Noggin improves ischemic brain tissue repair and promotes alternative activation of microglia in mice

Shin, Jeong-Ah; Lim, Soo Mee; Jeong, Sae Im; Kang, Jihee Lee; Park, Eun Mi

doi:10.1016/j.bbi.2014.03.013

Cited by 59 publications

(42 citation statements)

References 49 publications

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“…Furthermore, minocycline and some other experimental treatments potentiate microglia/macrophage M2 polarization while promoting angiogenesis or BBB remodeling after stroke. 301–303 These studies suggest that the polarization state of microglia/macrophage might be a key regulator of angiogenesis and BBB repair after stroke.…”

Section: Part II Neurovascular Injury and Repair After Ischemic Strokementioning

confidence: 98%

Cerebral Vascular Disease and Neurovascular Injury in Ischemic Stroke

Silva

Chen

et al. 2017

Circulation Research

314

237

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The consequences of cerebrovascular disease are among the leading health issues worldwide. Large and small cerebral vessel disease can trigger stroke and contribute to the vascular component of other forms of neurological dysfunction and degeneration. Both forms of vascular disease are driven by diverse risk factors, with hypertension as the leading contributor. Despite the importance of neurovascular disease and subsequent injury following ischemic events, fundamental knowledge in these areas lag behind our current understanding of neuroprotection and vascular biology in general. The goal of this review is to address select key structural and functional changes in the vasculature that promote hypoperfusion and ischemia, while also affecting the extent of injury and effectiveness of therapy. In addition, as damage to the blood-brain barrier (BBB) is one of the major consequences of ischemia, we discuss cellular and molecular mechanisms underlying ischemia-induced changes in BBB integrity and function, including alterations in endothelial cells and the contribution of pericytes, immune cells, and matrix metalloproteinases. Identification of cell types, pathways, and molecules that control vascular changes before and after ischemia may result in novel approaches to slow the progression of cerebrovascular disease and lessen both the frequency and impact of ischemic events.

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Section: Part II Neurovascular Injury and Repair After Ischemic Strokementioning

confidence: 98%

Cerebral Vascular Disease and Neurovascular Injury in Ischemic Stroke

Silva

Chen

et al. 2017

Circulation Research

314

237

View full text Add to dashboard Cite

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“…The role of the microglia in pathological NVU activity has been proposed to induce damage to the endothelium and the basal lamina via receptors for nucleotides, such as ATP, and opening new routes of communication between ECs, pericytes, astrocytes and microglia is important for BBB repair (Deitmer et al, 2001; Andersson et al, 2005). However, recent studies have demonstrated that enhancing the activation of microglia promotes tissue repair and remodeling after stroke by decreasing the levels of the inflammatory markers IL-1β and TNF-α and increasing IL-1ra, IL-10, and arginase 1 expression (Gelosa et al, 2014; Shin et al, 2014). …”

Section: Bbb Dysfunction In Cerebral Ischemiamentioning

confidence: 99%

Protection after stroke: cellular effectors of neurovascular unit integrity

Posada‐Duque

Barreto

Cardona‐Gómez

2014

Front. Cell. Neurosci.

106

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Neurological disorders are prevalent worldwide. Cerebrovascular diseases (CVDs), which account for 55% of all neurological diseases, are the leading cause of permanent disability, cognitive and motor disorders and dementia. Stroke affects the function and structure of blood-brain barrier, the loss of cerebral blood flow regulation, oxidative stress, inflammation and the loss of neural connections. Currently, no gold standard treatments are available outside the acute therapeutic window to improve outcome in stroke patients. Some promising candidate targets have been identified for the improvement of long-term recovery after stroke, such as Rho GTPases, cell adhesion proteins, kinases, and phosphatases. Previous studies by our lab indicated that Rho GTPases (Rac and RhoA) are involved in both tissue damage and survival, as these proteins are essential for the morphology and movement of neurons, astrocytes and endothelial cells, thus playing a critical role in the balance between cell survival and death. Treatment with a pharmacological inhibitor of RhoA/ROCK blocks the activation of the neurodegeneration cascade. In addition, Rac and synaptic adhesion proteins (p120 catenin and N-catenin) play critical roles in protection against cerebral infarction and in recovery by supporting the neurovascular unit and cytoskeletal remodeling activity to maintain the integrity of the brain parenchyma. Interestingly, neuroprotective agents, such as atorvastatin, and CDK5 silencing after cerebral ischemia and in a glutamate-induced excitotoxicity model may act on the same cellular effectors to recover neurovascular unit integrity. Therefore, future efforts must focus on individually targeting the structural and functional roles of each effector of neurovascular unit and the interactions in neural and non-neural cells in the post-ischemic brain and address how to promote the recovery or prevent the loss of homeostasis in the short, medium and long term.

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“…This release is critical for morphogenesis, eye development and skeletal muscle differentiation [1, 8]. Overexpression of Noggin has been shown to act as a neuroprotectant in rodent models of stroke[35–37]. Astrocytes, Muller cells and microglia exhibit a gliotic reaction in response to BMPs, and Noggin circumvents gliosis [36–40].…”

Section: Discussionmentioning

confidence: 99%

Role of Myo/Nog Cells in Neuroprotection: Evidence from the Light Damaged Retina

et al. 2017

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PurposeTo identify Myo/Nog cells in the adult retina and test their role in protecting retinal photoreceptors from light damage.MethodsLight damage was induced by exposing albino rats raised in dim cyclic light to 1000 lux light for 24 hours. In one group of rats, Myo/Nog cells were purified from rat brain tissue by magnetic cell sorting following binding of the G8 monoclonal antibody (mAb). These cells were injected into the vitreous humour of the eye within 2 hours following bright light exposure. Retinal function was assessed using full-field, flash electroretinogram (ERG) before and after treatment. The numbers of Myo/Nog cells, apoptotic photoreceptors, and the expression of glial fibrillary acidic protein (GFAP) in Muller cells were assessed by immunohistochemistry.ResultsMyo/Nog cells were present in the undamaged retina in low numbers. Light induced damage increased their numbers, particularly in the choroid, ganglion cell layer and outer plexiform layer. Intravitreal injection of G8-positive (G8+) cells harvested from brain mitigated all the effects of light damage examined, i.e. loss of retinal function (ERG), death of photoreceptors and the stress-induced expression of GFAP in Muller cells. Some of the transplanted G8+ cells were integrated into the retina from the vitreous.ConclusionsMyo/Nog cells are a subpopulation of cells that are present in the adult retina. They increase in number in response to light induced stress. Intravitreal injection of Myo/Nog cells was protective to the retina, in part, by reducing retinal stress as measured by the Muller cell response. These results suggest that Myo/Nog cells, or the factors they produce, are neuroprotective and may be therapeutic in neurodegenerative retinal diseases.

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Noggin improves ischemic brain tissue repair and promotes alternative activation of microglia in mice

Cited by 59 publications

References 49 publications

Cerebral Vascular Disease and Neurovascular Injury in Ischemic Stroke

Cerebral Vascular Disease and Neurovascular Injury in Ischemic Stroke

Protection after stroke: cellular effectors of neurovascular unit integrity

Role of Myo/Nog Cells in Neuroprotection: Evidence from the Light Damaged Retina

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