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. Author manuscript; available in PMC: 2022 Jan 1.
Published in final edited form as: Arterioscler Thromb Vasc Biol. 2020 Nov 5;41(1):346–359. doi: 10.1161/ATVBAHA.120.315472

Figure 2. TNF-α treatment sequesters septin 2 to the cytoplasm in association with the disorganization of junctional proteins.

Figure 2.

Immunofluorescence staining for endogenous septin 2 (green), cell-cell adhesion proteins (red) and actin filaments in HDMVECS and scoring of the organization of junctional molecules (A-D). Insets indicate enlarged area of the image. (A) Endogenous septin 2, nectin-2, actin filaments, and blind scores of nectin-2 organization are shown in untreated (Upper) and TNF-α-treated HDMVECs (Lower). (B) Endogenous septin 2, afadin, actin filaments, and blind scores of afadin organization are shown in untreated (Upper) and TNF-α-treated HDMVECs (Lower). (C) Endogenous septin 2, PECAM-1, actin filaments, and blind scores of PECAM-1 organization are shown in untreated (Upper) and TNF-α-treated HDMVECs (Lower). (D) Endogenous septin 2, ZO-1, actin filaments, and blind scores of ZO-1 organization are shown in untreated (Upper) and TNF-α-treated HDMVECs (Lower). Scale bars: 50 μm. Variances among observers are statistically not significant. Differences in the organization of junctional proteins between untreated and TNF-α-treated HDMVECs are statistically significant. p-values are < 0.0001.