Wnt/β-catenin signaling pathway is involved in early dopaminergic differentiation of trabecular meshwork-derived mesenchymal stem cells.
Sahebdel F, Parvaneh Tafreshi A, Arefian E, Roussa E, Nadri S, Zeynali B
This study shows that stem cells from the eye's trabecular meshwork convert into dopamine-producing neurons more effectively than bone marrow or fat stem cells when stimulated by specific signaling pathways. The researchers identify the Wnt/beta-catenin pathway as a key driver for this transformation, suggesting it could be a target for future cell-based therapies.
- Trabecular meshwork stem cells show higher neural potential than bone marrow or fat stem cells.
- Wnt/beta-catenin activation directs these stem cells toward a dopamine-producing fate.
- The study uses only cell cultures, with no animal or human testing involved.
- Nurr-1 expression confirms early differentiation into dopaminergic neurons in the lab setting.
Construction of lncRNA-miRNA-mRNA network based on ceRNA mechanism reveals the function of lncRNA in the pathogenesis of gout.
Chen F, Zhang X, Chen Y, Chai Y, Jiang X, Li H
This study found that a network of lncRNAs, miRNAs, and mRNAs helps drive gout by disrupting key inflammatory pathways, including NF-κB and IL-17 signaling, with NR4A2 identified as a central hub gene involved in this process.
- NR4A2 is a key hub gene in the ceRNA network of gout
- The lncRNA-miRNA-mRNA network affects inflammation and joint cell function
- Five lncRNAs and five miRNAs are linked to gout development
- The network influences NF-κB, IL-17, and TNF signaling pathways
- Findings may point to new treatment targets for gout
Prostaglandin A2 Interacts with Nurr1 and Ameliorates Behavioral Deficits in Parkinson's Disease Fly Model.
Rajan S, Toh HT, Ye H, Wang Z, Basil AH, Parnaik T, Yoo JY, Lim KL, Yoon HS
Prostaglandin A2 binds directly to the Nurr1 protein and rescues movement deficits in a fruit fly model of Parkinson's disease. This study provides structural evidence that PGA2 activates Nurr1, suggesting it could potentially modulate the pathway affected by NR4A2 mutations.
- PGA2 physically binds to the Nurr1 ligand-binding domain via covalent coupling.
- Binding shifts the AF-2 helix, activating Nurr1 transcriptional function.
- PGA2 rescues locomotor deficits in LRRK2 mutant fruit flies.
- Study uses insect models, not human patients or mammalian systems.
Orphan Nuclear Receptor NR4A2 Is Constitutively Expressed in Cartilage and Upregulated in Inflamed Synovium From hTNF-Alpha Transgenic Mice.
Lilley CM, Alarcon A, Ngo MH, Araujo JS, Marrero L, Mix KS
This study shows that NR4A2 levels rise in joint tissue during inflammation in a mouse model of rheumatoid arthritis. It confirms that NR4A2 is part of the inflammatory process in joints but does not address its role in dopaminergic neurons or movement disorders.
- NR4A2 increases in inflamed synovium of mice with rheumatoid arthritis.
- The study focuses on joint inflammation, not brain or dopamine pathways.
- Results validate the mouse model for testing drugs targeting NR4A2 in arthritis.
- No findings apply to NR4A2-related syndromes affecting movement or development.
Disrupted myelination network in the cingulate cortex of Parkinson's disease.
Xie S, Yang J, Huang S, Fan Y, Xu T, He J, Guo J, Ji X, Wang Z, Li P, Chen J, Zhang Y
This study identifies disrupted myelination in the cingulate cortex of Parkinson's disease patients and highlights NR4A2 as one of several genes implicated in this neurodegenerative process. The findings suggest that remyelination strategies could be a potential therapeutic approach for cognitive symptoms in Parkinson's.
- Myelin genes are downregulated in the cingulate cortex of Parkinson's patients.
- Oligodendrocytes, which produce myelin, are the primary damaged cell type.
- NR4A2 is listed among seven genes implicated in PD or neurodegeneration.
- Results validate findings from a separate dementia with Lewy Bodies cohort.
- Remyelination is proposed as a promising treatment strategy for Parkinson's.
Essential Roles of the Transcription Factor NR4A1 in Regulatory T Cell Differentiation under the Influence of Immunosuppressants.
