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Hypoxia Induces Endothelial Barrier Dysfunctions in Lungs: Nitric Oxide Perturbs Actin Dynamics in Endothelial Cells pp. 271-281 $100.00
Authors:  (Swaraj Sinha, Hima Bindu Reddy, Suvro Chatterjee, AU-KBC Research Centre, Anna University, Chennai, India)
Endothelium forms a physical barrier that separates blood from tissues.
Communication between blood and tissues occurs through the delivery of molecules and
circulating substances across the endothelial barrier by directed transport either through
or between cells. In response to different stress stimuli, the endothelial barrier becomes
less restrictive that results in increased water and protein permeability. Two mechanisms
together or independent of each other may account for such an increase in permeability:
paracellular (i.e., between cell) and transcytotic (i.e., through cell) transport. The role of
intercellular gaps in mediating paracellular permeability also has been determined by
osmotically shrinking endothelial cells.Vascular remodeling in response to stress is a
common complication of many pulmonary abnormalities such as pulmonary
hypertension; vein graft remodeling and high altitude induced pulmonary edema (HAPE).
The actin cytoskeleton is a dynamic structure that undergoes rearrangement under the
control of various actin binding, capping, nucleating, and severing proteins, which are
intimately involved in integration of endothelial monolayers. Therefore, actin filaments
are of critical importance to endothelial cells permeability. Although significant progress
has been made in understanding the cellular and molecular events that regulate
permeability, the mechanistic insight of endothelial barrier functions in clinical
conditions such as HAPE remains elusive. An alternative strategy to protect barrier
integrity could be achieved by focusing on the downstream signaling of cytoskeletal
rearrangements in the endothelial cells. To prevent the endothelial cells from cellular
contraction via reductions in hyperphosphorylation known to be essential for several
models of agonist-induced pulmonary edema and ventilator-induced lung injury might
facilitate restoration following endothelial barrier dysfunctions. The permeability of
epithelial surfaces has been studied more thoroughly than that of endothelial surfaces,
and several studies have suggested a role of cytoskeleton in regulating epithelial
permeability. We hypothesized that the cytoskeleton might also contribute to regulation
of endothelial permeability. Alterations of the endothelial cell cytoskeleton under
hypoxia may contribute to changes in pulmonary vascular permeability and thereby leads
to HAPE. Many studies have been reported that hypoxia disrupts the endothelial barrier
by creating gaps in cell- cell junctions that causes infiltration of blood proteins and cells
into vessel wall. Few biophysical studies also proved that under hypoxia cytoskeletal
changes occur that cause this remodeling of endothelium. Nitric oxide plays an important
role in maintaining endothelial cell morphology. Our study has demonstrated that
hypoxia attenuates nitric oxide levels that make the endothelium leaky [1]. In
pathological conditions like HAPE, the transvascular leakage occurs due to low
bioavailability of nitric oxide in endothelium. We deem that membrane permeability,
cytoskeletal re-arrangements and vascular leakage under hypoxia are associated
phenomena. Our work improvises the concept that nitric oxide aids to resist hypoxia
induced endothelial leakage, which may lead to the development of therapeutic strategies
for minimizing vascular leakage in various conditions under hypoxia. 

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Hypoxia Induces Endothelial Barrier Dysfunctions in Lungs: Nitric Oxide Perturbs Actin Dynamics in Endothelial Cells pp. 271-281