Fen Ji

ORCID: 0000-0002-2869-103X
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About
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Research Areas
  • Neurogenesis and neuroplasticity mechanisms
  • Epigenetics and DNA Methylation
  • MicroRNA in disease regulation
  • Genetics and Neurodevelopmental Disorders
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Pluripotent Stem Cells Research
  • Research in Cotton Cultivation
  • Circular RNAs in diseases
  • Mitochondrial Function and Pathology
  • Barrier Structure and Function Studies
  • Adipose Tissue and Metabolism
  • Phosphodiesterase function and regulation
  • Immune cells in cancer
  • interferon and immune responses
  • Congenital heart defects research
  • Phagocytosis and Immune Regulation
  • Silicon and Solar Cell Technologies
  • Autophagy in Disease and Therapy
  • Chromatin Remodeling and Cancer
  • Wnt/β-catenin signaling in development and cancer
  • FOXO transcription factor regulation
  • Climate Change, Adaptation, Migration
  • Semiconductor materials and devices
  • Biomarkers in Disease Mechanisms
  • Plant Water Relations and Carbon Dynamics

Institute of Zoology
2015-2025

Chinese Academy of Sciences
2016-2025

University of Chinese Academy of Sciences
2009-2025

State Key Laboratory of Stem Cell and Reproductive Biology
2016-2024

China Agricultural University
2023

Yutong (China)
2023

China Meteorological Administration
2023

Institute of Electrical Engineering
2019

Second People's Hospital of NanTong
2016

Nantong University
2016

Adult neurogenesis is thought to be crucial for preserving cognitive functions, which tightly controlled by various epigenetic regulators. As the methyltransferase of histone H3K27, role Ezh2 in adult mice and its mechanism action are largely unknown. Here, we show that expressed actively dividing neural stem cells (NSCs)/progenitor as well mature neurons, but not quiescent NSCs subgranular zone. The deletion NSCs/progenitor results a reduction progenitor cell proliferation. Furthermore,...

10.1523/jneurosci.4129-13.2014 article EN cc-by-nc-sa Journal of Neuroscience 2014-04-09

Summary. MicroRNAs (miRNAs) are stably present in human serum. The relationship between circulating miRNAs and hepatitis B virus (HBV) infected liver disease has not been previously reported. Applied Biosystems array‐based miRNA expression profiling was performed on pooled sera obtained from identified groups of chronic asymptomatic carriers (ASC), patients with (CHB) HBV‐associated acute‐on‐chronic failure (ACLF), as well healthy controls (HC). Nine were verified more clinical samples by...

10.1111/j.1365-2893.2011.01443.x article EN Journal of Viral Hepatitis 2011-03-07

Defects in neurogenesis alter brain circuit formations and may lead to neurodevelopmental disorders such as autism schizophrenia. Histone H2A.z, a variant of histone H2A, plays critical roles chromatin structure epigenetic regulation, but its function mechanism development remain largely unknown. Here, we find that the deletion H2A.z results enhanced proliferation neural progenitors reduced neuronal differentiation. In addition, neurons knockout mice exhibit abnormal dendrites during...

10.1093/nar/gkx1295 article EN cc-by-nc Nucleic Acids Research 2017-12-19

Chromodomain helicase DNA-binding protein 2 (CHD2) has been associated with a broad spectrum of neurodevelopmental disorders, such as autism disorders and intellectual disability. However, it is largely unknown whether how CHD2 involved in brain development. Here, we demonstrate that predominantly expressed Pax6(+) radial glial cells (RGs) but rarely Tbr2(+) intermediate progenitors (IPs). Importantly, the suppression expression inhibits self-renewal RGs increases generation IPs production...

