Shaogen Wu

ORCID: 0000-0001-5653-3357
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About
Contact & Profiles
Research Areas
  • Pain Mechanisms and Treatments
  • Botulinum Toxin and Related Neurological Disorders
  • Hereditary Neurological Disorders
  • Nerve injury and regeneration
  • Cancer-related molecular mechanisms research
  • Pain Management and Opioid Use
  • MicroRNA in disease regulation
  • RNA modifications and cancer
  • Circular RNAs in diseases
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Musculoskeletal pain and rehabilitation
  • Toxin Mechanisms and Immunotoxins
  • Pharmacological Effects of Natural Compounds
  • Cancer Treatment and Pharmacology
  • Healthcare and Venom Research
  • Fibromyalgia and Chronic Fatigue Syndrome Research
  • Histone Deacetylase Inhibitors Research
  • Spine and Intervertebral Disc Pathology
  • Kruppel-like factors research
  • Exercise and Physiological Responses
  • Pain Management and Treatment
  • Reproductive Biology and Fertility
  • Neuropeptides and Animal Physiology
  • Pain Management and Placebo Effect
  • Cancer-related gene regulation

Stanford University
2020-2024

Rutgers, The State University of New Jersey
2015-2023

Rutgers New Jersey Medical School
2015-2023

Huazhong University of Science and Technology
2021

Nanjing Drum Tower Hospital
2012-2016

Nanjing University
2013-2016

Nankai University
2016

Abstract Nerve injury induces changes in gene transcription dorsal root ganglion (DRG) neurons, which may contribute to nerve injury-induced neuropathic pain. DNA methylation represses expression. Here, we report that peripheral increases expression of the methyltransferase DNMT3a injured DRG neurons via activation factor octamer 1. Blocking this increase prevents voltage-dependent potassium (Kv) channel subunit Kcna2 promoter region and rescues attenuates Conversely, absence injury,...

10.1038/ncomms14712 article EN cc-by Nature Communications 2017-03-08

Maladaptive changes of nerve injury-associated genes in dorsal root ganglia (DRGs) are critical for neuropathic pain genesis. Emerging evidence supports the role long noncoding RNAs (lncRNAs) regulating gene transcription. Here we identified a conserved lncRNA, named injury-specific lncRNA (NIS-lncRNA) its upregulation injured DRGs exclusively response to injury. This was triggered by injury-induced increase DRG ELF1, transcription factor that bound NIS-lncRNA promoter. Blocking this...

10.1172/jci153563 article EN cc-by Journal of Clinical Investigation 2022-06-30

Activin, a member of the transforming growth factor-β superfamily, promotes preantral follicles and proliferation granulosa cells. However, little is known about role microRNAs in activin-mediated cell proliferation. Here, we reported dose- time-dependent suppression microRNA-181a (miR-181a) expression by activin A mouse cells (mGC). Overexpression miR-181a mGC suppressed receptor IIA (acvr2a) binding to its 3′-untranslated region (3′-UTR), resulting down-regulation cyclin D2 proliferating...

10.1371/journal.pone.0059667 article EN cc-by PLoS ONE 2013-03-20

Forkhead L2 (Foxl2) is expressed in ovarian granulosa cells and participates steroidogenesis by transcriptionally regulating target genes such as steroidogenic acute regulatory protein (StAR) CYP19A1. In this study, a direct link between microRNA‐133b (miR‐133b) Foxl2‐mediated estradiol release was established. miR‐133b involved follicle‐stimulating hormone (FSH)‐induced estrogen production. Luciferase assays confirmed that bound to the 3′ untranslated region (3′UTR) of Foxl2 mRNA....

10.1016/j.febslet.2013.06.023 article EN FEBS Letters 2013-06-26

Background Peripheral nerve injury leads to changes in gene expression primary sensory neurons of the injured dorsal root ganglia. These are believed be involved neuropathic pain genesis. Previously, these have been identified using microarrays or next generation RNA sequencing with poly-A tail selection, but approaches cannot provide a more thorough analysis alterations after injury. Methods The present study chose eliminate mRNA selection and perform strand-specific analyze whole...

10.1177/1744806916629048 article EN cc-by-nc Molecular Pain 2016-01-01

Abstract Nerve injury‐induced change in gene expression primary sensory neurons of dorsal root ganglion (DRG) is critical for neuropathic pain genesis. N 6 ‐methyladenosine (m A) modification RNA represents an additional layer regulation. Here, it reported that peripheral nerve injury increases the m A demethylase fat‐mass and obesity‐associated proteins (FTO) injured DRG via activation Runx1, a transcription factor binds to Fto promoter. Mimicking this increase erases euchromatic histone...

