Fig 2: Immunofluorescence staining demonstrates the localization of Cav-1 in the dorsal root ganglion. Cav-1 was mainly distributed in NF200-positive medium and large neurons and only a small part of it was distributed in the CGRP- and IB4-positive medium and small neurons (magnification, x200). The white arrows indicate the position of positive cells. Cav-1, caveolin-1; CPSP, chronic postsurgical pain; NF200, neurofilament 200; CGRP, calcitonin gene-related peptide; IB4, isolectin B4.

Fig 3: Effects of Cav-1 on ADSC developmental stages. (A) Immunofluorescence staining of undifferentiated hADSCs (upper), differentiated for 7 days (middle) and 14 days (lower). All samples were detected under fluorescence microscopy, and the merged images of Cav-1 (stained green) and nuclei (stained blue) are shown in the middle (Scale ba=200 µm). (B) Western blot analysis of Cav-1 in undifferentiated (control) and differentiated hADSCs for 7 and 14 days. (C) Semiquantitative reverse transcription-polymerase chain reaction analyses of ALB and HNF1A in differentiated and normal hADSCs. (D) Western blot analysis of the expression levels of p-MAPK and MAPK in differentiated and normal hADSCs. hADSCs, human adipose-derived stem cells; Cav-1, Caveolin-1; si, small interfering RNA; MAPK, mitogen-activated protein kinase; p-phosphorylated; GAPDH, glyceraldehyde 3-phosphate dehydrogenase.

Fig 4: Antagomir treatment restores BMECs function and OPC differentiation via Cav-1 in vitro.a BMECs transfected with Cy5-N.C. or Cy5-antagomir (yellow) were double immunostained by Cav-1 (green) and CD31 (red) (n = 5 independent primary cell cultures/group). Scale bar, 20 µm. b, c Immunoblotting and quantitative analyses of Cav-1, ZO-1, Occludin, and Claudin-5 levels. Results represent the mean for the relative band intensity of five replicates. d, e Representative co-immunostaining images and quantification of Cav-1 (green) and HSP90a (red) in control- or antagomir-treated endothelial cells in hypoxic conditions (n = 5 independent primary cell cultures/group). Scale bar, 20 µm. f ELISA for detection of HSP90a in CM from different groups (n = 5 independent primary cell cultures/group). g, h Representative immunofluorescent images and quantifications showing the differentiated cells (MBP+) cultured in CM from BMECs of different groups (n = 5 independent primary cell cultures/group). Scale bar, 20 µm. i, j Immunoblotting and quantifications of myelin proteins. Results represent the mean for the relative band intensity of five replicates. For immunoblotting experiments, protein samples derived from the same experiment and gels/blots were processed in parallel. All data are presented as the mean ± SD. The data in e were compared by paired t-test. The data in others were compared by one-way ANOVA with Tukey post hoc test. Source data are provided as a Source Data file.

Fig 5: Cav1-GLUT3 signaling is crucial for TKI-resistant NSCLC growth and is associated with cellular ATP production and glucose uptake. A. Cell viability (n=3) and B. ATP measurement (n=3) assays demonstrate the effects of Atorvastatin (ATV) at 1 µM, combination of ATV and Cav1-HALO (0.5 µg) vector, and combination of ATV, Cav1-HALO, and Cav1#1 siRNAs (25 nM) on tumor cells after 72 h using 96-well format, with vehicle acting as control. Cellular ATP is presented as percentages and normalized to vehicle. Significance in differences in viability indexes and cellular ATP percentages, in which ATV-treated or Cav1-HALO over expressing ATV-treated cells acted as controls, was determined by t test. C. Western blotting on Cav1, GLUT3, AMPK-a, and phospho-AMPKa T172, and ACTB protein expression from cells exposed to vehicle, ATV at 1 µM, combination of ATV and Cav1-HALO (6 µg) transfection and combination of ATV, Cav1-HALO and Cav1#1 siRNAs (25 nM) for 72 h. Protein size is indicated in kDa. D. Glucose uptake measurement in tumor cells treated with vehicle, ATV at 1 µM or combination of ATV and Cav1-HALO (2 µg) vector for 72 h (n=3). Glucose uptake is presented as percentages and normalized to vehicle. Significance in differences in glucose uptake, in which ATV-treated or Cav1-HALO over expressing ATV-treated cells acted as controls, was determined by t test.