Astroglial Connexins in Neurological and Neuropsychological Disorders and Radiation Exposure

Liu, Yuan Duo; Tang, Ge; Qian, Feng; Huang, Jiang Rong; Tang, Feng Ru

doi:10.2174/0929867327666200610175037

Cited by 4 publications

(4 citation statements)

References 187 publications

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“…The balance between pro- and anti-inflammatory factors sustains physiological interactions between microglia and astrocytes, resulting in homeostatic restoration at the NVU level [ 89 , 90 ].…”

Section: Connexins Signatures Of Nvu Componentsmentioning

confidence: 99%

Connexins Signatures of the Neurovascular Unit and Their Physio-Pathological Functions

Vicario

Parenti

2022

IJMS

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Central nervous system (CNS) homeostasis is closely linked to the delicate balance of the microenvironment in which different cellular components of the neurovascular unit (NVU) coexist. Intercellular communication plays a pivotal role in exchanges of signaling molecules and mediators essential for survival functions, as well as in the removal of disturbing elements that can lead to related pathologies. The specific signatures of connexins (Cxs), proteins which form either gap junctions (GJs) or hemichannels (HCs), represent the biological substrate of the pathophysiological balance. Connexin 43 (Cx43) is undoubtedly one of the most important factors in glia–neuro–vascular crosstalk. Herein, Cxs signatures of every NVU component are highlighted and their critical influence on functional processes in healthy and pathological conditions of nervous microenvironment is reviewed.

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Section: Connexins Signatures Of Nvu Componentsmentioning

confidence: 99%

Connexins Signatures of the Neurovascular Unit and Their Physio-Pathological Functions

Vicario

Parenti

2022

IJMS

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“…Impaired attention, slow processing speed, and hypersomnia are known complications of childhood brain tumor and its treatment, particularly radiotherapy 2,4,15,16 . There are multiple ways by which RT influences cognitive function, including gray and white matter volume loss, 2,5,17 and disruption of astroglial connexins 18 . Stimulants are effective in improving attention and processing speed in children with brain tumors, 6 but because of higher disposition to dysautonomia and cardiovascular morbidity, 12,13 it is possible that brain tumor survivors may react differently to stimulant medications.…”

Section: Discussionmentioning

confidence: 99%

Height, weight, and cardiovascular effects of stimulants on children with brain tumors

Khan

Bano

Wang

et al. 2020

Pediatric Blood & Cancer

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Introduction: Children with brain tumors may develop inattention, slow processing, and hypersomnia. Stimulant medications improve these problems, but their effect on growth, heart rate, and blood pressure (BP) are inadequately explored. Procedure: We retrospectively studied children with brain tumors treated at our institution that had data available for 1 year pre and 2 years on stimulant treatment. Tumor location, gender, radiation treatment (RT), age at RT, drug type, and hormone therapy were variables of interest. Results: We identified 65 children (35 males) that fulfilled eligibility criteria. Focal RT was utilized in 58; 11 additionally had whole brain RT; and seven received no RT. Thirty were treated for hypersomnia and inattention, eight for hypersomnia alone, and rest for inattention. Modafinil was the first drug in 18 (27.7%), and methylphenidate in the others. Forty-seven (72.3%), 45 (69.2%), and 49 (75.4%) were on thyroxine, cortisone, and growth hormones, respectively. There was no difference in pre-and post-stimulant body mass index (BMI), heart rate, and BP. There was also no difference between modafinil and methylphenidate groups. Rate of height acquisition slowed on stimulants (P = .0096). Thyroxine treatment correlated with increase in BMI after stimulants (P = .04). Younger age (P = .0003) and higher prestimulant BMI (P = .0063) correlated with increased heart rate on stimulants, while higher age at RT (P =.016) correlated with elevated systolic BP on stimulants. No associations were found with height acquisition and diastolic BP. Conclusion: Stimulants are well tolerated by children with brain tumors that are appropriately managed for endocrine deficiencies, but may reduce the trajectory of height attainment. K E Y W O R D S blood pressure, brain tumors, childhood, heart rate, stimulants, weight 1 INTRODUCTION A significant number of childhood brain tumor survivors develop neurocognitive impairment, particularly attention span, processing speed, Abbreviations: BMI, body mass index; BP, blood pressure; RT, radiation treatment and working memory. 1,2 Cognitive deficits may result from effect of radiation and chemotherapy on the brain, or due to the direct tumor effect. 3 Latter may represent involvement of eloquent areas of brain by the tumor or disruption of brain connectivity. Younger age and radiation treatment (RT) are the most important risk factors for cognitive impairment in childhood brain tumor survivors, and may be related to loss of gray and white matter volume. 1,2,4,5

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“…Microglia, neurons, astrocytes and pericytes exhibit the capacity to release inflammatory cytokines and chemokines in response to radiation‐induced brain injury (Figure 1). 30,31 These cellular interactions contribute to the amplification of neuroinflammation 23 . During the neuroinflammatory process, neurons communicate with microglia by secreting high mobility group box‐1 (HMGB1), which binds to Toll‐like receptor 4 (TLR4) on the membrane, indirectly activating microglia 32 .…”

Section: Microglial Activation After Radiationmentioning

confidence: 99%

Microglia in radiation‐induced brain injury: Cellular and molecular mechanisms and therapeutic potential

Wang,

Tian,

Liu

et al. 2024

CNS Neurosci Ther

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BackgroundRadiation‐induced brain injury is a neurological condition resulting from radiotherapy for malignant tumors, with its underlying pathogenesis still not fully understood. Current hypotheses suggest that immune cells, particularly the excessive activation of microglia in the central nervous system and the migration of peripheral immune cells into the brain, play a critical role in initiating and progressing the injury. This review aimed to summarize the latest advances in the cellular and molecular mechanisms and the therapeutic potential of microglia in radiation‐induced brain injury.MethodsThis article critically examines recent developments in understanding the role of microglia activation in radiation‐induced brain injury. It elucidates associated mechanisms and explores novel research pathways and therapeutic options for managing this condition.ResultsPost‐irradiation, activated microglia release numerous inflammatory factors, exacerbating neuroinflammation and facilitating the onset and progression of radiation‐induced damage. Therefore, controlling microglial activation and suppressing the secretion of related inflammatory factors is crucial for preventing radiation‐induced brain injury. While microglial activation is a primary factor in neuroinflammation, the precise mechanisms by which radiation prompts this activation remain elusive. Multiple signaling pathways likely contribute to microglial activation and the progression of radiation‐induced brain injury.ConclusionsThe intricate microenvironment and molecular mechanisms associated with radiation‐induced brain injury underscore the crucial roles of immune cells in its onset and progression. By investigating the interplay among microglia, neurons, astrocytes, and peripheral immune cells, potential strategies emerge to mitigate microglial activation, reduce the release of inflammatory agents, and impede the entry of peripheral immune cells into the brain.

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Astroglial Connexins in Neurological and Neuropsychological Disorders and Radiation Exposure

Cited by 4 publications

References 187 publications

Connexins Signatures of the Neurovascular Unit and Their Physio-Pathological Functions

Connexins Signatures of the Neurovascular Unit and Their Physio-Pathological Functions

Height, weight, and cardiovascular effects of stimulants on children with brain tumors

Microglia in radiation‐induced brain injury: Cellular and molecular mechanisms and therapeutic potential

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