10.1002/advs.201902402 article EN cc-by Advanced Science 2020-05-27

Nerve injury-induced maladaptive changes of gene expression in dorsal root ganglion (DRG) neurons contribute to neuropathic pain. Long non-coding RNAs (lncRNAs) are emerging as key regulators expression. Here, a conserved lncRNA is reported, named DRG-specifically enriched (DS-lncRNA) for its high DRG neurons. Peripheral nerve injury downregulates DS-lncRNA injured due, part, silencing POU domain, class 4, transcription factor 3, that interacts with the promoter. Rescuing downregulation...

10.1002/advs.202004515 article EN cc-by Advanced Science 2021-05-14

Abstract Nerve injury-induced downregulation of voltage-gated potassium channel subunit Kcna2 in the dorsal root ganglion (DRG) is critical for DRG neuronal excitability and neuropathic pain genesis. However, how nerve injury causes this still elusive. Euchromatic histone-lysine N-methyltransferase 2, also known as G9a, methylates histone H3 on lysine residue 9 to predominantly produce a dynamic dimethylation, resulting condensed chromatin gene transcriptional repression. We showed here that...

10.1038/srep37704 article EN cc-by Scientific Reports 2016-11-22

Opioids are the gold standard for pharmacological treatment of neuropathic pain, but their analgesic effects unsatisfactory in part due to nerve injury-induced downregulation opioid receptors dorsal root ganglia (DRG) neurons. How injury drives such remains elusive. DNA methyltransferase (DNMT)-triggered methylation represses gene expression. We show here that blocking increase DRG DNMT3a (a de novo DNMT) rescued expression Oprm1 and Oprk1 mRNAs respective encoding mu-opioid receptor (MOR)...

10.1097/j.pain.0000000000000894 article EN Pain 2017-03-04

MicroRNAs (miRNAs) are a class of 21‐ to 25‐nucleotide non‐coding RNAs, some which important gene regulators involved in folliculogenesis. In this study, we used CCK‐8, real‐time PCR and Western blot assays demonstrate that miR‐145 inhibits mouse granulosa cell (mGC) proliferation. Combined with the results luciferase reporter studied 3′‐untranslated region ACVRIB mRNA, these identified as direct target miR‐145. The ectopic expression reduced levels both mRNA protein also interfered...

10.1016/j.febslet.2012.06.048 article EN FEBS Letters 2012-07-13

Expressional changes of pain-associated genes in primary sensory neurons DRG are critical for neuropathic pain genesis. DNA methyltransferase (DNMT)-triggered methylation silences gene expression. We show here that DNMT1, a canonical maintenance methyltransferase, acts as the <i>de novo</i> DNMT and is required genesis likely through repressing at least <i>Kcna2</i> expression male mice. Peripheral nerve injury upregulated DNMT1 injured transcription factor cAMP response element binding...

10.1523/jneurosci.0695-19.2019 article EN Journal of Neuroscience 2019-06-10

Toll like receptor 7 (TLR7) is expressed in neurons of the dorsal root ganglion (DRG), but whether it contributes to neuropathic pain elusive. We found that peripheral nerve injury caused by ligation fourth lumbar (L4) spinal (SNL) or chronic constriction sciatic led a significant increase expression TLR7 at mRNA and protein levels mouse injured DRG. Blocking this through microinjection adeno-associated virus (AAV) 5 expressing shRNA into ipsilateral L4 DRG alleviated SNL-induced mechanical,...

10.1016/j.bbi.2020.03.019 article EN cc-by Brain Behavior and Immunity 2020-03-20

Abstract Nerve injury to peripheral somatosensory system causes refractory neuropathic pain. Maladaptive changes of gene expression in primary sensory neurons are considered molecular basis this disorder. Long non-coding RNAs (lncRNAs) key regulators transcription; however, their significance pain remains largely elusive.Here, we reported a novel lncRNA, named neuron-specific lncRNA (SS-lncRNA), for its exclusively dorsal root ganglion (DRG) and trigeminal ganglion. SS-lncRNA was...

10.1093/brain/awad110 article EN Brain 2023-04-04

Microglia are implicated as primarily detrimental in pain models; however, they exist across a continuum of states that contribute to homeostasis or pathology depending on timing and context. To clarify the specific contribution microglia progression, we take advantage temporally controlled transgenic approach transiently deplete microglia. Unexpectedly, observe complete resolution coinciding with microglial repopulation rather than depletion. We find repopulated mouse spinal cord...

