Transient activation of Wnt/β-catenin signaling reporter in fibrotic scar formation after compression spinal cord injury in adult mice

Yamagami, Takashi; Pleasure, David E; Lam, Kit S.; Zhou, Chengji J.

doi:10.1016/j.bbrc.2018.02.004

Cited by 11 publications

(7 citation statements)

References 43 publications

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“…For example, in a rat spinal cord transection model of SCI, direct signaling between fibrotic cells and astrocytes mediated the glial/fibrotic scar border formation ( Bundesen et al, 2003 ). In an SCI compression injury model, fibrotic scar fibroblasts transiently increased Wnt/β-catenin signaling ( Yamagami et al, 2018 ), and since Wnt signaling is known to drive fibrosis in other organs ( Chilosi et al, 2003 ), and Wnt ligand expression is increased following SCI ( Fernández-Martos et al, 2011 ; González-Fernández et al, 2014 ), induction of fibroblast WNT signaling likely contributes to fibrosis. In the photothrombotic stroke injury model, activation of TGF-β1 and retinoic acid signaling pathways in meningeal fibroblasts stimulated arachnoid barrier cells and facilitated reconstruction of the blood-CSF barrier ( Cha et al, 2014 ).…”

Section: Meningeal Response To Injury and Diseasementioning

confidence: 99%

Living on the Edge of the CNS: Meninges Cell Diversity in Health and Disease

Derk

Jones

Como

et al. 2021

Front. Cell. Neurosci.

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The meninges are the fibrous covering of the central nervous system (CNS) which contain vastly heterogeneous cell types within its three layers (dura, arachnoid, and pia). The dural compartment of the meninges, closest to the skull, is predominantly composed of fibroblasts, but also includes fenestrated blood vasculature, an elaborate lymphatic system, as well as immune cells which are distinct from the CNS. Segregating the outer and inner meningeal compartments is the epithelial-like arachnoid barrier cells, connected by tight and adherens junctions, which regulate the movement of pathogens, molecules, and cells into and out of the cerebral spinal fluid (CSF) and brain parenchyma. Most proximate to the brain is the collagen and basement membrane-rich pia matter that abuts the glial limitans and has recently be shown to have regional heterogeneity within the developing mouse brain. While the meninges were historically seen as a purely structural support for the CNS and protection from trauma, the emerging view of the meninges is as an essential interface between the CNS and the periphery, critical to brain development, required for brain homeostasis, and involved in a variety of diseases. In this review, we will summarize what is known regarding the development, specification, and maturation of the meninges during homeostatic conditions and discuss the rapidly emerging evidence that specific meningeal cell compartments play differential and important roles in the pathophysiology of a myriad of diseases including: multiple sclerosis, dementia, stroke, viral/bacterial meningitis, traumatic brain injury, and cancer. We will conclude with a list of major questions and mechanisms that remain unknown, the study of which represent new, future directions for the field of meninges biology.

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Section: Meningeal Response To Injury and Diseasementioning

confidence: 99%

Living on the Edge of the CNS: Meninges Cell Diversity in Health and Disease

Derk

Jones

Como

et al. 2021

Front. Cell. Neurosci.

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“…The Wnt pathway plays an indispensable role in disease processes in the CNS (Lie et al, 2005;Wang et al, 2011). The activity of Wnt signaling after SCI can be detected by performing Xgal staining in Wnt signaling reporter TOPgal transgenic mice (DasGupta and Fuchs, 1999;Yamagami et al, 2018). The Wnt/βcatenin pathway is transiently activated in FN + fibroblasts in the injured core after SCI (Yamagami et al, 2018).…”

Section: Wntmentioning

confidence: 99%

Fibrotic Scar After Spinal Cord Injury: Crosstalk With Other Cells, Cellular Origin, Function, and Mechanism

et al. 2021

Front. Cell. Neurosci.

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The failure of axonal regeneration after spinal cord injury (SCI) results in permanent loss of sensorimotor function. The persistent presence of scar tissue, mainly fibrotic scar and astrocytic scar, is a critical cause of axonal regeneration failure and is widely accepted as a treatment target for SCI. Astrocytic scar has been widely investigated, while fibrotic scar has received less attention. Here, we review recent advances in fibrotic scar formation and its crosstalk with other main cellular components in the injured core after SCI, as well as its cellular origin, function, and mechanism. This study is expected to provide an important basis and novel insights into fibrotic scar as a treatment target for SCI.

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“…When Wnt binds to this complex, disheveled (Dvl) proteins aggregate and the expression of the degradation complex is inhibited, thus stabilizing β-catenin in cells. The β-catenin is recruited by the cytoplasm and enters the nucleus where it activates the T-cell factor/lymphoid enhancer-binding factor (LEF/TCF) protein ( Yamagami et al, 2018 ). Interactions between β-catenin and LEF/TCF involve transcriptional regulators and histone-modification factors, which, in turn, mediate excessive developmental and homeostasis processes.…”

Section: The Wnt/β-catenin Signaling Pathwaymentioning

confidence: 99%

Regulatory Mechanisms of the Wnt/β-Catenin Pathway in Diabetic Cutaneous Ulcers

et al. 2018

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Skin ulcers are a serious complication of diabetes. Diabetic patients suffer from vascular lesions and complications such as peripheral neuritis, peripheral vascular lesions, and collagen abnormalities, which result in skin wounds that are refractory and often develop into chronic ulcers. The healing of skin ulcers requires an inflammatory reaction, wound proliferation, remodeling regulation, and control of stem cells. Studies investigating diabetic cutaneous ulcers have focused on cellular and molecular levels. Diabetes can cause nerve and blood vessel damage, and persistent high blood sugar levels can cause systemic multisite nerve damage based on peripheral neuropathy. The long-term hyperglycemia state enables the polyol glucose metabolism pathway to be activated, increasing the accumulation of toxic substances in the vascular injured nerve tissue cells. Sustained hyperglycemia leads to dysfunction of epithelial cells, leading to a decrease in pro-angiogenic signaling and nitric oxide production. In addition, due to impaired leukocyte function in hyperglycemia, immune function is impaired and the immune response at relevant sites is insufficient, making diabetic foot more difficult to heal. The Wnt/β-catenin pathway is a highly conserved signal transduction pathway involved in a variety of biological processes, such as cell proliferation, apoptosis, and differentiation. It is considered an important pathway involved in the healing of skin wounds. This article summarizes the mechanism of action of the Wnt/β-catenin pathway involved in the inflammatory responses to diabetic ulcers, wound proliferation, wound remodeling, and stem cells. The interactions between the Wnt signal pathway and other metabolic pathways are also discussed.

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Transient activation of Wnt/β-catenin signaling reporter in fibrotic scar formation after compression spinal cord injury in adult mice

Cited by 11 publications

References 43 publications

Living on the Edge of the CNS: Meninges Cell Diversity in Health and Disease

Living on the Edge of the CNS: Meninges Cell Diversity in Health and Disease

Fibrotic Scar After Spinal Cord Injury: Crosstalk With Other Cells, Cellular Origin, Function, and Mechanism

Regulatory Mechanisms of the Wnt/β-Catenin Pathway in Diabetic Cutaneous Ulcers

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