Sekiya T, Kasahara H, Takemura R, Fujita S, Kato J, Doki N, Katayama Y, Ozawa Y, Takada S, Eto T, Fukuda T, Ichinohe T, Takanashi M, Onizuka M, Atsuta Y, Okamoto S, Yoshimura A, Takaki S, Mori T
This study investigates NR4A1, a different gene from the NR4A2 gene affecting your child, focusing on immune system regulation rather than neurological development. The research demonstrates how NR4A1 influences regulatory T cells in the context of immunosuppressant therapy and transplant outcomes.
- The paper studies NR4A1, not NR4A2, which is the gene relevant to your child's condition.
- Research focuses on immune cell differentiation and transplant medicine, not brain development.
- Findings involve mouse models and human transplant patients regarding graft-versus-host disease.
- No direct implications for NR4A2-related neurodevelopmental disorders or treatments are presented.
Identification and Verification of Potential Hub Genes in Amphetamine-Type Stimulant (ATS) and Opioid Dependence by Bioinformatic Analysis.
Zhang W, Deng X, Liu H, Ke J, Xiang M, Ma Y, Zhang L, Yang M, Liu Y, Huang F
This bioinformatic study identifies Nr4a2 as a hub gene involved in neuron differentiation and proliferation within mouse models of drug dependence. The research confirms that Nr4a2 expression changes in response to amphetamine and opioid treatments, linking it to the PI3K/Akt signaling pathway.
- Nr4a2 appears as a key hub gene in mouse models of amphetamine and opioid dependence.
- The study links Nr4a2 to neuron differentiation, migration, and proliferation processes.
- Nr4a2 expression changes were observed in both bioinformatic data and cell line validation.
- The PI3K/Akt signaling pathway is implicated in the pathogenesis of substance dependence.
Pharmacological Rescue with SR8278, a Circadian Nuclear Receptor REV-ERBα Antagonist as a Therapy for Mood Disorders in Parkinson's Disease.
Kim J, Park I, Jang S, Choi M, Kim D, Sun W, Choe Y, Choi JW, Moon C, Park SH, Choe HK, Kim K
This preclinical study in mice shows that a drug targeting the REV-ERBα protein reduces anxiety and depression-like behaviors linked to circadian rhythms. The treatment also restores normal function of NURR1, a protein related to NR4A2, within dopamine-producing neurons.
- The study uses Parkinson's disease mouse models, not humans or NR4A2 patients.
- SR8278 reduces mood disorders and restores circadian rhythms in mice.
- The drug normalizes NURR1 binding to DNA in dopamine neurons.
- Findings suggest REV-ERBα antagonism may help with non-motor symptoms in Parkinson's.
ADRAM is an experience-dependent long noncoding RNA that drives fear extinction through a direct interaction with the chaperone protein 14-3-3.
Wei W, Zhao Q, Wang Z, Liau WS, Basic D, Ren H, Marshall PR, Zajaczkowski EL, Leighton LJ, Madugalle SU, Musgrove M, Periyakaruppiah A, Shi J, Zhang J, Mattick JS, Mercer TR, Spitale RC, Li X, Bredy TW
This study identifies a specific RNA molecule in mice that helps form fear extinction memories by interacting with the NR4A2 gene. The findings describe a molecular mechanism in mouse models and do not provide clinical evidence or treatment options for humans.
- Researchers studied fear extinction memory mechanisms in adult male mice.
- An RNA called ADRAM recruits the 14-3-3 protein to the Nr4a2 gene promoter.
- This interaction is required for forming fear extinction memories in mice.
- The study focuses on basic molecular biology without human clinical data.
Identification of differentially expressed genes and signaling pathways with Candida infection by bioinformatics analysis.
Zhu GD, Xie LM, Su JW, Cao XJ, Yin X, Li YP, Gao YM, Guo XG
This study used computational analysis to identify genes and pathways activated during Candida infections, finding that JUNB, ATF3, and EGR2 are consistently altered across different Candida species and may serve as potential biomarkers for infection.
- JUNB, ATF3, and EGR2 are consistently changed in Candida infections
- These genes may help detect Candida infections early
- The findings come from analyzing human infection data
- Results suggest possible new ways to diagnose Candida infections
Autistic-like behavior and cerebellar dysfunction in Bmal1 mutant mice ameliorated by mTORC1 inhibition.
