Fig 1: TGF-ß1 promotes PIEZO1 expression through C/EBPß. (A) TGF-ß1 dose-dependently induces PIEZO1 mRNA and protein expression. (B) PIEZO1, HIF-1a and TGF-ß1 protein expression were futher enhanced by addition of TGF-ß1 to cells subjectd to irradiation (IR). (C) Intracellular Ca2+ concentration was increased after TGF-ß1 co-culture. (D) TGF-ß1 inhibits C/EBPß protein expression. (E) C/EBPß protein expression was decreased after IR. (F) C/EBPß mRNA and protein expression were successful inhibited by specific siRNA to C/EBPß. (G) Compared to TGF-ß1 co-culture alone, PIEZO1 protein was further increased when C/EBPß expression was inhibited by siRNA targeting C/EBPß (si-C/EBPß). (H) The PROMO (prediction of transcription factor binding sites) database indicates a potential binding site of C/EBPß in the PEIZO1 promoter locus. (I) Dual-luciferase reporter assay suggests that C/EBPß binds to PIEZO1 gene promoter. (J) Chromatin immunoprecipitation (ChIP) reporter gene analyses found two binding sites of C/EBPß in the upstream region of the PIEZO1 promoter. Data are presented with the means ± SEMs (n = 3). *, p < 0.05; and **, p < 0.01.
Fig 2: The effect of Piezo1 and MCU in colon cancer cell metastasis. a–c Wound-healing assay was performed to investigate the effect of Piezo1 and MCU on cell motility in HCT-116 and SW-480 cells. d–g Transwell assay was used to evaluate the effect of Piezo1 and MCU on cell migration. *p < 0.05; **p < 0.01; ****p < 0.0001
Fig 3: PIEZO1 expression levels in diverse human cancers and pathological stages. (a) PIEZO1 expression level in TCGA tumors analyzed by the TIMER2 database. (b) Box plot data of CESE, CHOL, GBM, PAAD, PCPG, and PRAD in TCGA cohorts compared to healthy tissues in GTEx records. (c) Protein level of PIEZO1 in normal tissue and BRCA, KIRC, COAD, GBM, HNSC, LIHC, LUAD, OV, PAAD, and UCEC. The data of protein expression were obtained and analyzed by CPTAC. (d) The expression level of PIEZO1 analyzed and compared depending on different pathological stages (stages I–IV) of KIRC, PAAD, and STAD, based on the TCGA database. *P <0.05, ****p < 0.0001.
Fig 4: Piezo1 expression in normal skin and HS tissues.A The relative expression of Piezo1 and Piezo2 mRNA from HDFs was analyzed by real-time RT-PCR. B, C Images and quantitative analysis of Piezo1 in human normal skin and HS. (Scale bar = 50 µm). The basal epithelial layer was excluded from quantitation. D Images of immunofluorescence co-staining of Piezo1 and a-SMA in human normal skin and HS. Piezo1 are labeled in red and a-SMA in green. (Scale bar = 100 µm). Scale bars for the zoom images, 20 µm. E, F Images and quantitative analysis of immunohistochemistry staining of Piezo1 in rat normal skin and HS. (Scale bar = 50 µm). The basal epithelial layer was excluded from quantitation. G Images of immunofluorescence co-staining of Piezo1 and a-SMA in rat normal skin and HS. Piezo1 are labeled in red and a-SMA in green. (Scale bar = 100 µm). Scale bars for the zoom images, 20 µm. The arrowheads point to the fibroblasts. The results are expressed as the means with SD (n = 3). The T-test is used for all analysis. ***P < 0.005.
Fig 5: Piezo1 expression in the hippocampal dentate gyrus correlates with GFAP in aged rats with peripheral infection and strongly correlates with amyloid plaques in TgF344-AD rats. Sagittal brain sections were triple-stained for Piezo1, GFAP and conformation-specific Aß1-42 and Pearson correlations (r values) were performed to measure changes in Piezo1 channel expression in astrocytes (GFAP vs. Piezo1) with age and peripheral infection in WT (A–D) and TgF344-AD (E–H) rats. There was a moderate Pearson correlation between GFAP and Piezo1 in the infected 18-month WT (r = 0.523) and infected 18-month TgF344-AD rats (r = 0.519). However, the linear regression (R2) values were relatively weak for both groups suggesting that the GFAP fluorescence intensity is not a good predictor of Piezo1 channel expression. Next, Pearson correlations were performed to measure changes in GFAP expression around amyloid plaques (GFAP vs. Aß1-42) in the dentate gyrus with age and peripheral infection in TgF344-AD rats (I–L). There was a moderate Pearson correlation between GFAP and Aß1-42 in the infected 18-month old TgF344-AD rats (r = 0.586) but a relatively weak linear regression (R2) value suggesting that Aß1-42 fluorescence intensity is not a good predictor of GFAP expression. Finally, Pearson correlations were performed to measure changes in Piezo1 channel expression in and around amyloid plaques (Aß1-42 vs. Piezo1) in the dentate gyrus with age and peripheral infection in TgF344-AD rats (M–P). There were strong Pearson correlations between Aß1-42 and Piezo1 in 12-month old TgF344-AD rats (r = 0.917), 12-month old TgF344-AD rats with peripheral infection (r = 0.736), 18-month old TgF344-AD rats (r = 0.770), and 18-month old TgF344-AD rats with peripheral infection (r = 0.856). In addition, the high linear regression (R2) values for each group (M–P) suggests that Aß1-42 fluorescence intensity is a good predictor of Piezo1 channel expression in the dentate gyrus of TgF344-AD rats.
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