Vascular Endothelium - Tissue Functioning and Remodeling in the Circulatory and Ventilatory Systems - page 496

T lymphocytes lose PECAM1 with aging,
whereas thrombosis risk augments. Conversely, thrombosis reduces PECAM1 ex-
pression, thereby increasing T-cell proliferation. In humans, numbers of peripheral
CD4

In humans, both CD4 + and CD8 +

T lymphocytes decrease markedly
in patients with abdominal aortic aneurysms, whereas populations of CD4

+ ,PECAM1 + and CD8 + ,PECAM1 +

+ ,

PECAM1 − and CD8 + ,PECAM1 − T lymphocytes increase [ 915 ].

9.5.7 Miscellaneous

Endothelial cells can also store Arg vasopressin, angiotensin-2, histamine, atrial
natriuretic peptide, calcitonin gene-related peptide, neuropeptide-Y, and vasoactive
intestinal peptide [ 680 ].

9.5.8 Vessel Wall Homeostasis

9.5.8.1 Apoptosis Regulators

Apoptosis regulator through modulating IAP expression (ARIA) synthesized by
vascular endothelial cells induces endothelial apoptosis and hampers angiogenesis
via proteasomal degradation of inhibitor of apoptosis IAP1 and IAP2 [ 917 ].
X-box binding protein XBP1 that is involved in endoplasmic reticulum stress
response is highly expressed at areas of atheroma [ 918 ]. Sustained XBP1 activation
causes endothelial cell apoptosis and favors atherosclerotic lesion (Vol. 6 - Chap. 8.
Vascular Diseases).
Humanin (Hn) is a 24-amino acid peptide synthesized in vascular endothelial
cells (of both arteries and veins) that protects against oxidative stress and apop-
tosis [ 919 ]. 53

mol) to endothelial cell
cultures reduces oxidized LDL-induced formation of reactive oxygen species and
apoptosis [ 919 ]. 54 The binding of exogenous humanin to plasmalemmal receptors
involved in cell survival pathways and intracellular humanin that binds to BCL2-
associated X protein (BAX) can impede BAX pro-apoptotic effects.

Exogenous administration of humanin (0.1

53 During early stages of atherosclerosis, the arterial intima is damaged after LDL penetration
and accumulation into the subendothelial space. Endothelial cells and smooth myocytes are the
initial source of reactive oxygen species that oxidize LDL particles. Oxidized LDLs amplify ROS
generation.
54 Humanin limits the production of ceramide, a lipid second messenger involved in apoptosis.
Ceramide activates BCL2-associated X protein. Oxidized LDLs increase the concentration of
cellular ceramide.