Liu D, Nanclares C, Simbriger K, Fang K, Lorsung E, Le N, Amorim IS, Chalkiadaki K, Pathak SS, Li J, Gewirtz JC, Jin VX, Kofuji P, Araque A, Orr HT, Gkogkas CG, Cao R
Disrupting the Bmal1 gene in mice causes autism-like behaviors and problems in the cerebellum, including abnormal brain cell connections and impaired neuron function. These issues are linked to overactive mTORC1 signaling, which can be reversed by the drug metformin, improving both behavior and brain cell health.
- Bmal1 gene loss causes autism-like behaviors in mice
- Cerebellum cells show abnormal structure and function
- mTORC1 signaling is overactive and linked to symptoms
- Metformin reduces mTORC1 and improves symptoms
- Cerebellum-specific Bmal1 loss is enough to cause issues
The impact of pre-freezing storage time and temperature on gene expression of blood collected in EDTA tubes.
Martire S, Valentino P, Marnetto F, Mirabile L, Capobianco M, Bertolotto A
Storing blood in EDTA tubes before processing affects gene expression, especially for inflammation-related genes like NR4A2, even after just 2 hours at room temperature or 4°C. This means delays in handling blood samples can lead to inaccurate results in gene studies.
- Delays in processing blood affect NR4A2 and other inflammation genes
- Even 2 hours at 4°C or room temperature alters gene expression
- B2M is the most stable reference gene for normalization
- Standardized handling is critical for reliable results
- RNA quality remains stable, but expression levels change
Ferulic Acid Induces NURR1 Expression and Promotes Dopaminergic Differentiation in Neural Precursor Cells.
Sadeghi-Zadeh M, Homayouni Moghadam F, Nasr-Esfahani MH
Ferulic acid increases NURR1 expression and promotes the differentiation of neural precursor cells into dopaminergic neurons in mouse stem cell cultures. This study demonstrates a molecular mechanism by which ferulic acid supports dopaminergic development, but it does not provide evidence of clinical efficacy or safety in humans.
- Ferulic acid boosts NURR1 and TH gene expression in mouse neural stem cells.
- Treatment enhances neurite length and overall dopaminergic differentiation rates.
- The study uses only mouse cell cultures, with no human or animal data.
- No clinical trials or patient outcomes are reported for this intervention.
Structural, molecular hybridization and network based identification of miR-373-3p and miR-520e-3p as regulators of NR4A2 human gene involved in neurodegeneration.
Singh J, Raina A, Sangwan N, Chauhan A, Avti PK
Computational modeling identifies miR-373-3p and miR-520e-3p as strong candidates for regulating the NR4A2 gene by binding to its mRNA. This study provides theoretical evidence of potential molecular interactions but does not test these findings in biological systems or humans.
- The study uses computer simulations, not wet-lab experiments or human data.
- It predicts miR-373-3p and miR-520e-3p bind tightly to NR4A2 mRNA.
- No experimental validation confirms these interactions occur in living cells.
- The research focuses on theoretical network analysis of gene regulation.
Role of Nuclear-Receptor-Related 1 in the Synergistic Neuroprotective Effect of Umbilical Cord Blood and Erythropoietin Combination Therapy in Hypoxic Ischemic Encephalopathy.
Choi JW, Kang SJ, Choi JI, Kwack K, Kim M
This study identifies Nurr1 (NR4A2) as a key mediator of neuroprotection in a mouse model of neonatal brain injury treated with umbilical cord blood and erythropoietin. The combination therapy activates the Wnt/beta-catenin signaling pathway, which upregulates Nurr1 to reduce brain damage.
- Researchers used a mouse model of neonatal hypoxic-ischemic encephalopathy.
- Combination therapy with umbilical cord blood and erythropoietin reduced brain infarct size.
- Nurr1 expression increased significantly in treated mice compared to untreated controls.
- The Wnt/beta-catenin pathway activation drives Nurr1-mediated neuroprotection.
- Findings are preclinical and do not involve human patients or NR4A2 syndrome.
The Selective Agonist for Sphingosine-1-Phosphate Receptors Siponimod Increases the Expression Level of NR4A Genes in Microglia Cell Line.
Montarolo F, Martire S, Marnetto F, Valentino P, Valverde S, Capobianco MA, Bertolotto A
The multiple sclerosis drug siponimod increases NR4A2 gene expression in microglia cells in a laboratory setting. This finding identifies a potential molecular mechanism for the drug's protective effects in the central nervous system.
- Siponimod boosts NR4A2 levels specifically in microglial brain cells.
