Matrix Metalloproteinase 2 (MMP2) and MMP9 Secreted by Erythropoietin-Activated Endothelial Cells Promote Neural Progenitor Cell Migration

Wang, Lei; Zhang, Zheng Gang; Zhang, Rui Lan; Gregg, Sara R; Hozeska-Solgot, Ann; LeTourneau, Yvonne; Wang, Ying; Chopp, Michael

doi:10.1523/jneurosci.5380-05.2006

Cited by 284 publications

(235 citation statements)

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“…We have shown before that MMP‐9 and MCP‐1 are reduced in ischemic stroke with post‐stroke BML‐111 administration (Hawkins et al., 2014). These factors are important in neural stem cell proliferation and migration during neurogenesis after ischemic stroke (Lee et al., 2006; L. Wang et al., 2006; Widera et al., 2004; Yan et al., 2007). Additionally, MMP‐9 is important in vascular remodeling after stroke and inhibiting MMP‐9 1 week after stroke increases infarct size and worsens outcomes (Zhao et al., 2006).…”

Section: Discussionmentioning

confidence: 99%

Targeting resolution of neuroinflammation after ischemic stroke with a lipoxin A₄ analog: Protective mechanisms and long‐term effects on neurological recovery

et al. 2017

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BackgroundResolution of inflammation is an emerging new strategy to reduce damage following ischemic stroke. Lipoxin A4 (LXA 4) is an anti‐inflammatory, pro‐resolution lipid mediator that reduces neuroinflammation in stroke. Since LXA 4 is rapidly inactivated, potent analogs have been synthesized, including BML‐111. We hypothesized that post‐ischemic, intravenous treatment with BML‐111 for 1 week would provide neuroprotection and reduce neurobehavioral deficits at 4 weeks after ischemic stroke in rats. Additionally, we investigated the potential protective mechanisms of BML‐111 on the post‐stroke molecular and cellular profile.MethodsA total of 133 male Sprague‐Dawley rats were subjected to 90 min of transient middle cerebral artery occlusion (MCAO) and BML‐111 administration was started at the time of reperfusion. Two methods of week‐long BML‐111 intravenous administration were tested: continuous infusion via ALZET ® osmotic pumps (1.25 and 3.75 μg μl−1 hr−1), or freshly prepared daily single injections (0.3, 1, and 3 mg/kg). We report for the first time on the stability of BML‐111 and characterized an optimal dose and a dosing schedule for the administration of BML‐111.ResultsOne week of BML‐111 intravenous injections did not reduce infarct size or improve behavioral deficits 4 weeks after ischemic stroke. However, post‐ischemic treatment with BML‐111 did elicit early protective effects as demonstrated by a significant reduction in infarct volume and improved sensorimotor function at 1 week after stroke. This protection was associated with reduced pro‐inflammatory cytokine and chemokine levels, decreased M1 CD40+ macrophages, and increased alternatively activated, anti‐inflammatory M2 microglia/macrophage cell populations in the post‐ischemic brain.ConclusionThese data suggest that targeting the endogenous LXA 4 pathway could be a promising therapeutic strategy for the treatment of ischemic stroke. More work is necessary to determine whether a different dosing regimen or more stable LXA 4 analogs could confer long‐term protection.

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Section: Discussionmentioning

confidence: 99%

Targeting resolution of neuroinflammation after ischemic stroke with a lipoxin A₄ analog: Protective mechanisms and long‐term effects on neurological recovery

et al. 2017

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“…6,44,47 An enriched environment, however, increased the stroke-induced neurogenesis in the hippocampus, but decreased the cell genesis and migration of neuroblasts into striatum. 28 Recent studies have revealed that MCP-1, 44 erythropoietin, 40 and MMPs 22,43 are involved in the migration of neuroblasts to the site of injury. In addition, erythropoietin has also been shown to be involved in the proliferation of progenitor cells in the subventricular zone.…”

Section: Role Of Neural Stem Cellsmentioning

confidence: 99%

“…The MMPs have been shown to be involved in the migration of new cells derived from neural precursors, 43 and proteolytic processing of ECM proteins by MMPs was shown to regulate the migration of cells, perhaps by clearing the path for them. 19 It should be noted, however, that MMPs are also involved in the proteolytic degradation of IGFBP3, which releases IGF-I from the IGF-I-IGFBP3 complex (Fig.…”

