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. 2019 Mar 15;36(7):1060–1079. doi: 10.1089/neu.2018.5986

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© Volodymyr Gerzanich et al., 2018; Published by Mary Ann Liebert, Inc.

This Open Access article is distributed under the terms of the Creative Commons License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited.

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FIG. 3. — (A) Immunolabeling for sulfonylurea receptor 1 (SUR1) showed sparse immunoreactivity in the control specimen (CTR) vs. widespread expression in elongated structures and small round cells in a glial fibrillary acidic protein (GFAP)–negative specimen from contusion–traumatic brain injury (TBI). (B, C) Double immunolabeling for collagen IV (COLIV) (red) and SUR1 (B) or transient receptor potential cation channel subfamily M member 4 (TRPM4) (C) showed expression of SUR1 and TRPM4 in microvessels; merged images are also shown. (D-F) Double immunolabeling for CD68 (red) and SUR1 (D) or TRPM4 (E) or KIR6.2 (F) showed expression of SUR1, TRPM4 and KIR6.2 in microglia/macrophages; merged images are also shown. (G) Double immunolabeling for SUR1 (green) and TRPM4 (red) showed co-localization in a microvessel. (H) ImmunoFRET for SUR1 (red) and TRPM4 (magenta) shows co-assembly of SUR1-TRPM4 heteromers (yellow pseudocolor) in a microvessel. The findings illustrated are from the GFAP-negative specimen shown in Figure 2, left, and are representative of all GFAP-negative, SUR1-positive specimens from four cases of human contusion-TBI; (four cases with GFAP-negative specimens showed no immunoreactivity for SUR1). Case #2, 11 days post-TBI; case #3, 7 days post-TBI.