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Fig. 5 | Translational Neurodegeneration

Fig. 5

From: Blocking meningeal lymphatic drainage aggravates Parkinson’s disease-like pathology in mice overexpressing mutated α-synuclein

Fig. 5

AQP4 depolarization was worsened in midbrain of A53T mice following blocking of meningeal lymphatics. a Immunofluorescence showed that AQP4 was restrictively expressed at astrocyte endfeet (arrowheads) surrounding CD31 positive microvessels in SN of WT-sham mice, but AQP4 immunoreactive signals were abnormally present at the neuropil domains (stars) of the other three groups, especially in A53T mice that had Ldclns. b Percentage of AQP4 positive area significantly increased in both WT-LDclns mice and A53T-LDclns mice (genotype, F(1,12) = 32.82, p < 0.0001; ligament, F(1,12) = 46.37, p < 0.0001; interaction, F(1,12) = 0.1126, p = 0.7430). c AQP4 polarization, a ratio of perivascular AQP4 immunointensity to neutrophil AQP4 immunointensity, was lower in A53T-LDclns mice than WT-LDclns mice and A53T-sham controls respectively (genotype, F(1,12) = 23.4, p = 0.0004; ligament, F(1,12) = 26.22, p = 0.0003; interaction, F(1,12) = 0.1357, p = 0.7191). d-e Representative immunoblotting bands and densitometry analysis of AQP4 expression from ventral midbrain samples. Levels of AQP4 were increased in both A53T mice and WT mice after LDclns (genotype, F(1,12) = 15.69, p = 0.0019; ligament, F(1,12) = 27.04, p = 0.0002; interaction, F(1,12) = 0.2051, p = 0.6587). f Representative images showed the distribution pattern of AQP4 and α-syn. Notably, dense AQP4 immunoreactivity was closely surrounding α-syn positive cells. Data represent mean ± SEM from 4 mice per group; data in e are from two independent results

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