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      Inflammation & apoptosis in spinal cord injury

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          Abstract

          Spinal cord injury (SCI) consists of a two-steps process involving a primary mechanical injury followed by an inflammatory process and apoptosis. Secondary insult is characterized by further destruction of neuronal and glial cells, and leads to expansion of the damage, so that the paralysis can extend to higher segments. With the identification of mechanisms that either promote or prevent neuronal inflammation and apoptosis come new approaches for preventing and treating neurodegenerative disorders. From a clinical perspective, this article discusses novel targets for the development of therapeutic agents that have the potential to protect the spinal cord from irreversible damage and promote functional recovery.

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          Apoptosis in neurodegenerative disorders.

          Mark P. Mattson (2000)
          Neuronal death underlies the symptoms of many human neurological disorders, including Alzheimer's, Parkinson's and Huntington's diseases, stroke, and amyotrophic lateral sclerosis. The identification of specific genetic and environmental factors responsible for these diseases has bolstered evidence for a shared pathway of neuronal death--apoptosis--involving oxidative stress, perturbed calcium homeostasis, mitochondrial dysfunction and activation of cysteine proteases called caspases. These death cascades are counteracted by survival signals, which suppress oxyradicals and stabilize calcium homeostasis and mitochondrial function. With the identification of mechanisms that either promote or prevent neuronal apoptosis come new approaches for preventing and treating neurodegenerative disorders.
          Article 0 comments Cited 311 times – based on 0 reviews     Review now
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            Proinflammatory cytokine synthesis in the injured mouse spinal cord: multiphasic expression pattern and identification of the cell types involved.

            Isabelle Pineau, Steve Lacroix (2007)
            We have studied the spatial and temporal distribution of six proinflammatory cytokines and identified their cellular source in a clinically relevant model of spinal cord injury (SCI). Our findings show that interleukin-1beta (IL-1beta) and tumor necrosis factor (TNF) are rapidly (<5 and 15 minutes, respectively) and transiently expressed in mice following contusion. At 30-45 minutes post SCI, IL-1beta and TNF-positive cells could already be seen over the entire spinal cord segment analyzed. Multilabeling analyses revealed that microglia and astrocytes were the two major sources of IL-1beta and TNF at these times, suggesting a role for these cytokines in gliosis. Results obtained from SCI mice previously transplanted with green fluorescent protein (GFP)-expressing hematopoietic stem cells confirmed that neural cells were responsible for the production of IL-1beta and TNF for time points preceding 3 hours. From 3 hours up to 24 hours, IL-1beta, TNF, IL-6, and leukemia inhibitory factor (LIF) were strongly upregulated within and immediately around the contused area. Colocalization studies revealed that all populations of central nervous system resident cells, including neurons, synthesized cytokines between 3 and 24 hours post SCI. However, work done with SCI-GFP chimeric mice revealed that at least some infiltrating leukocytes were responsible for cytokine production from 12 hours on. By 2 days post-SCI, mRNA signal for all the above cytokines had nearly disappeared. Notably, we also observed another wave of expression for IL-1beta and TNF at 14 days. Overall, these results indicate that following SCI, all classes of neural cells initially contribute to the organization of inflammation, whereas recruited immune cells mostly contribute to its maintenance at later time points. (c) 2006 Wiley-Liss, Inc.
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              CD95's deadly mission in the immune system.

              P. H. Krammer (2000)
              Apoptosis in the immune system is a fundamental process regulating lymphocyte maturation, receptor repertoire selection and homeostasis. Thus, death by apoptosis is as essential for the function of lymphocytes as growth and differentiation. This article focuses on death receptor-associated apoptosis and the role of CD95 (Apo-1/Fas)-mediated signalling in T-cell and B-cell development and during the course of an immune response. Gaining an insight into these processes improves our understanding of the pathogenesis of diseases such as cancer, autoimmunity and AIDS, and opens new approaches to rational treatment strategies.
              Article 0 comments Cited 190 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Indian J Med Res
                Journal ID (iso-abbrev): Indian J. Med. Res
                Journal ID (publisher-id): IJMR
                Title: The Indian Journal of Medical Research
                Publisher: Medknow Publications & Media Pvt Ltd (India )
                ISSN (Print): 0971-5916
                Publication date (Print): March 2012
                Volume: 135
                Issue: 3
                Pages: 287-296
                Affiliations
                [* ] Department of Orthopaedics, 2 nd Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, PR of China
                [** ] Department of Orthopaedics, Institute of Clinical Research, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, PR of China
                Author notes
                Reprint requests: Dr Wei-Shan Chen, Department of Orthopaedics, 2 nd Affiliated Hospital, School of Medicine, Zhejiang University, Jiefang Road, Hangzhou, PR of China, 310 009 e-mail: zrspine@ 123456gmail.com
                [+]

                Corresponding authors

                Article
                Publisher ID: IJMR-135-287
                PMC ID: 3361863
                PubMed ID: 22561613
                SO-VID: ea9e12f2-17a6-4ea4-b007-6a9278fd2f31
                Copyright © Copyright: © The Indian Journal of Medical Research
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 24 December 2010
                Categories
                Subject: Review Article

                ScienceOpen disciplines: Medicine
                Keywords: mechanisms,spinal cord injury,inflammation,apoptosis,therapy
                Data availability:
                ScienceOpen disciplines: Medicine
                Keywords: mechanisms, spinal cord injury, inflammation, apoptosis, therapy

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