Preprint Article Version 1 Preserved in Portico This version is not peer-reviewed

Focal Traumatic Brain Injury Impairs Integrity of Basement Membrane of Hindlimb Muscle Fibers Revealed by Extracellular Matrix Immunoreactivity

Version 1 : Received: 13 February 2024 / Approved: 13 February 2024 / Online: 13 February 2024 (15:29:10 CET)

A peer-reviewed article of this Preprint also exists.

Kristensen, M.A.; Rich, K.K.; Mogensen, T.C.; Damsgaard Jensen, A.M.; Fex Svenningsen, Å.; Zhang, M. Focal Traumatic Brain Injury Impairs the Integrity of the Basement Membrane of Hindlimb Muscle Fibers Revealed by Extracellular Matrix Immunoreactivity. Life 2024, 14, 543. Kristensen, M.A.; Rich, K.K.; Mogensen, T.C.; Damsgaard Jensen, A.M.; Fex Svenningsen, Å.; Zhang, M. Focal Traumatic Brain Injury Impairs the Integrity of the Basement Membrane of Hindlimb Muscle Fibers Revealed by Extracellular Matrix Immunoreactivity. Life 2024, 14, 543.

Abstract

Traumatic brain injury (TBI) stands as a prominent global cause of disability, with motor deficits being a common consequence. Despite its widespread impact, the precise pathological mechanisms underlying motor deficits after TBI remain elusive. In this study, hindlimb postural asymmetry (HL-PA) development in rats subjected to focal TBI was investigated to explore the potential roles of laminin and collagen IV within the ECM of selected hindlimb muscles in the emergence of motor deficits following TBI. A focal TBI was induced by ablating the left sensorimotor cortex in rats and motor deficits were assessed by measuring HL-PA. The expression of laminin and collagen IV in eight selected muscles on each side of the hindlimbs from both TBI and sham-operated rats were studied using immunohistochemistry and semi-quantitatively analyzed. Results indicated that the TBI rats exhibited HL-PA, characterized by flexion of the contralateral (right) hindlimb. In the sham-operated rats the immunoreactive components of laminin and collagen IV were evenly and smoothly distributed along the border of the muscle fibers in all the investigated muscles. In contrast, in the TBI rats the pattern was broken into aggregated granule-like immunoreactive components. Such a labeling pattern was detected in all the investigated muscles both from the contra-and ipsilateral side of the TBI rats. However, in TBI rats most of the muscles from the contralateral hindlimb showed a significant increased expression of these two proteins in comparison with those from the ipsilateral hindlimb. In comparison to sham-operated rats, there was a significant increase in laminin and collagen IV expression in various contralateral hindlimb muscles in the TBI rats. These findings suggest potential implications of laminin and collagen IV in the development of motor deficits following a focal TBI.

Keywords

traumatic brain injury; hindlimb postural asymmetry; motor deficits; extracellular matrix; laminin; collagen type IV

Subject

Medicine and Pharmacology, Neuroscience and Neurology

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