scholarly journals Ionizing Radiation-Induced Brain Cell Aging and the Potential Underlying Molecular Mechanisms

Cells ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 3570
Author(s):  
Qin-Qi Wang ◽  
Gang Yin ◽  
Jiang-Rong Huang ◽  
Shi-Jun Xi ◽  
Feng Qian ◽  
...  

Population aging is occurring rapidly worldwide, challenging the global economy and healthcare services. Brain aging is a significant contributor to various age-related neurological and neuropsychological disorders, including Alzheimer’s disease and Parkinson’s disease. Several extrinsic factors, such as exposure to ionizing radiation, can accelerate senescence. Multiple human and animal studies have reported that exposure to ionizing radiation can have varied effects on organ aging and lead to the prolongation or shortening of life span depending on the radiation dose or dose rate. This paper reviews the effects of radiation on the aging of different types of brain cells, including neurons, microglia, astrocytes, and cerebral endothelial cells. Further, the relevant molecular mechanisms are discussed. Overall, this review highlights how radiation-induced senescence in different cell types may lead to brain aging, which could result in the development of various neurological and neuropsychological disorders. Therefore, treatment targeting radiation-induced oxidative stress and neuroinflammation may prevent radiation-induced brain aging and the neurological and neuropsychological disorders it may cause.

2019 ◽  
Vol 20 (6) ◽  
pp. 1272 ◽  
Author(s):  
Jungwoon Lee ◽  
Suk Yoon ◽  
Inpyo Choi ◽  
Haiyoung Jung

Many elderly people suffer from hematological diseases known to be highly age-dependent. Hematopoietic stem cells (HSCs) maintain the immune system by producing all blood cells throughout the lifetime of an organism. Recent reports have suggested that HSCs are susceptible to age-related stress and gradually lose their self-renewal and regeneration capacity with aging. HSC aging is driven by cell-intrinsic and -extrinsic factors that result in the disruption of the immune system. Thus, the study of HSC aging is important to our understanding of age-related immune diseases and can also provide potential strategies to improve quality of life in the elderly. In this review, we delineate our understanding of the phenotypes, causes, and molecular mechanisms involved in HSC aging.


2020 ◽  
Vol 21 (24) ◽  
pp. 9514
Author(s):  
Genevieve Saw ◽  
Feng Ru Tang

The hippocampus is crucial in learning, memory and emotion processing, and is involved in the development of different neurological and neuropsychological disorders. Several epigenetic factors, including DNA methylation, histone modifications and non-coding RNAs, have been shown to regulate the development and function of the hippocampus, and the alteration of epigenetic regulation may play important roles in the development of neurocognitive and neurodegenerative diseases. This review summarizes the epigenetic modifications of various cell types and processes within the hippocampus and their resulting effects on cognition, memory and overall hippocampal function. In addition, the effects of exposure to radiation that may induce a myriad of epigenetic changes in the hippocampus are reviewed. By assessing and evaluating the current literature, we hope to prompt a more thorough understanding of the molecular mechanisms that underlie radiation-induced epigenetic changes, an area which can be further explored.


Dose-Response ◽  
2020 ◽  
Vol 18 (1) ◽  
pp. 155932582091418
Author(s):  
Guangyao He ◽  
Anzhou Tang ◽  
Mao Xie ◽  
Wei Xia ◽  
Pengcheng Zhao ◽  
...  

Radiotherapy is an effective treatment for local solid tumors, but the mechanism of damage to human body caused by radiation therapy needs further study. In this study, gene expression profiles of human peripheral blood samples exposed to different doses and rates of ionizing radiation (IR) were used for bioinformatics analysis to investigate the mechanism of IR damage and radiation-induced bystander effect (RIBE). Differentially expressed genes analysis, weighted gene correlation network analysis, functional enrichment analysis, hypergeometric test, gene set enrichment analysis, and gene set variation analysis were applied to analyze the data. Moreover, receiver operating characteristic curve analysis was performed to identify core genes of IR damage. Weighted gene correlation network analysis identified 3 modules associated with IR damage, 2 were positively correlated and 1 was negatively correlated. The analysis showed that the positively correlated modules were significantly involved in apoptosis and p53 signaling pathway, and ESR1, ATM, and MYC were potential transcription factors regulating these modules. Thus, the study suggested that apoptosis and p53 signaling pathway may be the potential molecular mechanisms of IR damage and RIBE, which could be driven by ESR1, ATM, and MYC.


2014 ◽  
Vol 42 (3) ◽  
pp. 663-669 ◽  
Author(s):  
M. Carmen Ortells ◽  
William M. Keyes

Adult tissue homoeostasis requires continual replacement of cells that are lost due to normal turnover, injury and disease. However, aging is associated with an overall decline in tissue function and homoeostasis, suggesting that the normal regulatory processes that govern self-renewal and regeneration may become impaired with age. Tissue-specific SCs (stem cells) lie at the apex of organismal conservation and regeneration, ultimately being responsible for continued tissue maintenance. In many tissues, there are changes in SC numbers, or alteration of their growth properties during aging, often involving imbalances in tumour-suppressor- and oncogene-mediated pathways. Uncovering the molecular mechanisms leading to changes in SC function during aging will provide an essential tool to address tissue-specific age-related pathologies. In the present review, we summarize the age-related alterations found in different tissue SC populations, highlighting recently identified changes in aged HFSCs (hair-follicle SCs) in the skin.