- The effect does not occur in blood cells or oligodendrocytes.
- This is an in vitro study using cell lines, not human patients.
- NR4A2 functions as an anti-inflammatory gene in this context.
The Effects of Prenatal Exposure to Pregabalin on the Development of Ventral Midbrain Dopaminergic Neurons.
Alsanie WF, Alhomrani M, Gaber A, Habeeballah H, Alkhatabi HA, Felimban RI, Abdelrahman S, Hauser CAE, Chaudhary AG, Alamri AS, Raafat BM, Alamri A, Anwar S, Alswat KA, Althobaiti YS, Asiri YA
Prenatal exposure to pregabalin alters the development of ventral midbrain dopaminergic neurons in mice by increasing specific gene expression and reducing ATP release, even at therapeutic doses. This suggests that pregabalin use during pregnancy may interfere with the formation and function of brain cells critical for movement and behavior.
- Pregabalin increases genes linked to dopaminergic neuron development in mouse embryos.
- Therapeutic doses reduce ATP release in developing midbrain neurons without killing them.
- The study uses primary mouse embryonic neurons, not human subjects or clinical data.
- Findings highlight potential risks of pregabalin use during pregnancy for fetal brain development.
[Protective effect of nuclear receptor related 1 (Nurr1) on nerves in rats with cerebral occlusion/reperfusion injury and its mechanism].
Hu D, Xie X, Zhang H
Overexpressing Nurr1 protects brain cells and improves neurological outcomes in rats after stroke by reducing inflammation, oxidative stress, and cell death. This study demonstrates a neuroprotective mechanism of Nurr1 in an acute injury model rather than a chronic developmental or dopaminergic context.
- Nurr1 overexpression reduces brain damage and improves neurological scores in rats after stroke.
- The protection works by lowering inflammation, oxidative stress, and apoptotic cell death signals.
- This is an acute injury model in rats, not a study of NR4A2-related syndrome or Parkinson's.
Reprogramming by Cytosolic Extract of Human Embryonic Stem Cells to Improve Dopaminergic Differentiation Potential of Human Adipose Tissue-derived Stem Cells.
Mobasseri S, Javeri A, Fakhr Taha M
This study shows that treating human fat-derived stem cells with an extract from embryonic stem cells improves their ability to become dopamine-producing neurons in a lab dish. The reprogrammed cells express higher levels of key dopaminergic markers like NURR1 and TH compared to untreated cells. This suggests a potential method for generating neural cells for future therapies, but it remains strictly preclinical.
- ESC extract reprograms fat stem cells to enhance their plasticity in vitro.
- Reprogrammed cells show increased expression of dopaminergic genes like NURR1 and TH.
- The study uses human cells but lacks any animal or human clinical testing.
- No direct link to NR4A2 syndrome treatment or current clinical trials is established.
Integration of transcriptomics and metabolomics provides metabolic and functional insights into reduced insulin secretion in MIN6 β-cells exposed to deficient and excessive arginine.
Xu L, Lin X, Li X, Hu Z, Hou Q, Wang Y, Wang Z
This study uses mouse pancreatic beta cells to show that abnormal arginine levels disrupt insulin secretion through metabolic stress and oxidative damage. Nr4a2 appears as one of several transcription factors involved in this cellular response, but the findings do not address neurological function or human disease mechanisms.
- The research focuses on insulin-secreting pancreatic cells, not brain neurons.
- Nr4a2 is identified incidentally among many genes affected by arginine imbalance.
- No clinical data, patient phenotypes, or treatment outcomes are reported.
- Findings describe general cellular metabolism rather than NR4A2-specific biology.
Striatal dopaminergic neurons as a potential target for GDNF based ischemic stroke therapy.
Beker MÇ, Beker M, Çağlayan AB, Bolat B, Kılıç Ü, Torun Köse G, Kılıç E
GDNF delivery increases Nurr1 expression and reduces neuronal degeneration in a mouse model of ischemic stroke, but it does not protect or increase the number of dopaminergic neurons. This preclinical study focuses on stroke recovery mechanisms rather than NR4A2-related neurodevelopmental conditions.
- GDNF treatment increases Nurr1 expression in the ischemic striatum of mice.
- GDNF reduces neuronal degeneration but does not protect dopaminergic neurons.
- The study uses a mouse model of cerebral ischemia, not NR4A2 syndrome.
- No clinical data or human trials are reported in this paper.
