Background: Low-intensity pulsed ultrasound (LIPUS) has been highlighted as a potential therapy for tissue repair and regeneration. However, little is known about LIPUS effects on neuromodulation. This research was conducted to study LIPUS effect on the proliferation of human neural stem cells.
Materials and methods: The human SH-SY5Y neuroblastoma cell line was used as a neural stem cell model. The well-documented SH-SY5Y neurogenic protocol, which involves treatment with all trans-retinoic acid (ATRA) for 5 days and then brain-derived neurotrophic factor (BDNF) for 7 days, was used to synchronise the growth cell cycle to G1 phase of the cell cycle before proliferation testing. Subsequently, the neural stem cells were then treated with single or triple 20-min LIPUS exposures (Intensity ISATA: 60 mW/cm2, frequency: 1.5 MHz, pulse repetition: 100 Hz, and duty cycle: 20%). Cell proliferation was analysed using cell counting of β-tubulin and neurofilament medium-positive neural stem cells, Ki67-cell proliferation marker and metabolic-based assays (cell counting kit-8 and alamarBlue). The involvement of ERK signalling was investigated by quantification of phospho-ERK1/2 levels and cell proliferation with and without MEK/ERK inhibitor (U0126).
Results: The results show that LIPUS exposure(s) induced cell proliferation, as evidenced by an increase in the numbers of neural stem cells. ERK signalling is involved in LIPUS-induced neural stem cell proliferation, as evidenced by concurrent inhibition of LIPUS-induced phospho-ERK levels and cell proliferation in the presence of the MEK/ERK inhibitor.
Conclusion: This study provides original evidence that LIPUS can stimulate neural stem/progenitor cell proliferation. LIPUS may be suggested as a sole or an adjunct therapeutic application to promote the neural stem cell pool in stem cell therapies and tissue engineering approaches for nerve repair and regeneration for the management of traumatic nerve injuries and regenerative endodontic treatment.
Telocytes (TCs) are a new type of interstitial cell identified in multiple tissues of mammals, including the human lung, and mediate homocellular or heterocellular cell-cell communication. Acute respiratory distress syndrome (ARDS) is characterized by acute hypoxemia respiratory failure and combined with direct and indirect lung injury, which is induced by pneumonia, sepsis, burns, etc. Pulmonary fibrosis is a progressive lung disease that occurs due to increased fibrosis of lung tissue in response to chronic injury of the epithelium and gets more and more attention as a well-recognized sequela of ARDS or mechanical ventilation. However, the existing intervention measures could not prevent the progression of pulmonary fibrosis. Although the protective effect of TCs in acute lung injury had been demonstrated in both cellular and animal models in previous studies by our or other researchers, the roles of TCs mediated cell-cell communication in fibroproliferative ARDS is unclear. This review is aimed at integrating our understanding of TC-mediated cell–cell communication in lung diseases with pulmonary fibrosis after ARDS.
Malignant tumours pose significant challenges in terms of high morbidity and mortality rates, primarily due to the lack of large-scale applicable screening methods and efficient treatment strategies. However, the development of liquid biopsies, particularly circulating cell-free DNA (cfDNA), offers promising solutions characterised by their non-invasiveness and cost-effectiveness, providing comprehensive tumour information on a global scale. The release of cfDNA is predominantly associated with cell death and turnover, while its elimination occurs through nuclease digestion, renal excretion into the urine and uptake by the liver and spleen. Extensive research into the biological properties of cfDNA has led to the identification of novel applications, including non-invasive cancer screening, cancer subtype classification, tissue-of-origin detection and monitoring of treatment efficacy. Additionally, emerging fields such as methylation-omics, fragment-omics and nucleosome-omics show immense potential as tissue-and disease-specific markers. Therefore, this review aims to comprehensively introduce the latest detection techniques of cfDNA, along with detailed information on its characteristics and applications, providing valuable insights for cancer diagnosis and monitoring, which will assist us in purposefully enhancing relevant features for a more comprehensive application in clinical practice.
