Fig 1: NR1 suppressed ACR-induced autophagy by regulating ITGAV in the hippocampus. (A) The expression of Trx-1 in the hippocampus was detected by western blot analysis. NR1 restored the expression of Trx-1. (B) The expression of ITGAV in the hippocampus was detected by western blot analysis. NR1 restored the expression of ITGAV. (C) The expression of ATG4B in the hippocampus was detected by western blot analysis. NR1 restored the expression of ATG4B. (D) The expression of LC3II in the hippocampus was detected by western blot analysis. NR1 restored the expression of LC3II. (E) The expression of Cathepsin D in the hippocampus was detected by western blot analysis. NR1 restored the expression of Cathepsin D. (F) The expression of LAMP2a in the hippocampus was detected by western blot analysis. NR1 restored the expression of LAMP2a. Each bar represents the mean ± SE (n = 6). n.s. (no significance) >0.05, *P < 0.05, **P < 0.01, ***P < 0.001, statistically significant.
Fig 2: Bioinformatics analysis for gene transcriptional expression. (A) Heatmap showed that the expression of genes correlated with ITGAV in 12 samples. (B) Correlations between ITGAV and genes in the autophagy pathway or genes in the pathway containing TXN1. (C) The genes correlated with ITGAV in the pathway.
Fig 3: A new tumor initiating cell population with limited differentiation capacity from SCCs with EMT phenotypeA. Increased expression of integrin aV (Itgav) in cells from SCC with EMT phenotype. qRT-PCR shows decreased expression of known cancer stem cell markers CD34 and Lgr6 in Itgav+ cancer cells. Experiments were performed three times with similar results. Error bars indicate SEM. B. Itgav+ cancer cell (red) in SCC with EMT phenotype. Nuclei were counterstained with DAPI. Scale bar = 5 µm. A representative section is shown. C. Flow cytometric sorting of Itgav+ cancer cells from SCC with EMT phenotype. Itgav log and forward scatter linear (FS lin) scales are shown. A representative sort is shown. D. H&E stained section of poorly differentiated SCC arising from transplanted Itgav+ cancer cells. E. Itgav+ cancer cell (red) in transplanted SCC. Scale bar = 5 µm. F. Flow cytometric sorting of Itgav+ cancer cells from transplanted SCC. Itgav+ cancer cells fail to regenerate CD34+ or Lgr6+ cancer stem cells. CD34+ G. and Lgr6+ H. cancer stem cells were sorted from transplanted SCC by flow cytometry.
Fig 4: PLAUR contributes to Serpin E1-elicited response in cultured mTGNs. (A) Knockdown (KD) of PLAUR is revealed by Western blotting analysis. In mTGNs, PLAUR KD resulted in reduced calcium spikes elicited by Serpin E1, the number of responders to Serpin E1, and AUC of Serpin E1-induced calcium transients (B). (C) KD of ITGAV is confirmed by Western blotting analysis in mTGNs. (D) ITGAV KD failed to reduce Serpin E1-induced calcium spikes, the number of responders to Serpin E1, and AUC of calcium transients elicited by Serpin E1in mTGNs. Each cell intracellular calcium increases were normalized to F/F0, with F denoting the fluorescence and F0 the baseline fluorescence, and graphed relative to time. Responding cells were analyzed and presented as % total neurons. For all the data, means ± SEMs (n = 3); ns P > 0.05, and ***p < .001, student t-test, n = 3. Scales = 5 µm.
Fig 5: Transcription levels of PLAUR correlate with skin lesions of AD and psoriasis. Transcripts of PLAUR in human LAD and NLAD versus HC (A), and in LAD versus NLAD (B). Transcripts of PLAUR in LPS versus HC (C). Transcripts of ITGAV in LAD and NLAD versus HC (D), in LAD versus NLAD (E), and in LPS versus HC (F). Significances were defined with transcripts showing greater than a 2-fold change and an FDR value <0.05. Scales = 100 µm. For (A–C) ***FDR < .001, **0.001 < FDR < 0.01, *0.01 < FDR < 0.05, nsFDR > 0.05. For E, means ± SEMs (n = 3); N.S., ***p < .001, student t-test.
Supplier Page from Abcam for Anti-Integrin alpha V antibody [EPR16800]