Jyoti J. Watters

ORCID: 0000-0003-1051-506X
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About
Contact & Profiles
Research Areas
  • Neuroscience of respiration and sleep
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Obstructive Sleep Apnea Research
  • Neonatal Respiratory Health Research
  • Immune cells in cancer
  • Adenosine and Purinergic Signaling
  • Sleep and Wakefulness Research
  • Neonatal and fetal brain pathology
  • Neuroendocrine regulation and behavior
  • Immune Response and Inflammation
  • Respiratory Support and Mechanisms
  • Spinal Cord Injury Research
  • Estrogen and related hormone effects
  • High Altitude and Hypoxia
  • Circadian rhythm and melatonin
  • Stress Responses and Cortisol
  • Neurological Complications and Syndromes
  • Neuropeptides and Animal Physiology
  • Neuroscience and Neuropharmacology Research
  • Immune Cell Function and Interaction
  • Epigenetics and DNA Methylation
  • Congenital Diaphragmatic Hernia Studies
  • Growth Hormone and Insulin-like Growth Factors
  • Retinoids in leukemia and cellular processes
  • Sleep and related disorders

University of Wisconsin–Madison
2015-2024

Allen Institute for Brain Science
2024

University of Florida
2024

University of Wisconsin System
2022

University of Tennessee at Knoxville
2017

University of Wisconsin Health
2013

Abbott (United Kingdom)
2009

New York University
2008

Harvard University
2008

Philadelphia University
2008

Abstract Rapid effects of steroid hormones have been observed in neuronal cells for many years. We show here, that the human neuroblastoma cell line SK-N-SH, membrane impermeable conjugated 17β-estradiol (E2BSA) activates mitogen activated protein kinase (MAPKK or MEK) and induces phosphorylation activation both ERK-1 ERK-2 (mitogen MAPK). Additionally, E2BSA transcription a reporter gene construct driven by promoter mouse c-fos proto-oncogene. The this estrogen on are not inhibited receptor...

10.1210/endo.138.9.5489 article EN Endocrinology 1997-09-01

Although microglial activation is associated with all CNS disorders, many of which are sexually dimorphic or age-dependent, little known about whether basal gene expression altered age in the healthy it sex dependent. Analysis microglia from brains 3-day (P3)- to 12-month-old male and female C57Bl/6 mice revealed distinct profiles during postnatal development that differ significantly those adulthood. Microglia at P3 characterized by relatively high iNOS, TNFα arginase-I mRNA levels, whereas...

10.1002/jnr.23242 article EN Journal of Neuroscience Research 2013-05-17

Estrogen treatment of ovariectomized rats rapidly increases immunoreactivity for the phosphorylated form cAMP response element binding protein (CREB)in neurons preoptic area and bed nucleus stria terminalis. These effects were detected within 15 minutes after estrogen exposure. Since antisera used these studies detect CREB phosphorylation at ser133, which is important transcriptional activation data provide a possible explanation estrogen's on neuronal genes lacking elements (EREs) but...

10.1210/endo.137.5.8612562 article EN Endocrinology 1996-05-01

Estrogens are well known to exert antiinflammatory effects outside the central nervous system (CNS). They have also been shown neuroprotective in CNS after several types of injury, including neurodegeneration. However, molecular mechanisms by which these occur remain unclear. Because microglial hyperactivation and their production neurotoxins is associated with many brain injury for estrogens beneficial, we sought investigate ability estrogen modulate function. Furthermore, because little...

10.1210/en.2004-0619 article EN Endocrinology 2004-07-16

Abstract CNS inflammation mediated by microglial activation can result in neuronal and glial cell death a variety of neurodegenerative demyelinating diseases. Minocycline, second‐generation tetracycline, has profound anti‐inflammatory properties the mediated, part, inhibition microglia. MAPK nuclear factor‐κB (NF‐κB) are hallmarks activated microglia they critical for expression many inflammatory mediators. In present study, we investigated minocycline effects on p38, c‐Jun‐N‐terminal...

