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Fig. 1 | Journal of Translational Medicine

Fig. 1

From: Pro-atherosclerotic disturbed flow disrupts caveolin-1 expression, localization, and function via glycocalyx degradation

Fig. 1

Heparan sulfate regulates flow-induced cav-1 expression and, partially, cav-1 localization. Cav-1 immunofluorescence of RFPECs is shown for conditions of a static flow, b DF, c UF, d static flow with Hep III treatment, and e UF with Hep III treatment (scale bar: 30 μm). f Quantification of cav-1 MFI demonstrates a significant highest expression of cav-1 in UF conditioned cells compared to all other conditions. g Representative cav-1 signal intensity curves showing, for each experimental condition, the distribution of cav-1 from one cell to a neighboring cell. The signal intensity curves were determined along equidistant lines (see representative hatched lines) that connect the intracellular compartments of the neighboring cells and the cell-to-cell appositions are at the 0.0 μm positions along each line. On first glance, distribution of cav-1 looks consistent for all conditions (h) Kurtosis analysis of full sets of these curves clarifies that indeed there are small differences in cav-1 distribution. However, it is important to note that RFPECs exposed to UF exhibit statistically more appositional localization of cav-1 than RFPECs exposed to DF, and there is no strong statistical evidence that HepIII treatment impacts this difference in cav-1 distribution. i Schematic view of the subcellular zones that were examined to assess preferential cav-1 localization. To clarify, preferential localization of cav-1 was determined based on MFI and not kurtosis analysis. j Compared to all other experimental conditions, exposure to UF induces significantly higher localization of cav-1 in the subcellular region that lies upstream with respect to flow direction. f, h, j Number of independent experiments “N” are shown for each condition, and *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001 are indicated in this Fig. 2 or in the accompanying Additional file 4: Fig. S4

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