Abstract
Lipocalin 2 (LCN2), an immunomodulator, regulates various cellular processes such as iron transport and defense against bacterial infection. Under pathological conditions, LCN2 promotes neuroinflammation via the recruitment and activation of immune cells and glia, particularly microglia and astrocytes. Although it seems to have a negative influence on the functional outcome in spinal cord injury (SCI), the extent of its involvement in SCI and the underlying mechanisms are not yet fully known. In this study, using a SCI contusion mouse model, we first investigated the expression pattern of Lcn2 in different parts of the CNS (spinal cord and brain) and in the liver and its concentration in blood serum. Interestingly, we could note a significant increase in LCN2 throughout the whole spinal cord, in the brain, liver, and blood serum. This demonstrates the diversity of its possible sites of action in SCI. Furthermore, genetic deficiency of Lcn2 (Lcn2-/-) significantly reduced certain aspects of gliosis in the SCI-mice. Taken together, our studies provide first valuable hints, suggesting that LCN2 is involved in the local and systemic effects post SCI, and might modulate the impairment of different peripheral organs after injury.
Highlights
Spinal cord injury (SCI) is a devastating event that causes life-long health restrictions including paralysis, loss of sensation and vegetative functions, pain, and psychological impairment [1]
In SCI, the primary injury refers to the initial physical damage of the spinal cord (SC), which is accompanied by hemorrhage, ischemia and local neuronal death, while the secondary injury phase is characterized by progressive damage of the SC, demyelination, astrogliosis and neuroinflammation [4,5,6,7,8,9]
Lipocalin 2 (Lcn2) protein levels, which were examined by Western Blot, revealed a similar time course and profile with a short delay compared to mRNA expression, peaking at 72 h post SCI (Figs. 1b/c)
Summary
Spinal cord injury (SCI) is a devastating event that causes life-long health restrictions including paralysis, loss of sensation and vegetative functions, pain, and psychological impairment [1]. The glial scar limits the spread of inflammation but, at the same time, impedes axonal regeneration [19,20,21] Under pathological conditions such as traumatic SCI, reactive astrocytes promote cytotoxic edema formation and ischemia through an upregulation of aquaporin 4 [16]. They are an integral component of local immune responses by producing and secreting a wide range of cytokines and chemokines [22, 23]. A1 polarized astrocytes express pro-inflammatory cytokines and contribute to neuronal death, whereas A2 polarized astrocytes stimulate CNS recovery and repair [24, 25]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
