scholarly journals Hematogenous Macrophages: A New Therapeutic Target for Spinal Cord Injury

2021 ◽  
Vol 9 ◽  
Author(s):  
Yuanzhe Ding ◽  
Di Zhang ◽  
Sheng Wang ◽  
Xiaolei Zhang ◽  
Jingquan Yang
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Therapeutic Target ◽  
Pathological Process ◽  
Secondary Injury ◽  
Cord Injury ◽  
Peripheral Monocyte ◽  
Primary Injury ◽  
M1 Type

Spinal cord injury (SCI) is a devastating disease leading to loss of sensory and motor functions, whose pathological process includes mechanical primary injury and secondary injury. Macrophages play an important role in SCI pathology. According to its origin, it can be divided into resident microglia and peripheral monocyte-derived macrophages (hematogenous Mφ). And it can also be divided into M1-type macrophages and M2-type macrophages on the basis of its functional characteristics. Hematogenous macrophages may contribute to the SCI process through infiltrating, scar forming, phagocytizing debris, and inducing inflammatory response. Although some of the activities of hematogenous macrophages are shown to be beneficial, the role of hematogenous macrophages in SCI remains controversial. In this review, following a brief introduction of hematogenous macrophages, we mainly focus on the function and the controversial role of hematogenous macrophages in SCI, and we propose that hematogenous macrophages may be a new therapeutic target for SCI.

scholarly journals Sirtuins: Potential Therapeutic Targets for Defense against Oxidative Stress in Spinal Cord Injury

2021 ◽  
Vol 2021 ◽  
pp. 1-14
Author(s):  
Jialiang Lin ◽  
Zhencheng Xiong ◽  
Jionghui Gu ◽  
Zhuoran Sun ◽  
Jiang Shuai ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Pathological Process ◽  
Secondary Injury ◽  
Beneficial Effects ◽  
Cord Injury ◽  
Primary Injury ◽  
Antioxidant Mechanisms ◽  
Antioxidant Effects

Spinal cord injury (SCI) is one of the most incapacitating neurological disorders. It involves complex pathological processes that include a primary injury and a secondary injury phase, or a delayed stage, which follows the primary injury and contributes to the aggravation of the SCI pathology. Oxidative stress, a key pathophysiological event after SCI, contributes to a cascade of inflammation, excitotoxicity, neuronal and glial apoptosis, and other processes during the secondary injury phase. In recent years, increasing evidence has demonstrated that sirtuins are protective toward the pathological process of SCI through a variety of antioxidant mechanisms. Notably, strategies that modulate the expression of sirtuins exert beneficial effects in cellular and animal models of SCI. Given the significance and novelty of sirtuins, we summarize the oxidative stress processes that occur in SCI and discuss the antioxidant effects of sirtuins in SCI. We also highlight the potential of targeting sirtuins for the treatment of SCI.

scholarly journals CCL3 contributes to secondary damage after spinal cord injury

2020 ◽  
Vol 17 (1) ◽  
Author(s):  
Nicolas Pelisch ◽  
Jose Rosas Almanza ◽  
Kyle E. Stehlik ◽  
Brandy V. Aperi ◽  
Antje Kroner
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Inflammatory Response ◽  
Lesion Size ◽  
Secondary Injury ◽  
Wild Type ◽  
Locomotor Recovery ◽  
Secondary Damage ◽  
Cord Injury

Abstract Background Secondary damage after spinal cord injury (SCI) is characterized by a cascade of events including hemorrhage, apoptosis, oxidative stress, and inflammation which increase the lesion size which can influence the functional impairment. Thus, identifying specific mechanisms attributed to secondary injury is critical in minimizing tissue damage and improving neurological outcome. In this work, we are investigating the role of CCL3 (macrophage inflammatory protein 1-α, MIP-1α), a chemokine involved in the recruitment of inflammatory cells, which plays an important role in inflammatory conditions of the central and peripheral nervous system. Methods A mouse model of lower thoracic (T11) spinal cord contusion injury was used. We assessed expression levels of CCL3 and its receptors on the mRNA and protein level and analyzed changes in locomotor recovery and the inflammatory response in the injured spinal cord of wild-type and CCL3−/− mice. Results The expression of CCL3 and its receptors was increased after thoracic contusion SCI in mice. We then examined the role of CCL3 after SCI and its direct influence on the inflammatory response, locomotor recovery and lesion size using CCL3−/− mice. CCL3−/− mice showed mild but significant improvement of locomotor recovery, a smaller lesion size and reduced neuronal damage compared to wild-type controls. In addition, neutrophil numbers as well as the pro-inflammatory cytokines and chemokines, known to play a deleterious role after SCI, were markedly reduced in the absence of CCL3. Conclusion We have identified CCL3 as a potential target to modulate the inflammatory response and secondary damage after SCI. Collectively, this study shows that CCL3 contributes to progressive tissue damage and functional impairment during secondary injury after SCI.

scholarly journals Revascularization After Traumatic Spinal Cord Injury

2021 ◽  
Vol 12 ◽  
Author(s):  
Chun Yao ◽  
Xuemin Cao ◽  
Bin Yu
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Blood Vessel ◽  
Vascular System ◽  
Mechanical Damage ◽  
Pathological Process ◽  
Secondary Injury ◽  
Traumatic Spinal Cord Injury ◽  
Physical Stimulation ◽  
Cord Injury