Section: Role Of Neural Stem Cellsmentioning

confidence: 99%

Growth factors, stem cells, and stroke

Kalluri

Dempsey

2008

FOC

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✓ Postischemic neurogenesis has been identified as a compensatory mechanism to repair the damaged brain after stroke. Several factors are released by the ischemic tissue that are responsible for proliferation, differentiation, and migration of neural stem cells. An understanding of their roles may allow future therapies based on treatment with such factors. Although damaged cells release a variety of factors, some of them are stimulatory whereas some are inhibitory for neurogenesis. It is interesting to note that factors like insulin-like growth factor–I can induce proliferation in the presence of fibroblast growth factor–2 (FGF-2), and promote differentiation in the absence of FGF-2. Meanwhile, factors like transforming growth factor–β can induce the differentiation of neurons while inhibiting the proliferation of neural stem cells. Therefore, understanding the role of each factor in the process of neurogenesis will help physicians to enhance the endogenous response and improve the clinical outcome after stroke. In this article the authors discuss the role of growth factors and stem cells following stroke.

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“…67 EPO promotes endothelial cell secretion of MMP 2 and MMP 9, which are chemotactic for neuroblast migration. 79 VEGF and BDNF expression in the ischemic brain are increased in response to EPO, and may provide a vascular niche, a microenvironment supporting migrating neuroblasts. EPO infusion into the adult lateral ventricles increases the number of newly generated cells migrating to the olfactory bulb, and thereby increases new olfactory bulb interneurons.…”

Section: Erythropoietinmentioning

confidence: 99%

Neurorestorative treatment of stroke: Cell and pharmacological approaches

Chen

Chopp

2006

NeuroRX

154

114

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Summary:There is a compelling need to develop cell and pharmacological therapeutic approaches to be administered beyond the hyperacute phase of stroke. These therapies capitalize on the capacity of the brain for neuroregeneration and neuroplasticity and are designed to reduce neurological deficits after stroke. This review provides an update of bone marrowderived mesenchymal stem cells (MSCs) and select pharmacological agents in clinical use for other indications that promote the recovery process in the subacute and chronic phases after stroke. Among these agents are 3-hydroxy-3-methylglutarylcoenzyme A reductase inhibitors (statins), erythropoietin (EPO), and phosphodiesterase type 5 (PDE-5) inhibitors and nitric oxide (NO) donors. Both the MSCs and the pharmacologic agents potentiate brain plasticity and neurobehavioral recovery after stroke.

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Matrix Metalloproteinase 2 (MMP2) and MMP9 Secreted by Erythropoietin-Activated Endothelial Cells Promote Neural Progenitor Cell Migration

Cited by 284 publications

References 50 publications

Targeting resolution of neuroinflammation after ischemic stroke with a lipoxin A₄ analog: Protective mechanisms and long‐term effects on neurological recovery

Targeting resolution of neuroinflammation after ischemic stroke with a lipoxin A₄ analog: Protective mechanisms and long‐term effects on neurological recovery

Growth factors, stem cells, and stroke

Neurorestorative treatment of stroke: Cell and pharmacological approaches

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Matrix Metalloproteinase 2 (MMP2) and MMP9 Secreted by Erythropoietin-Activated Endothelial Cells Promote Neural Progenitor Cell Migration

Cited by 284 publications

References 50 publications

Targeting resolution of neuroinflammation after ischemic stroke with a lipoxin A4 analog: Protective mechanisms and long‐term effects on neurological recovery

Targeting resolution of neuroinflammation after ischemic stroke with a lipoxin A4 analog: Protective mechanisms and long‐term effects on neurological recovery

Growth factors, stem cells, and stroke

Neurorestorative treatment of stroke: Cell and pharmacological approaches

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Targeting resolution of neuroinflammation after ischemic stroke with a lipoxin A₄ analog: Protective mechanisms and long‐term effects on neurological recovery

Targeting resolution of neuroinflammation after ischemic stroke with a lipoxin A₄ analog: Protective mechanisms and long‐term effects on neurological recovery