Publications by authors named "Libo Su"

Background: Hepatic stellate cell (HSC) activation is a critical factor in the development of liver fibrosis. Recent research indicates that mesoderm/mesenchyme homeobox 1 (Meox1) contributes to fibrosis in organs like the skin and heart.

Objectives: To investigate the potential impact of Meox1 on HSC activation and provide an available target for hepatic fibrosis research.

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Astrocytes are crucial for central nervous system (CNS) development and function, with their differentiation being stringently controlled by epigenetic mechanisms, such as histone modifications. Enhancer of Zeste Homologue 2 (EZH2), a histone methyltransferase, is essential for the suppression of gene expression. However, the role of EZH2 in astrocyte early morphogenesis has remained unclear.

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Article Synopsis
  • - Oligodendrocyte precursor cells (OPCs) rely on blood vessels for migration during central nervous system development, but the mechanisms that regulate their growth and transformation into oligodendrocytes are not yet fully understood.
  • - The study found that removing the endothelial stimulator of interferon genes (STING) hampers blood vessel formation by affecting cholesterol synthesis, which negatively influences OPC development and myelination.
  • - Disrupted metabolic balance in endothelial cells leads to increased interleukin 17D levels, which sends inhibitory signals to OPCs, resulting in abnormal behavior in adult mice, highlighting the importance of endothelial STING in OPC development in the neocortex.
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  • Microglia, the immune cells of the central nervous system, show a lot of variability and their inflammatory state is linked to metabolic changes during diseases.
  • This study explores how microglial metabolism affects the growth of astrocytes in developing brains, focusing on the role of the transcription factor Bach1 in regulating lactate production.
  • Findings suggest that maintaining proper microglial metabolism is crucial for astrocyte development and overall brain health, with implications for understanding related neurological conditions.
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  • Embryonic neurogenesis is crucial for proper cortical development, and disruptions can lead to behavioral issues; a study highlights that deleting the immune molecule Pd1 impairs this process in mice.
  • The absence of Pd1 results in increased neural progenitor cell proliferation, reduced neuron differentiation, and structural abnormalities in neurons, leading to behaviors associated with depression.
  • The research shows that Pd1 affects neurogenesis by interacting with the Pax3 and β-catenin signaling pathways, suggesting potential therapeutic targets for brain development and mood regulation.
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The regulation of neural stem cell (NSC) proliferation and differentiation during brain development is a precisely controlled process, with the production of different neuronal subtypes governed by strict timelines. Glutamate is predominantly used as a neurotransmitter by the subtypes of neurons in the various layers of the cerebral cortex. The expression pattern of BCAT1, a gene involved in glutamate metabolism, in the different layers of neurons has yet to be fully understood.

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The vascular system and the neural system processes occur simultaneously, the interaction among them is fundamental to the normal development of the central nervous system. Arid1a (AT-rich interaction domain 1A), which encodes an epigenetic subunit of the SWI/SNF chromatin-remodelling complex, is associated with promoter-mediated gene regulation and histone modification. However, the molecular mechanism of the interaction between cerebrovascular and neural progenitor cells (NPCs) remains unclear.

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Neocortex expansion and folding are related to human intelligence and cognition, but the molecular and cellular mechanisms underlying cortical folding remain poorly understood. Here, we report that the human gene SERPINA3 is linked to gyrification. Specifically, the overexpression of SERPINA3 induced neocortical folding, increased the abundance of neurons, and improved cognitive abilities.

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The intimate communication between the vascular and nervous systems is critical for maintaining central nervous system (CNS) development. However, whether cerebrovascular endothelial cells (ECs) can orchestrate neural precursor cell (NPC) proliferation and differentiation, and the identity of the signals involved therein, is unclear. Here, we find that the development of ECs is often accompanied by DNA damage.

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Microglia are resident macrophages of the central nervous system that selectively emerge in embryonic cortical proliferative zones and regulate neurogenesis by altering molecular and phenotypic states. Despite their important roles in inflammatory phagocytosis and neurodegenerative diseases, microglial homeostasis during early brain development has not been fully elucidated. Here, we demonstrate a notable interplay between microglial homeostasis and neural progenitor cell signal transduction during embryonic neurogenesis.

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During mammalian cortical development, neural stem/progenitor cells (NSCs) gradually alter their characteristics, and the timing of generation of neurons and glial cells is strictly regulated by internal and external factors. However, whether the blood vessels located near NSCs affect the neurogenic-to-gliogenic transition remain unknown. Here, it is demonstrated that endothelial uncoupling protein 2 (UCP2) deletion reduces blood vessel diameter and affects the transition timing of neurogenesis and gliogenesis.

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Cortical expansion and folding are key processes in human brain development and evolution and are considered to be principal elements of intellectual ability. How cortical folding has evolved and is induced during embryo development is not well understood. Here, we show that the expression of human FOXM1 promotes basal progenitor cell proliferation and induces cortical thickening and folding in mice.

