TGFβ1 alleviates axonal injury by regulating microglia/macrophages alternative activation in traumatic brain injury

Zhao, Junjie; Wang, Bo; Wu, Xiang; Yang, Zhongbo; Huang, Tingqin; Guo, Xiaoye; Guo, Dan; Liu, Zunwei; Song, Jin‐Ning

doi:10.1016/j.brainresbull.2020.04.011

Cited by 9 publications

(8 citation statements)

References 49 publications

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“…On the contrary, multiple studies in preclinical models reported a reduced expression of TGF-β pathway components. The expression of Tgfb1 and Tgfbr1 is reduced in the rat brain after cortical contusion [114]. Similar results were obtained by employing NanoString gene expression analysis, where genes in the TGF-β signaling pathway (Tgfb1, Tgfbr1, Tgfbr2, Smad3, and Ski) were shown to be significantly downregulated in mouse microglia after cortical impact injury [115].…”

Section: Traumatic Brain Injurysupporting

confidence: 69%

“…For instance, increased levels of TGF-β are found in the brain following traumatic injuries in patients and in animal models [110]. TGF-β1, -β2, and -β3 [111], Tgfbr1 and Tgfbr2 [112], and Smads and p-Smads [113,114] are upregulated after injury and usually in astrocytes, oligodendrocytes, microglia, and neurons in a variety of TBI models. We observed that stab lesions resulted in the consistent induction of TGF-β1 and PAI-1 mRNA, as well as rapid activation of TGF-β signaling in SBE-luc mice [23].…”

Section: Traumatic Brain Injurymentioning

confidence: 99%

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TGF-β as a Key Modulator of Astrocyte Reactivity: Disease Relevance and Therapeutic Implications

Luo

2022

Biomedicines

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Astrocytes are essential for normal brain development and functioning. They respond to brain injury and disease through a process referred to as reactive astrogliosis, where the reactivity is highly heterogenous and context-dependent. Reactive astrocytes are active contributors to brain pathology and can exert beneficial, detrimental, or mixed effects following brain insults. Transforming growth factor-β (TGF-β) has been identified as one of the key factors regulating astrocyte reactivity. The genetic and pharmacological manipulation of the TGF-β signaling pathway in animal models of central nervous system (CNS) injury and disease alters pathological and functional outcomes. This review aims to provide recent understanding regarding astrocyte reactivity and TGF-β signaling in brain injury, aging, and neurodegeneration. Further, it explores how TGF-β signaling modulates astrocyte reactivity and function in the context of CNS disease and injury.

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Section: Traumatic Brain Injurysupporting

confidence: 69%

Section: Traumatic Brain Injurymentioning

confidence: 99%

TGF-β as a Key Modulator of Astrocyte Reactivity: Disease Relevance and Therapeutic Implications

Luo

2022

Biomedicines

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“…However, the M2-like responses become dissipated over time, resulting in development of pathological M1-like phenotypes, which may eventually elicit secondary expansion of injury after trauma (Wang et al, 2013;Kumar et al, 2016a). Thus, inhibiting M1 phenotype while inducing M2 phenotype activation of microglia/macrophages by regulating key molecules such as NADPH oxidase 2 (NOX2) (Wang et al, 2017), histone deacetylases (HDACs) (Wang et al, 2015), high-mobility group box 1 (HMGB1) (Gao et al, 2018) and transforming growth factor-β1 (TGF-β1) (Zhao et al, 2020) can modify inflammatory responses, reduce neuronal damage, alleviate white matter injury and facilitate neurological functional recovery after TBI. Multiple types of drugs targeting microglia have been applied in experimental models of TBI to alleviate neuronal damage.…”

Section: Microglial Activities In Experimental Traumatic Brain Injurymentioning

confidence: 99%

Microglia and Neuroinflammation: Crucial Pathological Mechanisms in Traumatic Brain Injury-Induced Neurodegeneration

Shao

Wang

et al. 2022

Front. Aging Neurosci.

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Traumatic brain injury (TBI) is one of the most common diseases in the central nervous system (CNS) with high mortality and morbidity. Patients with TBI usually suffer many sequelae in the life time post injury, including neurodegenerative disorders such as Alzheimer’s disease (AD) and Parkinson’s disease (PD). However, the pathological mechanisms connecting these two processes have not yet been fully elucidated. It is important to further investigate the pathophysiological mechanisms underlying TBI and TBI-induced neurodegeneration, which will promote the development of precise treatment target for these notorious neurodegenerative consequences after TBI. A growing body of evidence shows that neuroinflammation is a pivotal pathological process underlying chronic neurodegeneration following TBI. Microglia, as the immune cells in the CNS, play crucial roles in neuroinflammation and many other CNS diseases. Of interest, microglial activation and functional alteration has been proposed as key mediators in the evolution of chronic neurodegenerative pathology following TBI. Here, we review the updated studies involving phenotypical and functional alterations of microglia in neurodegeneration after injury, survey key molecules regulating the activities and functional responses of microglia in TBI pathology, and explore their potential implications to chronic neurodegeneration after injury. The work will give us a comprehensive understanding of mechanisms driving TBI-related neurodegeneration and offer novel ideas of developing corresponding prevention and treatment strategies for this disease.

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“…These results suggest that TGF-β as an inflammatory factor enhances the inflammatory response during the progression of dementia. However, TGF-β secreted by astrocytes showed protective effects against brain injury caused by ischemia ( Zhao et al, 2020 ). TGF-β exerted anti-inflammatory effects by inhibiting the proliferation and activation of microglia and astrocytes.…”

Section: The Role Of Oxidative Stress and Inflammation In Dementiamentioning

confidence: 99%

Traditional Chinese medicine promotes the control and treatment of dementia

Tao

Wang

et al. 2022

Front. Pharmacol.

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Dementia is a syndrome that impairs learning and memory. To date, there is no effective therapy for dementia. Current prescription drugs, such as cholinesterase inhibitors, fail to improve the condition of dementia and are often accompanied by severe adverse effects. In recent years, the number of studies into the use of traditional Chinese medicine (TCM) for dementia treatment has increased, revealing a formula that could significantly improve memory and cognitive dysfunctions in animal models. TCM showed fewer adverse effects, lower costs, and improved suitability for long-term use compared with currently prescribed drugs. Due to the complexity of ingredients and variations in bioactivity of herbal medicines, the multi-target nature of the traditional Chinese formula affected the outcome of dementia therapy. Innovations in TCM will create a platform for the development of new drugs for the prevention and treatment of dementia, further strengthening and enhancing the current influence of TCM.

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TGFβ1 alleviates axonal injury by regulating microglia/macrophages alternative activation in traumatic brain injury

Cited by 9 publications

References 49 publications

TGF-β as a Key Modulator of Astrocyte Reactivity: Disease Relevance and Therapeutic Implications

TGF-β as a Key Modulator of Astrocyte Reactivity: Disease Relevance and Therapeutic Implications

Microglia and Neuroinflammation: Crucial Pathological Mechanisms in Traumatic Brain Injury-Induced Neurodegeneration

Traditional Chinese medicine promotes the control and treatment of dementia

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