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Long-term peritoneal dialysis is associated with progressive fibrosis of the peritoneum. Epithelial-mesenchymal transition (EMT) of mesothelial cells is an important mechanism involved in peritoneal fibrosis, and TGF-β1 is considered central in this process. However, targeting currently known TGF-β1-associated pathways has not proven effective to date. Therefore, there are still gaps in understanding the mechanisms underlying TGF-β1-associated EMT and peritoneal fibrosis. We conducted network-based integrated analysis of transcriptomic and proteomic data to systemically characterize the molecular signature of TGF-β1-stimulated human peritoneal mesothelial cells (HPMCs). To increase the power of the data, multiple expression datasets of TGF-β1-stimulated human cells were employed, and extended based on a human functional gene network. Dense network sub-modules enriched with differentially expressed genes by TGF-β1 stimulation were prioritized and genes of interest were selected for functional analysis in HPMCs. Through integrated analysis, ECM constituents and oxidative stress-related genes were shown to be the top-ranked genes as expected. Among top-ranked sub-modules, TNFAIP6, ZC3H12A, and NNT were validated in HPMCs to be involved in regulation of E-cadherin, ZO-1, fibronectin, and αSMA expression. The present data shows the validity of network-based integrated analysis in discovery of novel players in TGF-β1-induced EMT in peritoneal mesothelial cells, which may serve as new prognostic markers and therapeutic targets for peritoneal dialysis patients.

The aim of this study was to elucidate the width and length of the superior palpebral muscle by using anti-α-smooth muscle actin antibody. Ten orbits of 5 adult Korean cadavers were used. Eyelids were cut in vertical planes through midpupilliary, medial limbus, and lateral limbus and in horizontal planes at the anterior border of the superior transverse ligament and 2 mm proximal to the upper tarsal border. Superior palpebral muscle was localized using mouse monoclonal anti-α-smooth muscle actin and counterstained with light green for collagen. In enlarged pictures of sections, widths, lengths, and thicknesses of the superior palpebral involuntary muscle were measured with a curved scale and were analyzed. The levator palpebrae superioris muscle was divided into superficial and deep parts below the superior transverse ligament. The levator aponeurosis originated from the superficial part and the superior palpebral muscle originated from the deep part of the levator palpebrae superioris muscle. The aponeurosis was inserted into the upper border of tarsus. The superior palpebral muscle fibers arose 2.71 ± 0.64 mm posterior to the anterior border of the superior transverse ligament. The superior palpebral muscle was trapezoidal. The lengths of its sides were 15.58 ± 1.82 and 22.30 ± 5.25 mm, and its height was 13.70 ± 2.74 mm. The levator aponeurosis covered the superior palpebral muscle anteriorly. The width of the levator aponeurosis was approximately 4 mm wider than the superior palpebral muscle. The thicknesses of the superior palpebral muscle were 0.14 ± 0.13 mm at the anterior border of the superior transverse ligament, 0.45 ± 0.11 mm at the superior fornix level, and 0.10 ± 0.03 mm at the upper border of the tarsal plate. One vascular layer was between the levator aponeurosis and the superior palpebral muscle (upper vascular layer), and the other was between the superior palpebral muscle and the conjunctiva (lower vascular layer). At the superior fornix level, thickness of the upper and lower vascular layers was 0.28 ± 0.06 and 0.38 ± 0.21 mm, respectively. The result of our study might contribute to corrective blepharoptosis surgery.