SDF-1 stimulates neurite growth on inhibitory CNS myelin

Opatz, Jessica; Küry, Patrick; Schiwy, Nora; Järve, Anne; Estrada, Veronica; Brazda, Nicole; Bosse, Frank; Müller, Hans

doi:10.1016/j.mcn.2008.11.002

Cited by 67 publications

(54 citation statements)

References 43 publications

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“…24 SDF-1 has been shown to promote neurite outgrowth in the presence of growth-inhibitory central nervous system myelin in vitro. 25 Local intrathecal infusion of SDF-1 in spinal cord injury resulted in enhanced sprouting of CST axons into both white matter and gray matter. 25 Moreover, there was evidence suggesting that SDF-1 has the ability to inhibit the function of RhoA and its downstream effector, ROCK.…”

Section: Discussionmentioning

confidence: 99%

“…25 Local intrathecal infusion of SDF-1 in spinal cord injury resulted in enhanced sprouting of CST axons into both white matter and gray matter. 25 Moreover, there was evidence suggesting that SDF-1 has the ability to inhibit the function of RhoA and its downstream effector, ROCK. 26 All these results indicate that SDF-1 may be involved in the enhanced CST sprouting induced by CIMT by counteracting the hostile microenvironment for axonal growth.…”

Section: Discussionmentioning

confidence: 99%

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Constraint-Induced Movement Therapy Overcomes the Intrinsic Axonal Growth–Inhibitory Signals in Stroke Rats

Zhao

Xiao

et al. 2013

Stroke

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Forty-two male Wistar rats (200-250 g) were randomly assigned as sham-operated rats (SHAM; n=12), rats subjected to cerebral ischemia (ISC; n=15), and rats with cerebral ischemia that were later treated with CIMT (ISC+CIMT; n=15). All rats were housed under controlled temperature in a 12-hour light/dark cycle with easy access to food and water and assigned to groups with a minimum of 4 animals per enclosure. Protocols and procedures were approved by the Institutional Animal Care and Use Committee of China Medical University (permit No. SCXK [Liao] 2008-0005).Background and Purpose-Constraint-induced movement therapy (CIMT) improves functional outcome in patients with stroke possibly through structural plasticity. We hypothesized that CIMT could enhance axonal growth by overcoming the intrinsic growth-inhibitory signals, leading eventually to improved behavioral performance in stroke rats. Methods-Focal cerebral ischemia was induced by intracerebral injection of endothelin-1. Adult Wistar rats were divided into a sham-operated group, an ischemic group, and an ischemic group treated with CIMT. CIMT started at postoperative day 7 and continued for 3 weeks. Biotinylated dextran amine was injected into the contralateral sensorimotor cortex at postoperative day 14 to trace crossing axons at the cervical spinal cord. The expressions of Nogo-A, Nogo receptor, RhoA, and Rho-associated kinase in the peri-infarct cortex, and the expressions of biotinylated dextran amine, growth associated protein-43, synaptophysin, vGlut1, and postsynaptic density-95 in the denervated spinal cord were measured by immunohistochemistry and Western blots. Behavioral recovery was analyzed at postoperative days 29 to 32. Results-Infarct volumes were not different between groups after stroke. CIMT significantly increased the length and the number of midline crossings of contralateral corticospinal axons to the denervated cervical spinal cord. CIMT significantly decreased the expressions of Nogo-A/Nogo receptor and RhoA/Rho-associated kinase in the peri-infarct cortex, and increased the expressions of growth associated protein-43, synaptophysin, vGlut1, and postsynaptic density-95 in the denervated cervical spinal cord. Behavioral performances assessed by the beam-walking test and the water maze test were improved significantly by CIMT. Conclusions-CIMT promoted poststroke synaptic plasticity and axonal growth at least partially by overcoming the intrinsic growth-inhibitory signaling, leading to improved behavioral outcome. (Stroke. 2013;44:1698-1705.)

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Constraint-Induced Movement Therapy Overcomes the Intrinsic Axonal Growth–Inhibitory Signals in Stroke Rats

Zhao

Xiao

et al. 2013

Stroke

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“…Moreover, we identified several matrix-and membrane-associated proteins, e.g. decorin (46), fibulin-1 (47), netrin-4 (48), neuronal growth regulator 1 (49), neuroplastin (50 -51), noelin-2 (52), SPARC (53), tenascin (54), and the cytokines colony-stimulating factor 1 (CSF-1) (55), macrophage migration inhibitory factor (MIF) (56) as well as the chemokine stromal cell-derived factor 1 (SDF-1) (15). In addition, the serine protease inhibitors glia-derived nexin (serpinE2) (57), neuroserpin (58), and plasminogen activator inhibitor 1 (serpinE1) (59) as well as the extracellular chaperone clusterin (60 -61) were secreted by USSC.…”