Scaffold Hopping from Amodiaquine to Novel Nurr1 Agonist Chemotypes via Microscale Analogue Libraries.
Willems S, Müller M, Ohrndorf J, Heering J, Proschak E, Merk D
Researchers designed new chemical compounds that activate the Nurr1 protein more effectively than existing templates. These novel molecules share no structural similarity to previous candidates but demonstrate superior potency in laboratory tests.
- New Nurr1 agonists show higher potency than the amodiaquine template.
- The compounds are structurally distinct from prior known activators.
- Pharmacophore modeling identified key features required for Nurr1 activation.
Genome-Wide Identification of Immune-Related Alternative Splicing and Splicing Regulators Involved in Abdominal Aortic Aneurysm.
Wu S, Liu S, Chen N, Zhang C, Zhang H, Guo X
This study found that immune-related gene splicing and splicing factors are disrupted in abdominal aortic aneurysm (AAA), with two key genes, NR4A1 and NR4A2, significantly downregulated. These genes are part of a broader network involving immune cell changes and splicing regulation, suggesting a role in disease development.
- NR4A1 and NR4A2 are downregulated in AAA
- Immune-related splicing events are altered in AAA
- Splicing factors like SF3B1 are linked to immune gene regulation
- Macrophages and plasma cells are increased in AAA
- Splicing changes distinguish AAA samples from controls
Monocyte Gene and Molecular Expression Profiles Suggest Distinct Effector and Regulatory Functions in Beninese HIV Highly Exposed Seronegative Female Commercial Sex Workers.
Blondin-Ladrie L, Fourcade L, Modica A, Aranguren M, de Montigny N, Labbé AC, Alary M, Guédou F, Poudrier J, Roger M
This study identifies NR4A2 as one of several immune-related genes with altered expression in the blood monocytes of women naturally resistant to HIV infection. It does not provide information on NR4A2's role in neurodevelopment, Parkinson's disease, or any treatment options for NR4A2-related syndromes.
- NR4A2 appears as an incidental marker in an unrelated immunology study.
- The research focuses on HIV resistance in commercial sex workers.
- No findings relate to dopaminergic neurons or neurological function.
- The paper offers no clinical guidance for NR4A2-related conditions.
CB2 receptor activation inhibits the phagocytic function of microglia through activating ERK/AKT-Nurr1 signal pathways.
Han QW, Shao QH, Wang XT, Ma KL, Chen NH, Yuan YH
Activating the CB2 receptor suppresses microglial inflammation by boosting Nurr1 levels in cell culture models. This mechanism suggests that targeting this pathway could reduce neurotoxicity, but the findings are limited to laboratory cells and do not yet demonstrate clinical benefit.
- CB2 activation increases nuclear Nurr1 protein in microglial cell lines.
- Nurr1 activation inhibits the phagocytic function of microglia.
- ERK/AKT signaling pathways mediate this regulatory effect.
- Results are derived from BV-2 cells and primary midbrain microglia cultures.
- No human data or animal model efficacy is reported.
BMS-470539 Attenuates Oxidative Stress and Neuronal Apoptosis via MC1R/cAMP/PKA/Nurr1 Signaling Pathway in a Neonatal Hypoxic-Ischemic Rat Model.
Yu S, Doycheva DM, Gamdzyk M, Gao Y, Guo Y, Travis ZD, Tang J, Chen WX, Zhang JH
This study shows that activating the MC1R receptor reduces brain damage and cell death in rats after oxygen deprivation, a process that depends on Nurr1. The drug BMS-470539 protects neurons by triggering a signaling pathway involving Nurr1, but this work is limited to animal models of stroke rather than genetic syndromes.
- BMS-470539 reduces brain injury and cell death in rats after hypoxic-ischemic events.
- Neuroprotection requires both MC1R activation and the presence of Nurr1 protein.
- CRISPR knockout of Nurr1 eliminates the drug's protective effects in this model.
- The study uses a rat model of stroke, not NR4A2-related genetic syndrome.
Genome-Wide DNA Methylation in Policemen Working in Cities Differing by Major Sources of Air Pollution.
Honkova K, Rossnerova A, Chvojkova I, Milcova A, Margaryan H, Pastorkova A, Ambroz A, Rossner P, Jirik V, Rubes J, Sram RJ, Topinka J
This study links specific air pollution exposures to changes in DNA methylation patterns in human blood, including alterations near the NR4A2 gene. These epigenetic changes are associated with pathways involved in neuronal function and neurodegenerative diseases.