10.1016/j.celrep.2024.113683 article EN cc-by-nc-nd Cell Reports 2024-01-22

Peripheral nerve injury-induced changes in gene transcription and translation primary sensory neurons of the dorsal root ganglion (DRG) are considered to contribute neuropathic pain genesis. Transcription factors control expression. injury increases expression myeloid zinc finger protein 1 (MZF1), a factor, promotes its binding voltage-gated potassium 1.2 (Kv1.2) antisense (AS) RNA injured DRG. However, whether DRG MZF1 participates is still unknown. Here, we report that blocking increase...

10.1097/j.pain.0000000000000103 article EN Pain 2015-01-28

Changes in gene transcription the dorsal root ganglion (DRG) after nerve trauma contribute to genesis of neuropathic pain. We report that peripheral caused by chronic constriction injury (CCI) increased abundance factor C/EBPβ (CCAAT/enhancer binding protein β) DRG. Blocking this increase mitigated development and maintenance CCI-induced mechanical, thermal, cold pain hypersensitivities without affecting basal responses acute locomotor activity. Conversely, mimicking produced...

10.1126/scisignal.aam5345 article EN Science Signaling 2017-07-11

Estrogen synthesis is an important function of the mammalian ovary. plays roles in many biological processes, including follicular development, oocyte maturation and endometrial proliferation, dysfunctions estrogen contribute to development polycystic ovary syndrome premature ovarian failure. Classical signaling cascades triggered by follicle-stimulating hormone induce via upregulation Cyp19a1 granulosa cells (GCs). This study aimed determine effect microRNA-132 (miR-132) on estradiol GCs....

10.1186/s12958-015-0095-z article EN cc-by Reproductive Biology and Endocrinology 2015-08-18

Neuropathic pain, a distressing and debilitating disorder, is still poorly managed in clinic. Opioids, like morphine, remain the mainstay of prescribed medications treatment this but their analgesic effects are highly unsatisfactory part due to nerve injury-induced reduction opioid receptors first-order sensory neurons dorsal root ganglia. G9a repressor gene expression. We found that increases its catalyzed repressive marker H3K9m2 responsible for epigenetic silencing Oprm1, Oprk1, Oprd1...

10.1177/1744806916682242 article EN cc-by-nc Molecular Pain 2016-01-01

The transmission of normal sensory and/or acute noxious information requires intact expression pain-associated genes within the pain pathways nervous system. Expressional changes these after peripheral nerve injury are also critical for neuropathic induction and maintenance. Methyl-CpG-binding domain protein 1 (MBD1), an epigenetic repressor, regulates gene transcriptional activity. We report here that MBD1 in primary neurons DRG is genesis as MBD1-deficient mice exhibit reduced responses to...

10.1523/jneurosci.0880-18.2018 article EN cc-by-nc-sa Journal of Neuroscience 2018-09-28

Antineoplastic drugs induce dramatic transcriptional changes in dorsal root ganglion (DRG) neurons, which may contribute to chemotherapy‐induced neuropathic pain. K 2p 1.1 controls neuronal excitability by setting the resting membrane potential. Here, we report that systemic injection of chemotherapy agent paclitaxel time‐dependently downregulates expression mRNA and its coding protein DRG neurons. Rescuing this downregulation mitigates development maintenance paclitaxel‐induced mechanical...

10.1002/ijc.32155 article EN International Journal of Cancer 2019-01-26

Complex regional pain syndrome (CRPS) is a chronic disorder with clear acute-to-chronic transition. Preclinical studies demonstrate that toll-like receptor 4 (TLR4), expressed by myeloid-lineage cells, astrocytes, and neurons, mediates sex-dependent transition to pain; however, evidence lacking on which exact TLR4-expressing cells are responsible. We used complementary pharmacologic transgenic approaches in mice more specifically manipulate TLR4 outline its contribution the from CRPS based...

10.1523/jneurosci.1940-20.2021 article EN cc-by-nc-sa Journal of Neuroscience 2021-04-12

Dysregulation of pain-associated genes in the dorsal root ganglion (DRG) is considered to be a molecular basis neuropathic pain genesis. Fused sarcoma (FUS), DNA/RNA-binding protein, critical regulator gene expression. However, whether it contributes unknown. This study showed that peripheral nerve injury caused by fourth lumbar (L4) spinal ligation (SNL) or chronic constriction (CCI) sciatic produced marked increase expression FUS protein injured DRG neurons. Blocking this through...

10.1523/jneurosci.2082-22.2022 article EN cc-by-nc-sa Journal of Neuroscience 2023-01-10
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