Microglial TREM2 Mitigates Inflammatory Responses and Neuronal Apoptosis in Angiotensin II-Induced Hypertension in Middle-Aged Mice

Xu, Xiequn; Du, Lin; Jiang, Jianxiong; Yang, Meifeng; Wang, Zhaoxia; Wang, Yingge; Tang, Tieyu; Fu, Xuetao; Hao, Jiukuan

doi:10.3389/fnagi.2021.716917

Cited by 16 publications

(10 citation statements)

References 69 publications

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“… 53 , 54 Recently, TREM2 was reported to be significantly upregulated in microglia in a hypertension model induced by Ang II infusion, and the overexpression of microglial TREM2 mitigated the microglial inflammatory response, suggesting its possible beneficial effects on BP regulation. 55 …”

Section: The Potential Role Of Microglia In Cardiovascular Diseasesmentioning

confidence: 99%

“…Controversy remains regarding whether TREM2 participates in the regulation of BP. [ 55 ] Male C57BL/6 mice (25±5 g) Electric foot shock with noises induced a stressed condition RAGE knockout via Cre-CX3CR1/RAGE fl/fl mice 1. Stress exposure increased the cytoplasmic translocation of HMGB1 in microglia.…”

Section: The Potential Role Of Microglia In Cardiovascular Diseasesmentioning

confidence: 99%

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Microglia-Mediated Neuroinflammation: A Potential Target for the Treatment of Cardiovascular Diseases

Wang¹,

Pan²,

Xu³

et al. 2022

JIR

156

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Microglia are tissue-resident macrophages of the central nervous system (CNS). In the CNS, microglia play an important role in the monitoring and intervention of synaptic and neuron-level activities. Interventions targeting microglia have been shown to improve the prognosis of various neurological diseases. Recently, studies have observed the activation of microglia in different cardiovascular diseases. In addition, different approaches that regulate the activity of microglia have been shown to modulate the incidence and progression of cardiovascular diseases. The change in autonomic nervous system activity after neuroinflammation may be a potential intermediate link between microglia and cardiovascular diseases. Here, in this review, we will discuss recent updates on the regulatory role of microglia in hypertension, myocardial infarction and ischemia/reperfusion injury. We propose that microglia serve as neuroimmune modulators and potential targets for cardiovascular diseases.

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Section: The Potential Role Of Microglia In Cardiovascular Diseasesmentioning

confidence: 99%

Section: The Potential Role Of Microglia In Cardiovascular Diseasesmentioning

confidence: 99%

Microglia-Mediated Neuroinflammation: A Potential Target for the Treatment of Cardiovascular Diseases

Wang¹,

Pan²,

Xu³

et al. 2022

JIR

156

View full text Add to dashboard Cite

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“…The mouse primary microglial cultures were prepared as we previously described [ 39 , 40 ]. Briefly, cortical tissues were isolated from newborn C57BL/6 mouse pups (P1) and were dissected in ice-cold Hank’s balanced salt solution (HBSS, Corning).…”

Section: Methodsmentioning

confidence: 99%

Ablation of Siglec-E augments brain inflammation and ischemic injury

Chen

Sluter

et al. 2022

J Neuroinflammation

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Sialic acid immunoglobulin-like lectin E (Siglec-E) is a subtype of pattern recognition receptors found on the surface of myeloid cells and functions as a key immunosuppressive checkpoint molecule. The engagement between Siglec-E and the ligand α2,8-linked disialyl glycans activates the immunoreceptor tyrosine-based inhibitory motif (ITIM) in its intracellular domain, mitigating the potential risk of autoimmunity amid innate immune attacks on parasites, bacteria, and carcinoma. Recent studies suggest that Siglec-E is also expressed in the CNS, particularly microglia, the brain-resident immune cells. However, the functions of Siglec-E in brain inflammation and injuries under many neurological conditions largely remain elusive. In this study, we first revealed an anti-inflammatory role for Siglec-E in lipopolysaccharide (LPS)-triggered microglial activation. We then found that Siglec-E was induced within the brain by systemic treatment with LPS in mice in a dose-dependent manner, while its ablation exacerbated hippocampal reactive microgliosis in LPS-treated animals. The genetic deficiency of Siglec-E also aggravated oxygen–glucose deprivation (OGD)-induced neuronal death in mouse primary cortical cultures containing both neurons and glial cells. Moreover, Siglec-E expression in ipsilateral brain tissues was substantially induced following middle cerebral artery occlusion (MCAO). Lastly, the neurological deficits and brain infarcts were augmented in Siglec-E knockout mice after moderate MCAO when compared to wild-type animals. Collectively, our findings suggest that the endogenous inducible Siglec-E plays crucial anti-inflammatory and neuroprotective roles following ischemic stroke, and thus might underlie an intrinsic mechanism of resolution of inflammation and self-repair in the brain.

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“…Models of hypertension increased the number of activated microglia in the cortex and hippocampus of mice, upregulated triggering receptor expressed on myeloid cells 2 (TREM2) produced by microglia, and increased amyloid-beta deposition [ 102 ]. In mice with transverse aortic constriction, it was demonstrated that hypertension per se triggered neuroinflammation before amyloid-beta deposition occurred [ 103 ].…”

Section: Neuroinflammatory Sequelae Of Cardiac Disordersmentioning

confidence: 99%

Chronic Neuroinflammation and Cognitive Decline in Patients with Cardiac Disease: Evidence, Relevance, and Therapeutic Implications

Traub

Frey

Störk

2023

Life

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Acute and chronic cardiac disorders predispose to alterations in cognitive performance, ranging from mild cognitive impairment to overt dementia. Although this association is well-established, the factors inducing and accelerating cognitive decline beyond ageing and the intricate causal pathways and multilateral interdependencies involved remain poorly understood. Dysregulated and persistent inflammatory processes have been implicated as potentially causal mediators of the adverse consequences on brain function in patients with cardiac disease. Recent advances in positron emission tomography disclosed an enhanced level of neuroinflammation of cortical and subcortical brain regions as an important correlate of altered cognition in these patients. In preclinical and clinical investigations, the thereby involved domains and cell types of the brain are gradually better characterized. Microglia, resident myeloid cells of the central nervous system, appear to be of particular importance, as they are extremely sensitive to even subtle pathological alterations affecting their complex interplay with neighboring astrocytes, oligodendrocytes, infiltrating myeloid cells, and lymphocytes. Here, we review the current evidence linking cognitive impairment and chronic neuroinflammation in patients with various selected cardiac disorders including the aspect of chronic neuroinflammation as a potentially druggable target.

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Microglial TREM2 Mitigates Inflammatory Responses and Neuronal Apoptosis in Angiotensin II-Induced Hypertension in Middle-Aged Mice

Cited by 16 publications

References 69 publications

Microglia-Mediated Neuroinflammation: A Potential Target for the Treatment of Cardiovascular Diseases

Microglia-Mediated Neuroinflammation: A Potential Target for the Treatment of Cardiovascular Diseases

Ablation of Siglec-E augments brain inflammation and ischemic injury

Chronic Neuroinflammation and Cognitive Decline in Patients with Cardiac Disease: Evidence, Relevance, and Therapeutic Implications

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