Supplementary Material for: Faster Macular Vessel Density Loss in More Advanced Primary Open Angle Glaucoma Eyes

Purpose: To characterize and compare the longitudinal change of macular vessel density (VD) in primary open angle glaucoma (POAG) eyes across different disease stages. Methods: This is a sub-analysis of a prospective cohort study. A total of 103 eyes (53 eyes in the mild stage, 50 eyes in the moderate-to-advanced stage) of 75 POAG patients followed for more than 1 year with at least 2 qualified optical coherence tomography (OCT) angiography (OCTA) images were included. The rates of macular VD change were determined by linear regression and compared using the generalized linear mixed models between groups. Mixed effect models were used to evaluate the demographic and ocular parameters associated with the VD loss rate. Results: With a mean follow-up time of 2.36 years, the rates of macular VD change were significantly different from zero in both groups. The rates of macular VD loss were significantly faster in moderate-to-advanced stage group than in mild stage group in whole image (-2.46%/yr vs -1.47%/yr, p=0.002), superior hemifield (-2.42%/yr vs -1.30%/yr, p=0.001), para fovea (-2.35%/yr vs -1.26, p=0.001), superior (-2.20%/yr vs -1.01%/yr, p=0.002), nasal (-2.41%/yr vs -1.04%/yr p=0.001), inferior (-2.46%/yr vs -1.43%/yr, p=0.018) and temporal sectors (-2.32%/yr vs -1.58%/yr, p=0.012). Baseline mean deviation (MD) and OCT parameters were associated with the rates of macular VD loss. Conclusions: OCTA measurements could detect vascular deterioration over time in POAG eyes at different stages. The rates of macular VD loss were significantly faster in more advanced POAG eyes

Supplementary Material for: Hsp27 Acts as a Master Molecular Chaperone and Plays an Essential Role in Hepatocellular Carcinoma Progression

<strong><em>Aims:</em></strong> Hsp27, a master molecular chaperone, plays an important role in cancer. However, the specific co-chaperones that partner with Hsp27 and the role of Hsp27 in hepatocellular carcinoma (HCC) are not fully enumerated. The present study focuses on the role of Hsp27 in HCC and explores its potential co-chaperones in HCC development. <b><i>Methods:</i></b> Gene overexpression or knockdown was used to observe the role of Hsp27 in HCC. Co-immunoprecipitation and mass spectrometry were used to explore apoptosis resistance by regulating multiple co-chaperones of Hsp27. Hsp27 protein-protein interaction (PPI) networks were constructed by the MetaCore software. <b><i>Results:</i></b> Hsp27 was upregulated in HCC tissues, and Hsp27 overexpression significantly facilitated formation of HCC cell colony and invasion in normoxia and tolerance in hypoxia by interacting with HIF-1α. Next, the analysis of microarrays revealed that Hsp27 regulated several cellular signaling pathways, including Wnt, ErbB and TGF-β signaling. Moreover, we characterized the Hsp27 PPI map, which indicated that Hsp27 along with its co-chaperones formed different complexes and exerts transcription regulation activity by activating sp1, c-Myc, p53 and ESR1. <b><i>Conclusions:</i></b> Hsp27 along with its co-chaperones was related to the development of HCC by regulating multiple signaling pathways, and drugs that target Hsp27 along with its co-chaperones may be a potential therapy for HCC.<br

Supplementary Material for: Transplantation of Telocytes Attenuates Unilateral Ureter Obstruction-Induced Renal Fibrosis in Rats

<b><i>Background/Aims:</i></b> Previous studies imply that telocytes may have a protective effect on fibrosis in various organs, including the liver, colon, and heart. The effect of telocytes on renal fibrosis remains unknown. Herein, this study was designed to investigate the effect of telocytes on renal fibrosis and the potential mechanisms involved. <b><i>Methods:</i></b> In a unilateral ureteral obstruction (UUO)-induced renal fibrosis model, telocytes were injected via the tail vein every other day for 10 days. The degree of renal damage and fibrosis was determined using histological assessment. The expression of collagen I, fibronectin, epithelial-mesenchymal transition markers, and Smad2/3 phosphorylation was examined by western blot analyses. Real-time PCR and enzyme-linked immunosorbent assay were performed <i>in vivo</i> to detect the levels of transforming growth factor (TGF)-β1 and various growth factors. <b><i>Results:</i></b> Telocytes attenuated renal fibrosis, as evidenced by reduced interstitial collagen accumulation, decreased expression of fibronectin and collagen I, upregulation of E-cadherin, and downregulation of α-smooth muscle actin. Furthermore, telocytes decreased serum TGF-β1 levels, suppressed Smad2/3 phosphorylation, and increased the expression of hepatocyte growth factor (HGF) in rat kidney tissue following UUO. Blockage of HGF counteracted the protective effect of telocytes on UUO-treated kidneys. Through the detection of HGF mRNA levels <i>in vitro</i>, we found that telocytes had no effect on HGF expression compared with renal fibroblasts. <b><i>Conclusion:</i></b> Telocytes attenuated UUO-induced renal fibrosis in rats, likely through enhancing the expression of HGF in an indirect manner