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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. 6. — Glial fibrillary acidic protein (GFAP)–positive specimens from human contusion- traumatic brain injury (TBI) exhibit KIR6.2 expression in astrocytes. (A) Immunolabeling for KIR6.2 showed sparse immunoreactivity in the control specimen (CTR) vs. widespread expression in a GFAP-positive specimen from contusion-TBI. (B) Double immunolabeling for GFAP (red) and KIR6.2 (green) showed astrocyte expression of KIR6.2; merged images confirm co-localization (yellow); in situ hybridization of the same tissue section for Kcnj11 messenger RNA showed positive signal co-localized with GFAP-positive, KIR6.2-expressing astrocytes; arrowheads point to cells with all three signals. (C) Double immunolabeling showed that KIR6.2 (red) and sulfonylurea receptor 1 (SUR1; green) were co-localized (yellow) in astrocytes. (D) ImmunoFRET for SUR1 (magenta) and KIR6.2 (red) showed co-assembly of SUR1-KIR6.2 heteromers (yellow pseudocolor) in astrocytes. (E) Double immunolabeling showed that KIR6.2 (green) and transient receptor potential cation channel subfamily M member 4 (TRPM4) (red) were co-localized in astrocytes. The findings illustrated are representative of all GFAP-positive specimens from eight cases of human contusion-TBI. (case #2, 11 days post-TBI; case #5, 1 day post-TBI)