Ultraviolet (UV) radiation, a component of sunlight, holds both advantageous anddetrimental effects on human health. While shorter wavelengths of UV radiationaid in melanin and vitamin D synthesis, longer wavelengths pose risks like skincancer and premature aging due to DNA damage. To combat such stress, cellsemploy various mechanisms, including the heat shock response (HSR). Activation of this response involves a highly regulated transcriptional processorchestrated by heat shock factors (HSFs). While HSF1 has been observed as a keytranscription factor for HSR, other HSFs are also found to be associated withdiverse cellular functions, including stress responses. Here, we discuss arecent study by Feng et al., published in Clinical and Translational Medicine, shedding light on the novel function of HSF4 in regulating inflammation and senescence following UV exposure. The researchers observed acomplex of HSF4 and the cofactor COIL (Coilin) at R-loops–aberrant DNA-RNAhybrid structures arising from UV-induced DNA damage in human skin cells. Inthe study, they proposed the HSF4-COIL complex at R-loops as a potential therapeutic target to mitigate UV-induced skin damage.
Background: The brain is a central key organ of the body containing the second highest lipid content only after adipose tissue. Lipids as the main structural components of biological membranes play important roles in a vast number of biological processes within the brain such as energy homeostasis, material transport, signal transduction, neurogenesis and synaptogenesis, providing a balanced cellular environment required for proper functioning of brain cells. Lipids and their metabolism are of great physiological importance in view of the crucial roles of lipids in brain development and function. Astrocytes are the most abundant glial cells in the brain and involved in various processes including metabolic homeostasis, blood brain barrier maintenance, neuronal support and crosstalk.
Results: Disturbances in lipid metabolism and astrocytic functions may lead to pathological alterations associated with numerous neurological diseases like Alzheimer's disease (AD) recognised as the most frequent cause of dementia leading to major progressive memory and cognitive deficits as well as glioblastoma (GBM) known as the most aggressive malignant brain tumour with a poor prognosis.
Conclusions: Herein, we not only review the level and role of altered lipid metabolism in correlation with astrocytic function and astrocyte-neuron crosstalk in AD and GBM, but also discuss important lipid-related metabolites and proteins participating in possible mechanisms of pathologically dysregulated lipid metabolism, offering potential therapeutic targets in targeted molecular therapies for AD and GBM.
Understanding the interplay between immune cells and the bone marrow microenvironment is crucial for elucidating age-related musculoskeletal changes. In this commentary manuscript, we summarized that studies have shown that proinflammatory immune cells in the bone marrow, such as macrophages and neutrophils, can inhibit bone formation by secreting grancalcin. Research on skeletal stem cells (SSCs) in aged mice reveals a shift towards pro-inflammatory gene expression, affecting their osteogenic potential, while another study maps age-related changes in cranial SSC niches, emphasizing the role of the CXCL12–CXCR4 axis in stem cell-immune cell communication, Additionally, the immune system influences hematopoietic stem cells (HSCs); Niche ageing and accumulation of mutations with age lead to HSC exhaustion and a bias towards myeloid differentiation, with toll-like receptors playing a key role in maintaining hematopoiesis and bone metabolism balance.
Background: Single-cell sequencing (SCS) marks the advent of a transformative period in biomedical studies, enabling unprecedented insight into the cellular intricacies of health and disease.
Methods: By dissecting the genetic, epigenetic and proteomic landscapes at the single-cell level, SCS transcends traditional bulk sequencing methodologies, illuminating the heterogeneity and dynamics of individual cells.
Results: This analytical leap facilitates a deeper understanding of disease mechanisms, offers novel diagnostic and therapeutic targets and underpins the development of precision medicine across diverse fields such as neurology, oncology and immunology.
Conclusions: Despite its profound potential, SCS encounters challenges, including complex sample preparation, sophisticated data analysis and cost considerations. Nevertheless, ongoing advancements promise to overcome these barriers, integrating SCS with other omics data and leveraging machine learning to enhance biological understanding and clinical application. With the advancement of SCS technologies, personalised healthcare might be fundamentally altered, facilitating tailored and efficacious treatment strategies.
Amino acids are necessary for all life forms, which play various roles. Disorder of amino acid metabolism is now considered an important driving mechanism in diverse pulmonary conditions, particularly chronic lung diseases like chronic obstructive pulmonary disease, idiopathic pulmonary fibrosis and lung cancer. Glutamate actively participates in multiple vital biological processes, while the intricate glutamate metabolism, glutamate receptors and glutamate transporters assume crucial regulatory functions in the development of chronic lung diseases. This review aims to discuss the relationship between glutamate dysfunction and chronic lung diseases. By discussing the physiological and pathological function of glutamate, we probe the potential drug targets for chronic lung diseases in the glutamate pathway.