Traumatic spinal cord injury (SCI) is a complex pathological process. The initial mechanical damage is followed by a progressive secondary injury cascade. The injury ruptures the local microvasculature and disturbs blood-spinal cord barriers, exacerbating inflammation and tissue damage. Although endogenous angiogenesis is triggered, the new vessels are insufficient and often fail to function normally. Numerous blood vessel interventions, such as proangiogenic factor administration, gene modulation, cell transplantation, biomaterial implantation, and physical stimulation, have been applied as SCI treatments. Here, we briefly describe alterations and effects of the vascular system on local microenvironments after SCI. Therapies targeted at revascularization for SCI are also summarized.

scholarly journals CCL3 contributes to secondary damage after spinal cord injury

2020 ◽  
Author(s):  
Nicolas Pelisch ◽  
Jose Rosas Almanza ◽  
Kyle Edward Stehlik ◽  
Brandy V Aperi ◽  
Antje Kroner
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Inflammatory Response ◽  
Lesion Size ◽  
Secondary Injury ◽  
Wild Type ◽  
Locomotor Recovery ◽  
Secondary Damage ◽  
Cord Injury

Abstract Background: Secondary damage after spinal cord injury (SCI) is characterized by a cascade of events including hemorrhage, apoptosis, oxidative stress and inflammation which increase the lesion size which can influence the functional impairment. Thus, identifying specific mechanisms attributed to secondary injury is critical in minimizing tissue damage and improving neurological outcome. In this work, we are investigating the role of CCL3 (Macrophage inflammatory protein 1- α, MIP-1α), a chemokine involved in the recruitment of inflammatory cells, which plays an important role in inflammatory conditions of the central and peripheral nervous system. Methods: A mouse model of lower thoracic (T11) spinal cord contusion injury was used. We assessed expression levels of CCL3 and its receptors on the mRNA and protein level and analyzed changes in locomotor recovery and the inflammatory response in the injured spinal cord of wild-type and CCL3-/- mice.Results: The expression of CCL3 and its receptors is increased after thoracic contusion SCI in mice. We then examined the role of CCL3 after SCI and its direct influence on the inflammatory response, locomotor recovery and lesion size using CCL3 −/− mice. CCL3 −/− mice showed mild but significant improvement of locomotor recovery and a smaller lesion size compared to wild-type controls. In addition, neutrophil numbers as well as the pro-inflammatory cytokines and chemokines, known to play a deleterious role after SCI, were markedly reduced in the absence of CCL3 .Conclusion: We have identified CCL3 as a potential target to modulate the inflammatory response and secondary damage after SCI. Collectively, this study shows that the absence of CCL3 can contribute to reduced tissue damage and better functional recovery during secondary injury after SCI.

scholarly journals Role of Melatonin in Traumatic Brain Injury and Spinal Cord Injury

2014 ◽  
Vol 2014 ◽  
pp. 1-13 ◽  
Author(s):  
Mehar Naseem ◽  
Suhel Parvez
Keyword(s):  
Traumatic Brain Injury ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Brain Injury ◽  
Protective Role ◽  
Secondary Injury ◽  
Severe Injuries ◽  
Cord Injury ◽  
Injured Part

Brain and spinal cord are implicated in incidences of two of the most severe injuries of central nervous system (CNS). Traumatic brain injury (TBI) is a devastating neurological deficit involving primary and secondary injury cascades. The primary and secondary mechanisms include complex consequences of activation of proinflammatory cytokines, cerebral edema, upregulation of NF-κβ, disruption of blood-brain barrier (BBB), and oxidative stress. Spinal cord injury (SCI) includes primary and secondary injury cascades. Primary injury leads to secondary injury in which generation of free radicals and oxidative or nitrative damage play an important pathophysiological role. The indoleamine melatonin is a hormone secreted or synthesized by pineal gland in the brain which helps to regulate sleep and wake cycle. Melatonin has been shown to be a versatile hormone having antioxidative, antiapoptotic, neuroprotective, and anti-inflammatory properties. It has a special characteristic of crossing BBB. Melatonin has neuroprotective role in the injured part of the CNS after TBI and SCI. A number of studies have successfully shown its therapeutic value as a neuroprotective agent in the treatment of neurodegenerative diseases. Here in this review we have compiled the literature supporting consequences of CNS injuries, TBI and SCI, and the protective role of melatonin in it.

scholarly journals Role of melatonin in the dynamics of acute spinal cord injury in rats

2021 ◽  
Author(s):  
Jiaqi Bi ◽  
Jianxiong Shen ◽  
Chong Chen ◽  
Zheng Li ◽  
Haining Tan ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Acute Spinal Cord Injury ◽  
Cord Injury

scholarly journals Exoskeletons, Rehabilitation and Bodily Capacities

2021 ◽  
pp. 1357034X2110256
Author(s):  
Denisa Butnaru
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Crucial Role ◽  
Spinal Cord Injuries ◽  
Main Task ◽  
Cerebrovascular Accidents ◽  
Complex Processes ◽  
Cord Injury ◽  
Neurological Conditions

Motility impairments resulting from spinal cord injuries and cerebrovascular accidents are increasingly prevalent in society, leading to the growing development of rehabilitative robotic technologies, among them exoskeletons. This article outlines how bodies with neurological conditions such as spinal cord injury and stroke engage in processes of re-appropriation while using exoskeletons and some of the challenges they face. The main task of exoskeletons in rehabilitative environments is either to rehabilitate or ameliorate anatomic functions of impaired bodies. In these complex processes, they also play a crucial role in recasting specific corporeal phenomenologies. For the accomplishment of these forms of corporeal re-appropriation, the role of experts is crucial. This article explores how categories such as bodily resistance, techno-inter-corporeal co-production of bodies and machines, as well as body work mark the landscape of these contemporary forms of impaired corporeality. While defending corporeal extension rather than incorporation, I argue against the figure of the ‘cyborg’ and posit the idea of ‘residual subjectivity’.

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