AQP1 Antibody - #AF5231

Figure 3 HUA activated the RIG-I/caspase-1/GSDMD pyroptosis pathway in renal tubules (A) Clustered heatmap of the relative proteins in HN (n = 3 animals per group). The color scale from blue (reduction) to white (low intensity) to red (increases). (B) Schematic diagram of RIG-I and caspase-1 molecular structure. (C–F) Western blot showing cleaved-caspase-1 (C and D) and caspase-1 (C and E) levels in the kidneys of control and OXO/adenine-induced mice (n = 5 animals per group). Western blot showing RIG-I (C and F) levels in the kidneys of control and OXO/adenine-induced mice (n = 5 animals per group). (G–I) Representative fluorescence microscopy images of normal renal tissue stained for AQP-1, RIG-I and caspase-1 to identify the colocalization of caspase-1 and RIG-I in renal tubules. Scale bar 50 μm. (J) Co-IP assay results showing the interplay between RIG-I and caspase-1 in NRK-52E cells treated with UA for 48 h. Data for (D–F) are presented as mean ± SEM. One-way ANOVA with Student-Newman-Keuls test for (D–F). Norm-diet, normal diet. UA, uric acid. See also Figure S1.

FIGURE 4 Ectopic expression of MMP-7 enhanced AQP-1 expression and then altered cell volume in peritoneal mesothelial cells. HMrSV5 cells were infected with lentivirus expressing MMP-7. (a, b) The expression of MMP-7 in the lentivirus-transfected cells was determined by quantitative RT-PCR (a) and Western blotting analysis (b). (c) The MMP-7-overexpressing cells (Lv-MMP-7) and control cells (Lv-NC) were incubated in NS or dialysate with 4.25% glucose for 1 minute. The cell diameter of peritoneal mesothelial cells was evaluated by the Scepter 2.0 cell counter. The changes of cell diameter after glucose stimulation were calculated. (d-f) The mRNA level of AQP-1 was detected by quantitative RT-PCR (d), and the protein expression of AQP-1 was assessed by Western blotting assay (e). Besides, the cells were permeabilized by Triton-X 100 and immunofluorescence assay was used to detect the expression of AQP-1 (f). (g, h) The cells were treated with the indicated 50 ng/ml MMP-7 for 12 hours. The expression of AQP-1 in the HMrSV5 cell membrane was evaluated by Western blotting (g) and immunofluorescence assay (h), HMrSV5 cells were transfected with AQP-1-targeting siRNAs for 36 hours. The expression level of AQP-1 protein was assayed by immunoblotting. The #3 siRNA against AQP-1 was selected for the further analysis. (I) After transfecting with AQP-1-targeting siRNAs for 36 hours, HMrSV5 cells were incubated with 100 ng/ml MMP-7 for another 24 hours. Cell diameter of the peritoneal mesothelial cells was evaluated by the Scepter 2.0 cell counter (J). *P < 0.05, **P < 0.01, one of the three independent experiments is shown

FIGURE 4 Ectopic expression of MMP-7 enhanced AQP-1 expression and then altered cell volume in peritoneal mesothelial cells. HMrSV5 cells were infected with lentivirus expressing MMP-7. (a, b) The expression of MMP-7 in the lentivirus-transfected cells was determined by quantitative RT-PCR (a) and Western blotting analysis (b). (c) The MMP-7-overexpressing cells (Lv-MMP-7) and control cells (Lv-NC) were incubated in NS or dialysate with 4.25% glucose for 1 minute. The cell diameter of peritoneal mesothelial cells was evaluated by the Scepter 2.0 cell counter. The changes of cell diameter after glucose stimulation were calculated. (d-f) The mRNA level of AQP-1 was detected by quantitative RT-PCR (d), and the protein expression of AQP-1 was assessed by Western blotting assay (e). Besides, the cells were permeabilized by Triton-X 100 and immunofluorescence assay was used to detect the expression of AQP-1 (f). (g, h) The cells were treated with the indicated 50 ng/ml MMP-7 for 12 hours. The expression of AQP-1 in the HMrSV5 cell membrane was evaluated by Western blotting (g) and immunofluorescence assay (h), HMrSV5 cells were transfected with AQP-1-targeting siRNAs for 36 hours. The expression level of AQP-1 protein was assayed by immunoblotting. The #3 siRNA against AQP-1 was selected for the further analysis. (I) After transfecting with AQP-1-targeting siRNAs for 36 hours, HMrSV5 cells were incubated with 100 ng/ml MMP-7 for another 24 hours. Cell diameter of the peritoneal mesothelial cells was evaluated by the Scepter 2.0 cell counter (J). *P < 0.05, **P < 0.01, one of the three independent experiments is shown

Fig. 1 Effect of Pseudoephedrine + emodin on pathological changes of lung tissues (×200), expression of AQP‐1, AQP‐5 in LPS‐induced ALI rats. A The chemical structure of Pseudoephedrine and Emodin. B Stained with hematoxylin and eosin. C The lung injury score was determined following a five-point scale from 0 to 4 as follows: 0, l, 2, 3, and 4 represent no damage, mild damage, moderate damage, severe damage, and very severe damage, respectively. Representative histological sections of the lungs were stained with hematoxylin and eosin (H & E staining, magnification ×200). D–F Western blot analysis was performed to detect AQP‐1 and AQP‐5 protein expression. K The dry/wet weight ratio and lung weight/body weight ratio were used to reflect the pulmonary edema. All data are expressed as mean ± S.D. (n = 5). ##p < 0.01, ###p < 0.001 vs. control group. *p < 0.05, **p < 0.01, ***p < 0.001 vs. LPS alone group. +p < 0.05, +++p < 0.001 vs. combined treatment group (5 + 20 mg/kg)

FIGURE 1 | The miR-3194-3p and AQP1 expression levels in BC tissues and cell lines. Comparing differences in the expression levels of miR-3194-3p between(A) BC and adjacent non-tumor tissues (n = 30); (B) BC cell lines and the control breast epithelial cells (MCF-10A); differences in AQP1 mRNA level between (C) BC and adjacent non-tumor tissue; (D) BC cell lines and MCF-10A; differences in AQP1 protein level between (E) BC cell lines and MCF-10A.