2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Yun-feng Rui ◽  
Min-hao Chen ◽  
Ying-juan Li ◽  
Long-fei Xiao ◽  
Peng Geng ◽  
...  

Aged tendon-derived stem/progenitor cells (TSPCs) lead to age-related tendon disorders and impair tendon healing. However, the underlying molecular mechanisms of TSPC aging remain largely unknown. Here, we investigated the role of connective tissue growth factor (CTGF) in TSPC aging. CTGF protein and mRNA levels were markedly decreased in the aged TSPCs. Moreover, recombinant CTGF attenuates TSPC aging and restores the age-associated reduction of self-renewal and differentiation of TSPCs. In addition, cell cycle distribution of aged TSPCs was arrested in the G1/S phase while recombinant CTGF treatment promoted G1/S transition. Recombinant CTGF also rescued decreased levels of cyclin D1 and CDK4 and reduced p27kip1 expression in aged TSPCs. Our results demonstrated that CTGF plays a vital role in TSPC aging and might be a potential target for molecular therapy of age-related tendon disorders.


2021 ◽  
Vol 12 ◽  
Author(s):  
Anna Allué-Guardia ◽  
Juan I. García ◽  
Jordi B. Torrelles

In the last two decades, multi (MDR), extensively (XDR), extremely (XXDR) and total (TDR) drug-resistant Mycobacterium tuberculosis (M.tb) strains have emerged as a threat to public health worldwide, stressing the need to develop new tuberculosis (TB) prevention and treatment strategies. It is estimated that in the next 35 years, drug-resistant TB will kill around 75 million people and cost the global economy $16.7 trillion. Indeed, the COVID-19 pandemic alone may contribute with the development of 6.3 million new TB cases due to lack of resources and enforced confinement in TB endemic areas. Evolution of drug-resistant M.tb depends on numerous factors, such as bacterial fitness, strain’s genetic background and its capacity to adapt to the surrounding environment, as well as host-specific and environmental factors. Whole-genome transcriptomics and genome-wide association studies in recent years have shed some insights into the complexity of M.tb drug resistance and have provided a better understanding of its underlying molecular mechanisms. In this review, we will discuss M.tb phenotypic and genotypic changes driving resistance, including changes in cell envelope components, as well as recently described intrinsic and extrinsic factors promoting resistance emergence and transmission. We will further explore how drug-resistant M.tb adapts differently than drug-susceptible strains to the lung environment at the cellular level, modulating M.tb–host interactions and disease outcome, and novel next generation sequencing (NGS) strategies to study drug-resistant TB.


Author(s):  
Laura R. Goldberg

Extracellular vesicles (EVs), important mediators of intercellular communication, play a critical role in modulating hematopoiesis within the bone marrow microenvironment. Although few studies have explicitly examined the connections between EVs and hematopoietic stem cell (HSC) aging, there is a growing body of evidence that implicates EVs in numerous age-related biologic processes and diseases. This, coupled with their tremendous capacity to influence hematopoiesis, suggests EVs may be key mediators of HSC aging. This review provides an overview of the effects of aging on HSCs, the role of EVs in aging in general, and then details key work in EV modulation of normal and malignant hematopoiesis, with a particular focus on how these effects may translate into the ability of EVs to drive HSC aging. Finally, it describes an exciting emerging literature that provides direct evidence for EV modulation of HSC phenotypes during natural aging and highlights their potential in HSC rejuvenation. Taken collectively, this body of research has profound implications for the future of HSC aging studies. More clearly defining how EVs modify HSC function in an age-dependent fashion and determining the molecular mechanisms by which they drive these age-related HSC phenotype changes will undoubtedly yield innovative strategies to delay or even reverse age-related hematologic dysfunction.


2020 ◽  
Vol 82 (1) ◽  
pp. 203-226 ◽  
Author(s):  
Heinrich Jasper

Regenerative processes that maintain the function of the gastrointestinal (GI) epithelium are critical for health and survival of multicellular organisms. In insects and vertebrates, intestinal stem cells (ISCs) regenerate the GI epithelium. ISC function is regulated by intrinsic, local, and systemic stimuli to adjust regeneration to tissue demands. These control mechanisms decline with age, resulting in significant perturbation of intestinal homeostasis. Processes that lead to this decline have been explored intensively in Drosophila melanogaster in recent years and are now starting to be characterized in mammalian models. This review presents a model for age-related regenerative decline in the fly intestine and discusses recent findings that start to establish molecular mechanisms of age-related decline of mammalian ISC function.


2021 ◽  
Vol 65 (6) ◽  
pp. 11-16
Author(s):  
D Isaev ◽  
D. Guryev ◽  
T. Blohina ◽  
E. Yashkina ◽  
A. Osipov

The review considers investigations presenting experimental data on the embryotoxic and teratogenic effects of exposure to ionizing radiation in zebrafish (Danio rerio) which is a convenient model for experimental embryology and radiation biology. The molecular mechanisms involved in response to the ionizing radiation influence as well as determining the embryonic death level, development disorders of embryos are examined. The data on acute and chronic effects of ionizing radiation on embryos of various stages of development with wide range of dose rates are presented. It was shown that the influence of γ-radiation on the death and development of zebrafish embryos is nonmonotonic and depends both on the irradiation conditions and on the stage of embryogenesis. The results of such studies are extremely important for understanding the mechanisms of radiation-induced biological effects formation in the embryogenesis of vertebrates, including humans, as well as for developing methods and approaches to assessing radiation risk for a developing organism.


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