Perturbation of such pathways can potentially skew vascular homeostatic equilibrium towards altered vascular permeability. We also observed significant upregulation of genes involved in paracrine signaling through chemokines and lymphocyte activation pathways during HAPE represented by transcripts of TNF, JAK2, MAP2K2, MAP2K7, MAPK10, PLCB1, ARAF, SOS1, PAK3 and RELA amongst others. Further, several important regulators of systemic/pulmonary hypertension including ADRA1D, ECE1, and EDNRA were upregulated in HAPE. Some notable genes within these pathways included MYLK rho family members ARGEF11, ARHGAP24 cell adhesion molecules such as CLDN6, CLDN23, PXN and VCAM1 besides other signaling intermediates. These pathways included those which regulate vasoconstriction through smooth muscle contraction, cellular actin cytoskeleton rearrangements and endothelial permeability/dysfunction. Our data suggests concurrent modulation of multiple pathways which regulate vascular homeostasis and consequently lung fluid dynamics.

We performed global gene expression profiling in individuals with established HAPE compared to acclimatized individuals.

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