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. 2018 Aug 4;19(8):2289. doi: 10.3390/ijms19082289

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© 2018 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Upstream factors linked to hereditary PAH modulate the PPARγ-APOE-LRP8 axis, which in turn controls pulmonary vascular matrix stiffening. (A–C) Following transfection with the indicated siRNAs, transcripts related to the PPARγ-APOE-LRP8-matrix remodeling axis were analyzed by RT-qPCR in PAAFs (A), PAECs (B), and PASMCs (C). Mean expression of a given miRNA in the control group (si-NC) was assigned a fold change of 1, to which corresponding miRNA levels in experimental groups were compared. Data are expressed as mean ± SD (* p < 0.05, ** p < 0.01, *** p < 0.001) of three independent experiments. One-way ANOVA and post-hoc Tukey tests were used for group comparisons. (D) Schematic of the main results. In each cell type, the central downstream PPARγ-APOE-LRP8-LOX-collagen axis is drawn. Factors genetically linked to PAH are strategically placed next to the portion of the axis which they regulate; font is also color-coded based on these connections. Blue: genes related to the PPARγ-APOE-LRP8 axis; Red: genes related to fibrillar collagen; Orange: genes related to LOX.