then enhance the
activity of macrophages and recruit eosinophils.
Prolonged antigenic stimulation by resistant microbes or tissue-derived auto-
antigens leads to chronic inflammation. During chronic inflammation, endothelial
cells respond to angiogenic factors to generate new blood vessels. Endothelial
cells subjected to lymphotoxin- acquire features of high endothelial venules and

secondary lymphoid organs, characterized by the recruitment of naive T cells and
central memory B and T cells (sometimes called tertiary lymphoid organs).

β

9.7.10.1 ED1L3

Whereas selectins, integrins, and immunoglobulin-like cell adhesion molecules
promote inflammatory cell recruitment, EGF-like repeat- and discoidin-1-like
domain-containing protein ED1L3 119 prevents leukocyte adhesion [ 999 ]. Inhibitor
ED1L3 is synthesized and secreted by endothelial cells. This anti-adhesive factor is
a ligand of

α L β 2 -integrin.

9.7.10.2 ELAV1

In human umbilical vein endothelial cells, the nucleocytoplasmic shuttling protein
Embryonic lethal, abnormal vision homolog ELAV1 120 contributes to the regulation
of inflammation by endothelial cells under mechanical and chemical stresses.
It regulates stress-sensitive genes that encode Kr uppel-like factor KLF2, endothelial
nitric oxide synthase NOS3, and bone morphogenic protein BMP4 [ 1000 ].
Synthesis of ELAV1 is controlled by hemodynamic stress. Agent ELAV1
promotes inflammation supported by endothelial cells, as it upregulates production
of ICAM1 and VCAM1 and causes NF κ B phosphorylation and adhesion of

monocytes.

9.8 Hemostasis

Hemostasis stops hemorrhage. Several processes participate in bleeding arrest when
a blood vessel is wounded: (1) vasoconstriction to reduce blood input in the
damaged region; (2) primary hemostasis induced by platelets bound to collagen that
forms the hemostatic plug within seconds after an injury; (3) blood coagulation, or

119 A.k.a. integrin-binding Developmentally regulated endothelial cell locus-1 (DEL1).
120 A.k.a. Hu antigen-R.