- The study analyzes DNA methylation in 125 non-smoking policemen exposed to different air pollution levels.
- Researchers identified thousands of differentially methylated loci associated with specific geographic locations.
- Changes near NR4A2 link air pollution exposure to dopaminergic system and neurodegenerative disease pathways.
- Affected biological processes include neuronal functions, axon guidance, and cell adhesion.
Overexpression of miR-200b-3p in Menstrual Blood-Derived Mesenchymal Stem Cells from Endometriosis Women.
de Oliveira RZ, de Oliveira Buono F, Cressoni ACL, Penariol LBC, Padovan CC, Tozetti PA, Poli-Neto OB, Ferriani RA, Orellana MD, Rosa-E-Silva JC, Meola J
miR-200b-3p is significantly overexpressed in menstrual stem cells from women with endometriosis, which may contribute to abnormal cell behavior and tissue implantation. This finding highlights a potential molecular mechanism in endometriosis but does not directly involve NR4A2-related syndrome.
- miR-200b-3p is overexpressed in endometriosis stem cells
- Overexpression links to increased cell proliferation and stemness
- May promote tissue implantation in endometriosis
- Not directly related to NR4A2/NURR1 syndrome
- Findings are specific to endometriosis biology
Potential role of inducible GPR3 expression under stimulated T cell conditions.
Shiraki H, Tanaka S, Guo Y, Harada K, Hide I, Yasuda T, Sakai N
This study investigates the role of GPR3 in T cell activation and its interaction with NR4A2, but it does not provide evidence relevant to NR4A2-related syndromes or dopaminergic function. The findings are limited to immune cell biology and do not translate to clinical insights for this condition.
- GPR3 expression increases in T cells after stimulation.
- NR4A2 modulation by GPR3 occurs in human T cell lines.
- Mouse models show no NR4A2 change without GPR3.
- GPR3 helps suppress effector T cell activation.
- No link to dopaminergic neurons or NR4A2 syndrome phenotypes.
Retinoid X Receptor: Cellular and Biochemical Roles of Nuclear Receptor with a Focus on Neuropathological Involvement.
Sharma S, Shen T, Chitranshi N, Gupta V, Basavarajappa D, Sarkar S, Mirzaei M, You Y, Krezel W, Graham SL, Gupta V
This review summarizes how Retinoid X Receptors (RXRs) regulate gene expression and influence neuroinflammation in various neurological disorders. It highlights that targeting RXRs with specific ligands shows protective effects in animal and cell models of conditions like Parkinson's disease.
- RXRs are nuclear receptors that modulate genes involved in neuronal stress and inflammation.
- Pharmacological activation of RXRs protects neurons in models of Alzheimer's and Parkinson's.
- The paper is a review of existing knowledge, not new clinical data.
- No direct link to NR4A2 genetics or specific treatments for NR4A2 syndrome is established.
Synergistic Effects of Combined Nurr1 Overexpression and Natural Inducers on the More Efficient Production of Dopaminergic Neuron-Like Cells From Stem Cells.
Beiki R, Khaghani M, Esmaeili F, Dehghanian F
Overexpressing the Nurr1 gene alongside brain extract factors efficiently converts stem cells into dopaminergic neuron-like cells in a laboratory setting. This preclinical study demonstrates that combining genetic modification with specific environmental cues enhances the production of these specialized neurons from stem cell lines.
- Nurr1 overexpression combined with neonatal rat brain extract boosts dopaminergic differentiation.
- The study uses P19 stem cells, not human patient cells or clinical trials.
- Results show synergistic effects on creating neuron-like cells in vitro.
- This is basic molecular biology research with no direct human application yet.
Integrative Analysis of Long Non-coding RNAs, Messenger RNAs, and MicroRNAs Indicates the Neurodevelopmental Dysfunction in the Hippocampus of Gut Microbiota-Dysbiosis Mice.
Liu L, Wang H, Chen X, Zhang Y, Li W, Rao X, Liu Y, Zhao L, Pu J, Gui S, Yang D, Fang L, Xie P
This study identifies Nr4a2 as part of a gene regulatory network in mouse brains affected by gut microbiota changes linked to depression. It does not provide evidence for treatment or understanding specific to NR4A2-related syndromes in humans.
- The research uses mice with altered gut bacteria to model depression.