10.1002/stem.2001 article EN Stem Cells 2015-03-18

Highlights•Nap1l1 knockdown or knockout causes abnormal embryonic neurogenesis•Nap1l1 depletion induces neuronal dendrites and morphology•Nap1l1 regulates cortical development via regulation of RassF10SummaryThe precise function role nucleosome assembly protein 1-like 1 (Nap1l1) in brain are unclear. Here, we find that Nap1l1 decreases neural progenitor cell (NPC) proliferation premature differentiation during development. A similar deficiency neurogenesis was observed (KO) mice, which were...

10.1016/j.celrep.2018.02.019 article EN cc-by-nc-nd Cell Reports 2018-02-01

Regulatory cell death is an important way to eliminate the DNA damage that accompanies rapid proliferation of neural stem cells during cortical development, including pyroptosis, apoptosis, and so on. Here, study reports absence GSDMD-mediated pyroptosis results in defective sensor pathways accompanied by aberrant neurogenesis autism-like behaviors adult mice. Furthermore, GSDMD involved organizing mitochondrial electron transport chain regulating AMPK/PGC-1α pathway target Aifm3. This...

10.1002/advs.202402285 article EN cc-by Advanced Science 2024-07-21

Oligodendrocyte precursor cells (OPCs) migrate extensively using blood vessels as physical scaffolds in the developing central nervous system. Although association of OPCs with vasculature is critical for migration, regulatory mechanisms important proliferative and oligodendrocyte development are unknown. Here, a correlation demonstrated between response during brain development. Deletion endothelial stimulator interferon genes (STING) disrupts angiogenesis by inhibiting farnesyl-diphosphate...

10.1002/advs.202308508 article EN cc-by Advanced Science 2024-08-13

Abstract Appropriate vascular and neural development is essential for central nervous system (CNS). Although programmed cell death receptor 1 (PD‐1) mediates neurogenesis, its role in cerebrovascular remains poorly understood. Here, a correlation between cerebral vessels oligodendrocyte precursor cells (OPCs) revealed during brain development. The ablation of endothelial PD‐1 triggers cortical hypervascularization through excessive angiogenic sprouting, concomitantly driving OPC...

10.1002/advs.202417410 article EN cc-by Advanced Science 2025-02-27

ABSTRACT 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 methyltransferase, is essential the suppression gene expression. However, role EZH2 in astrocyte early morphogenesis has remained unclear. Using an astrocyte‐specific Ezh2 knockout (cKO) mouse model, we examined effects deletion on morphogenesis,...

10.1111/cpr.70015 article EN cc-by Cell Proliferation 2025-02-28

Abstract Mitochondrial metabolism is a fundamental process in tissue development. How this play functions embryonic neurogenesis remains largely unknown. Here, we show that mitochondrial uncoupling protein 2 (UCP2) regulates the by inhibiting production of reactive oxygen species (ROS), which affect proliferation progenitors. In brains UCP2 knockdown or condition knockout mice, progenitors significantly increased, while differentiation reduced. Furthermore, identify Yap response...

10.1002/stem.2605 article EN Stem Cells 2017-03-09

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

10.1002/advs.202105208 article EN cc-by Advanced Science 2022-04-30

Disrupted in schizophrenia 1 (DISC1) is known as a high susceptibility gene for schizophrenia. Recent studies have indicated that might be caused by glia defects and dysfunction. However, there no direct evidence of link between the DISC1 gliogenesis defects. Thus, an investigation into involvement (a ubiquitously expressed brain protein) astrogenesis during late stage mouse embryonic development warranted. Here, we show suppression expression represses vitro vivo, overexpression...

10.1242/dev.133066 article EN Development 2016-06-11

The intimate communication between the vascular and nervous systems is critical for maintaining central system (CNS) development. However, whether cerebrovascular endothelial cells (ECs) can orchestrate neural precursor cell (NPC) proliferation differentiation, identity of signals involved therein, unclear. Here, we find that development ECs often accompanied by DNA damage. RNF20, an E3 ubiquitin ligase, required damage response (DDR). deletion RNF20 causes accumulation in ECs, which fails...

10.1016/j.celrep.2022.111350 article EN cc-by-nc-nd Cell Reports 2022-09-01
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