The role of Tenascin C in intracerebral hemorrhage-induced secondary brain injury in rats via induction of neuronal cell death and neuroinflammation

Ding, Jiasheng; Lian, Jinrong; Wang, Jiahe; Yang, Siyuan; Li, Haiying; Shen, Haitao; Sun, Qing; Li, Xiang; Chen, Gang

doi:10.1016/j.jchemneu.2022.102147

Cited by 1 publication

(2 citation statements)

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“…We did not find tenascin-C to be increased in our ICH lesions at day 7 while staining was observed in the EAE lesion control. Our results are thus discrepant with those of others where tenascin-C was found to be elevated after ICH in rats, and in the serum of patients with ICH (Wang et al, 2018;Ding et al, 2022). Further work would need to be conducted to resolve this discrepancy.…”

Section: Discussioncontrasting

confidence: 99%

“…(Continued) Li et al 10.3389/fnmol.2023.1251432 Frontiers in Molecular Neuroscience 13 frontiersin.org hemorrhage and may cause cytotoxic and vasogenic edema (Midwood and Orend, 2009;Suzuki et al, 2020). Tenascin-C is found to be elevated after ICH in rats, and in the serum of patients with ICH (Wang et al, 2018;Ding et al, 2022). Overall, despite the pathologic significance of ECM, the expression and functions of ECM members in ICH have largely not been elucidated.…”

Section: Discussionmentioning

confidence: 99%

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Prominent elevation of extracellular matrix molecules in intracerebral hemorrhage

Li,

Ghorbani,

Zhang

et al. 2023

Front. Mol. Neurosci.

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BackgroundIntracerebral hemorrhage (ICH) is the predominant type of hemorrhagic stroke with high mortality and disability. In other neurological conditions, the deposition of extracellular matrix (ECM) molecules is a prominent obstacle for regenerative processes and an enhancer of neuroinflammation. Whether ECM molecules alter in composition after ICH, and which ECM members may inhibit repair, remain largely unknown in hemorrhagic stroke.MethodsThe collagenase-induced ICH mouse model and an autopsied human ICH specimen were investigated for expression of ECM members by immunofluorescence microscopy. Confocal image z-stacks were analyzed with Imaris 3D to assess the association of immune cells and ECM molecules. Sections from a mouse model of multiple sclerosis were used as disease and staining controls. Tissue culture was employed to examine the roles of ECM members on oligodendrocyte precursor cells (OPCs).ResultsAmong the lectican chondroitin sulfate proteoglycan (CSPG) members, neurocan but not aggrecan, versican-V1 and versican-V2 was prominently expressed in perihematomal tissue and lesion core compared to the contralateral area in murine ICH. Fibrinogen, fibronectin and heparan sulfate proteoglycan (HSPG) were also elevated after murine ICH while thrombospondin and tenascin-C was not. Confocal microscopy with Imaris 3D rendering co-localized neurocan, fibrinogen, fibronectin and HSPG molecules to Iba1+ microglia/macrophages or GFAP+ astrocytes. Marked differentiation from the multiple sclerosis model was observed, the latter with high versican-V1 and negligible neurocan. In culture, purified neurocan inhibited adhesion and process outgrowth of OPCs, which are early steps in myelination in vivo. The prominent expression of neurocan in murine ICH was corroborated in human ICH sections.ConclusionICH caused distinct alterations in ECM molecules. Among CSPG members, neurocan was selectively upregulated in both murine and human ICH. In tissue culture, neurocan impeded the properties of oligodendrocyte lineage cells. Alterations to the ECM in ICH may adversely affect reparative outcomes after stroke.

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Section: Discussioncontrasting

confidence: 99%