- Nr4a2 appears in a gene network associated with neurodevelopmental dysfunction.
- Findings focus on inflammatory and neurodevelopmental pathways in the hippocampus.
- No human data or clinical trials for NR4A2 syndromes are included.
LincRNA-p21 Upregulates Nuclear Orphan Receptor Nr4a2 and Aggravates Myocardial Ischemia/Reperfusion Injury via Targeting MiR-466i-5p.
Zhai X, Liu R, Li J, Wang F, Liu L, Wei S, Bian Y, Pang J, Xue M, Qin D, Wang S, Xu T, Xu F, Cao S, Yuan Q, Chen Y
This study found that a molecule called LincRNA-p21 worsens heart damage after a heart attack by reducing a protective protein called Nr4a2. The molecule works by trapping a microRNA that normally keeps Nr4a2 levels in check. Blocking LincRNA-p21 improved heart function and reduced cell death in mice and heart cells.
- LincRNA-p21 increases heart damage after a heart attack
- It reduces Nr4a2, a protective protein in heart cells
- LincRNA-p21 traps a microRNA that controls Nr4a2
- Blocking LincRNA-p21 protects heart cells and improves recovery
- This pathway could be a target for future heart attack treatments
Hydroxychloroquine improves motor function and affords neuroprotection without inhibition of inflammation and autophagy in mice after intracerebral hemorrhage.
Yoshimizu A, Kinoshita K, Ichihara Y, Kurauchi Y, Seki T, Katsuki H
Hydroxychloroquine improved motor function and protected brain cells in mice after stroke-like brain bleeding, likely by preserving nerve fiber connections, even though it didn’t reduce inflammation or autophagy as expected.
- Hydroxychloroquine improved movement and brain function after brain bleeding in mice
- It protected neurons and preserved nerve fiber structure
- Benefits occurred without blocking inflammation or autophagy
- May act through direct neuroprotection, not immune or cellular cleanup pathways
Developmental Patterning and Neurogenetic Gradients of Nurr1 Positive Neurons in the Rat Claustrum and Lateral Cortex.
Fang C, Wang H, Naumann RK
This study maps the developmental timeline and spatial organization of Nurr1-positive neurons in the rat claustrum and lateral cortex. It establishes that these specific neurons are generated sequentially during embryonic days 13.5 to 17.5, forming distinct neurogenetic gradients.
- Nurr1 expression begins as an elongated line on embryonic day 13.5 in rats.
- Most dorsal endopiriform neurons are born between days 13.5 and 14.5.
- Claustrum sub-regions form primarily between embryonic days 14.5 and 15.5.
- Deep layer cortical neurons arise from day 14.5 to 15.5.
- Superficial layer cortical neurons arise from day 15.5 to 17.5.
Nuclear receptors of NR1 and NR4 subfamilies in the regulation of microglial functions and pathology.
Katsuki H
This review summarizes how activating specific nuclear receptors, including Nurr1 (NR4A2), can reduce inflammation and improve microglial function in animal models of neurological diseases. It highlights that while these pathways show therapeutic potential for conditions like Parkinson's disease, the evidence remains preclinical and does not yet translate to human treatments.
- Nurr1 activation reduces neuroinflammation and improves outcomes in animal disease models.
- NR1 receptor agonists also show promise in treating neurological disorders in animals.
- The paper is a review of existing literature, not a new clinical study.
- No human data or direct treatment recommendations for NR4A2 syndrome are provided.
Exosomal lncRNA Nuclear Paraspeckle Assembly Transcript 1 (NEAT1)contributes to the progression of allergic rhinitis via modulating microRNA-511/Nuclear Receptor Subfamily 4 Group A Member 2 (NR4A2) axis.
Wang T, Cai W, Wu Q, Chen D, Wang P, Xu Z
This study shows that NR4A2 promotes inflammation and cell death in nasal tissue during allergic rhinitis, suggesting it acts as a driver of this specific immune condition rather than a neurodevelopmental factor. The findings are based on human nasal epithelial cells and do not provide evidence regarding the neurological symptoms or treatment responses associated with NR4A2 syndrome.
- NR4A2 increases inflammation and cell death in nasal tissue during allergic rhinitis.
- The study uses human nasal cells, not brain tissue or animal models of neurodevelopment.
- Results focus on immune response mechanisms unrelated to dopaminergic pathways.
- No clinical data or treatment implications for NR4A2-related neurodevelopmental disorders are presented.