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Endothelial cells and cathepsins: Biochemical and biomechanical regulation
#MMPMID26458976
Platt MO
; Shockey WA
Biochimie
2016[Mar]; 122
(?): 314-23
PMID26458976
show ga
Cathepsins are mechanosensitive proteases that are regulated not only by
biochemical factors, but are also responsive to biomechanical forces in the
cardiovascular system that regulate their expression and activity to participate
in cardiovascular tissue remodeling. Their elastinolytic and collagenolytic
activity have been implicated in atherosclerosis, abdominal aortic aneurysms, and
in heart valve disease, all of which are lined by endothelial cells that are the
mechanosensitive monolayer of cells that sense and respond to fluid shear stress
as the blood flows across the surfaces of the arteries and valve leaflets.
Inflammatory cytokine signaling is integrated with biomechanical signaling
pathways by the endothelial cells to transcribe, translate, and activate either
the cysteine cathepsins to remodel the tissue or to express their inhibitors to
maintain healthy cardiovascular tissue structure. Other cardiovascular diseases
should now be included in the study of the cysteine cathepsin activation because
of the additional biochemical cues they provide that merges with the already
existing hemodynamics driving cardiovascular disease. Sickle cell disease causes
a chronic inflammation including elevated TNF? and increased numbers of
circulating monocytes that alter the biochemical stimulation while the more
viscous red blood cells due to the sickling of hemoglobin alters the hemodynamics
and is associated with accelerated elastin remodeling causing pediatric strokes.
HIV-mediated cardiovascular disease also occurs earlier in than the broader
population and the influence of HIV-proteins and antiretrovirals on endothelial
cells must be considered to understand these accelerated mechanisms in order to
identify new therapeutic targets for prevention.
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