Fig. 4
From: Loss of TRPV4 is insufficient to promote repair in a spinal cord injury contusion model
Full absence of TRPV4 does not contribute to recovery after spinal cord injury in a heterozygous model of Cx3cr1. (A) Timeline of the experimental procedures. (B) Functional recovery of 12-week-old Trpv4 WT Cx3cr1eGFP/+ (n = 14) and Trpv4 KO Cx3cr1eGFP/+ (n = 12) mice over 28 days after contusion injury at T8, of two individual experiments. (C) Overview of MBP, Laminin, GFAP+ astrocytes, and eGFP+ phagocytes around the lesion of a sagittal spinal cord section. (D) Quantification of lesion area surrounded by MBP, laminin, and GFAP+ astrocytes at 28 dpi. (E) Phagocytic (eGFP) and astrocytic (GFAP) density at different distances from the lesion at 28 dpi. Two-way ANOVA (B), Unpaired T-test (D), and Multiple unpaired T-test (E). Data are presented as means ± SEM. Scale bar: 1 mm. WT; wild-type, KO; knockout, T8, thoracic level 8; eGFP, enhanced green fluorescent protein; MBP, myelin basic protein; GFAP, glial fibrillary acidic protein; SCI, spinal cord injury; BMS, Basso Mouse Scale; dpi, days post-injury; IMV, intensity mean value.
