4.2 Article

Integrated analysis of gait parameters and gene expression profiles in a murine model of subarachnoid hemorrhage

Journal

GENES BRAIN AND BEHAVIOR
Volume 20, Issue 5, Pages -

Publisher

WILEY
DOI: 10.1111/gbb.12728

Keywords

CatWalk; gait variability; SP1; stroke; subarachnoid hemorrhage

Funding

  1. SDIVF RD Centre
  2. Chinese University of Hong Kong Direct Grant for Research [MD16622]

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This study investigated the correlation between gait variability and SAH-associated gene expression in a murine model, identifying a strong relationship between gait deficits and the regulation of these genes. Furthermore, the study suggests that p-SP1(453) expression could serve as a potential biomarker for monitoring SAH pathogenesis and a therapeutic target for the condition.
Gait analysis has been widely used to examine the behavioral presentation of numerous neurological disorders. Thorough murine model evaluation of the subarachnoid hemorrhage (SAH)-associated gait deficits is missing. This study measures gait deficits using a clinically relevant murine model of SAH to examine associations between gait variability and SAH-associated gene expressions. A total of 159 dynamic and static gait parameters from the endovascular perforation murine model for simulating clinical human SAH were determined using the CatWalk system. Eighty gait parameters and the mRNA expression levels of 35 of the 88 SAH-associated genes were differentially regulated in the diseased models. Totals of 42 and 38 gait parameters correlated with the 35 SAH-associated genes positively and negatively with Pearson's correlation coefficients of >0.7 and <-0.7, respectively. p-SP1(453) expression in the motor cortex in SAH animal models displays a significant correlation with a subset of gait parameters associated with muscular strength and coordination of limb movements. Our data highlights a strong correlation between gait variability and SAH-associated gene expression. p-SP1(453) expression could act as a biomarker to monitor SAH pathological development and a therapeutic target for SAH.

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