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Short interspersed nuclear elements (SINEs) play a key role in regulating gene expression, and SINE RNAs are involved in age-related diseases. We investigated the anti-aging effects of a genetically engineered murine SINE B1 antisense RNA (B1as RNA) and explored its mechanism of action in naturally senescent BALB/c (≥14 months) and moderately senscent C57BL/6N (≥9 months) mice. After tail vein injection, B1as RNA was available in the blood of mice for approximately 30 min, persisted for approximately 2-4 h in most detected tissues and persisted approximately 48 h in lungs.

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The development of the nervous system requires precise regulation. Any disturbance in the regulation process can lead to neurological developmental diseases, such as autism and schizophrenia. Histone variants are important components of epigenetic regulation.

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RNAs have been elucidated to play the critical role in regulating gene expression and to be expected as effective drugs in the treatment of cancer and age-related diseases. RNAs are extracted by SDS-NaCl centrifugation after transformation of by expression vectors, which is a method to obtain genetically engineered RNAs. But the prepared RNAs by this method contain endotoxin, which limits their application and in cell experments.

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During embryonic brain development, neurogenesis requires the orchestration of gene expression to regulate neural stem cell (NSC) fate specification. Epigenetic regulation with specific emphasis on the modes of histone variants and histone post-translational modifications are involved in interactive gene regulation of central nervous system (CNS) development. Here, we provide a broad overview of the regulatory system of histone variants and histone modifications that have been linked to neurogenesis and diseases.

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Recently, de novo mutations of transcription factor 20 (TCF20) were found in patients with autism by large-scale exome sequencing. However, how TCF20 modulates brain development and whether its dysfunction causes ASD remain unclear. Here, we show that TCF20 deficits impair neurogenesis in mouse.

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Astrogenesis is repressed in the early embryonic period and occurs in the late embryonic period. A variety of external and internal signals contribute to the sequential differentiation of neural stem cells. Here, we discovered that immune-related CD93 plays a critical negative role in the regulation of astrogenesis in the mouse cerebral cortex.

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Angiogenesis plays crucial roles in maintaining the complex operation of central nervous system (CNS) development. The architecture of communication between neurogenesis and angiogenesis is essential to maintain normal brain development and function. Hence, any disruption of neuron-vascular communications may lead to the pathophysiology of cerebrovascular diseases and blood-brain barrier (BBB) dysfunction.

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Networks of coupled systems may exhibit a form of incomplete synchronization called partial synchronization or cluster synchronization, which refers to the situation where only some, but not all, systems exhibit synchronous behavior. Moreover, due to perturbations or uncertainties in the network, exact partial synchronization in the sense that the states of the systems within each cluster become identical, cannot be achieved. Instead, an approximate synchronization may be observed, where the states of the systems within each cluster converge up to some bound, and this bound tends to zero if (the size of) the perturbations tends to zero.

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Background: Hepatocellular carcinoma is a common malignant cancer and the second most common cause of cancer-related deaths worldwide. Collagen triple helix repeat containing 1 (CTHRC1) has been increasingly reported to be involved in tumorigenesis and/or tumor progression. However, limited data are available regarding the role of CTHRC1 in hepatocellular carcinoma.

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In mammals, a constant body temperature is an important basis for maintaining life activities. Here, we show that when pregnant mice are subjected to cold stress, the expression of RBM3, a cold-induced protein, is increased in the embryonic brain. When RBM3 is knocked down or knocked out in cold stress, embryonic brain development is more seriously affected, exhibiting abnormal neuronal differentiation.

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Astrocytes play crucial roles in the central nervous system, and defects in astrocyte function are closely related to many neurological disorders. Studying the mechanism of gliogenesis has important implications for understanding and treating brain diseases. Epigenetic regulations have essential roles during mammalian brain development.

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The B-cell activating factor (BAFF) is a member of tumour necrosis factor (TNF) superfamily that specifically regulates B lymphocyte proliferation and survival. Excess BAFF leads to overproduction of antibodies for secretion, anti-dsDNA antibodies and a lupus-like syndrome in mice. To investigate whether transgenic overexpression of the zebrafish BAFF leads to immunoglobulin changes and/or early maturing of the immune system, a Tol2-GFP-2A-BAFF/His recombinant plasmid was constructed by inserting a 2A peptide between the green fluorescent protein (GFP) and BAFF sequences.

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Infections with intestinal helminth and bacterial pathogens, such as enteropathogenic Escherichia coli, continue to be a major global health threat for children. To determine whether and how an intestinal helminth parasite, Heligomosomoides polygyrus, might impact the TLR signaling pathway during the response to a bacterial enteropathogen, MyD88 knockout and wild-type C57BL/6 mice were infected with H. polygyrus, the bacterial enteropathogen Citrobacter rodentium, or both.

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