Section: Characterization Of Ussc Secretome By Mass Spectrometry-mentioning

confidence: 99%

Characterization of Regenerative Phenotype of Unrestricted Somatic Stem Cells (USSC) from Human Umbilical Cord Blood (hUCB) by Functional Secretome Analysis

Schira¹,

Falkenberg

Hendricks

et al. 2015

Molecular & Cellular Proteomics

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Stem cell transplantation is a promising therapeutic strategy to enhance axonal regeneration after spinal cord injury. Unrestricted somatic stem cells (USSC) isolated from human umbilical cord blood is an attractive stem cell population available at GMP grade without any ethical concerns. It has been shown that USSC transplantation into acute injured rat spinal cords leads to axonal regrowth and significant locomotor recovery, yet lacking cell replacement. Instead, USSC secrete trophic factors enhancing neurite growth of primary cortical neurons in vitro. Here, we applied a functional secretome approach characterizing proteins secreted by USSC for the first time and validated candidate neurite growth promoting factors using primary cortical neurons in vitro. By mass spectrometric analysis and exhaustive bioinformatic interrogation we identified 1156 proteins representing the secretome of USSC. Using Gene Ontology we revealed that USSC secretome contains proteins involved in a number of relevant biological processes of nerve regeneration such as cell adhesion, cell motion, blood vessel formation, cytoskeleton organization and extracellular matrix organization. We found for instance that 31 well-known neurite growth promoting factors like, e.g. Injury to the spinal cord leads to a multiple damaging process including axonal contusion and transection with subsequent degeneration, massive apoptosis of oligodendrocytes and break-down of the blood-spinal cord barrier accompanied by invasion of immune cells resulting in sustained motoric and sensory impairments. Glial-fibrotic scarring and the lack of growth promoting factors impair axonal regrowth, which is currently the main target for therapeutic interventions to treat spinal cord injury. In addition, modulation of neuronal survival, remyelination of axons, and the immune reaction could promote functional regeneration (1-3). The inhibition of axonal regeneration might be overcome by exogenous application of growth factors or by transplantation of stem cells directly into the lesion site, which locally release trophic factors and thus support axonal regrowth. For clinical applications, stem cells should be ideally available on a clinical scale without ethical concerns or invasive interventions. Human umbilical cord blood (hUCB) 1 is

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“…These homeostatic functions take on added significance within the context of neuroinflammatory disease, as the CXCL12/CXCR4 signaling axis aids recovery by promoting survival of mature neurons, recruitment of neural and glial progenitor cells (6)(7)(8), and neuronal-glial communication (9).…”

Section: Introductionmentioning

confidence: 99%

Neuronal ferritin heavy chain and drug abuse affect HIV-associated cognitive dysfunction

Pitcher¹,

Abt²,

Myers³

et al. 2014

J. Clin. Invest.

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Interaction of the chemokine CXCL12 with its receptor CXCR4 promotes neuronal function and survival during embryonic development and throughout adulthood. Previous studies indicated that μ-opioid agonists specifically elevate neuronal levels of the protein ferritin heavy chain (FHC), which negatively regulates CXCR4 signaling and affects the neuroprotective function of the CXCL12/CXCR4 axis. Here, we determined that CXCL12/CXCR4 activity increased dendritic spine density, and also examined FHC expression and CXCR4 status in opiate abusers and patients with HIV-associated neurocognitive disorders (HAND), which is typically exacerbated by illicit drug use. Drug abusers and HIV patients with HAND had increased levels of FHC, which correlated with reduced CXCR4 activation, within cortical neurons. We confirmed these findings in a nonhuman primate model of SIV infection with morphine administration. Transfection of a CXCR4-expressing human cell line with an iron-deficient FHC mutant confirmed that increased FHC expression deregulated CXCR4 signaling and that this function of FHC was independent of iron binding. Furthermore, examination of morphine-treated rodents and isolated neurons expressing FHC shRNA revealed that FHC contributed to morphine-induced dendritic spine loss. Together, these data implicate FHC-dependent deregulation of CXCL12/CXCR4 as a contributing factor to cognitive dysfunction in neuroAIDS.

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SDF-1 stimulates neurite growth on inhibitory CNS myelin

Cited by 67 publications

References 43 publications

Constraint-Induced Movement Therapy Overcomes the Intrinsic Axonal Growth–Inhibitory Signals in Stroke Rats

Constraint-Induced Movement Therapy Overcomes the Intrinsic Axonal Growth–Inhibitory Signals in Stroke Rats

Characterization of Regenerative Phenotype of Unrestricted Somatic Stem Cells (USSC) from Human Umbilical Cord Blood (hUCB) by Functional Secretome Analysis

Neuronal ferritin heavy chain and drug abuse affect HIV-associated cognitive dysfunction

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