10.1111/j.1471-4159.2005.03520.x article EN Journal of Neurochemistry 2005-12-08

Acute intermittent hypoxia elicits a form of spinal, brain-derived neurotrophic factor (BDNF)-dependent respiratory plasticity known as phrenic long-term facilitation. Ligands that activate G(s)-protein-coupled receptors, such the adenosine 2a receptor, mimic effects neurotrophins in vitro by transactivating their high-affinity receptor tyrosine kinases, Trk receptors. Thus, we hypothesized A2a agonists would elicit facilitation mimicking BDNF on TrkB Here demonstrate spinal transactivate...

10.1523/jneurosci.3570-07.2008 article EN cc-by-nc-sa Journal of Neuroscience 2008-02-27

Microglial activation plays a key role in the neuroinflammation associated with virtually all CNS disorders, although their normal physiology is becoming increasingly appreciated. Neuroinflammation often assessed by analyzing pro-inflammatory mediators tissue homogenates, under assumption that microglia are main source of these molecules. However, other cell types can also synthesize inflammatory Hence, to enable direct analysis microglial activities ex vivo, an efficient, reliable, and...

10.1186/1742-2094-9-147 article EN cc-by Journal of Neuroinflammation 2012-06-28

Experimental allergic encephalomyelitis, an autoimmune disorder mediated by T cells, results in demyelination, inflammation, and axonal loss the central nervous system (CNS). Microglia play a critical role major histocompatibility complex class II (MHC II)-dependent antigen presentation reactivation of CNS-infiltrated encephalitogenic cells. Minocycline, tetracycline anti-biotic, has profound anti-inflammatory properties is experimentally used for treatment many CNS disorders; however,...

10.1074/jbc.m611907200 article EN cc-by Journal of Biological Chemistry 2007-03-30

Abstract The nucleotide receptor P2X7 has been shown to modulate LPS-induced macrophage production of numerous inflammatory mediators. Although the C-terminal portion is thought be essential for multiple functions, little known regarding structural motifs that lie within this region. We show here domain contains several apparent protein-protein and protein-lipid interaction with potential importance signaling LPS action. Surprisingly, also a conserved LPS-binding domain. In report, we...

10.4049/jimmunol.167.4.1871 article EN The Journal of Immunology 2001-08-15

Steroid hormones exert dramatic effects on neuronal expression of genes that encode neuropeptides. Expression the neurotensin/neuromedin (NT/N) gene in preoptic area neurons is dramatically enhanced by estrogen <i>in vivo</i>, even though its promoter lacks palindromic response elements. We report here promotes transcription this interactions with cAMP cascade a cell line, SK-N-SH, and mouse model. In neuroblastoma cells, increases phosphorylation element-binding protein time frame precedes...

10.1523/jneurosci.18-17-06672.1998 article EN Journal of Neuroscience 1998-09-01

Abstract Extracellular nucleotides regulate macrophage function via P2X nucleotide receptors that form ligand-gated ion channels. In particular, P2X7 activation is characterized by pore formation, membrane blebbing, and cytokine release. also linked to mitogen-activated protein kinases (MAPK) Rho-dependent pathways, which are known affect cytoskeletal structure in other systems. As critical for behavior, we have tested the importance of these pathways actin filament reorganization during...

10.1189/jlb.1203648 article EN Journal of Leukocyte Biology 2004-04-09

Microglia are implicated in multiple neurodegenerative disorders, many of which display sexual dimorphisms and have symptom onsets at different ages. P2 purinergic receptors critical for regulating various microglial functions, but little is known about how their expression varies with age or sex. Therefore, comprehensive information receptor normal microglia, both sexes, over necessary if we to better understand roles the healthy diseased CNS. We analyzed all fourteen rodent P2X P2Y CD11b+...

10.1186/1742-2094-6-24 article EN cc-by Journal of Neuroinflammation 2009-08-25

Intermittent hypoxia (IH) during sleep is a hallmark of apnea, causing significant neuronal apoptosis, and cognitive behavioral deficits in CNS regions underlying memory processing executive functions. IH-induced neuroinflammation thought to contribute after IH. In the present studies, we tested hypothesis that IH would differentially induce inflammatory factor gene expression microglia region-dependent manner, effects differ temporally. To test this hypothesis, adult rats were exposed...

10.1371/journal.pone.0081584 article EN cc-by PLoS ONE 2013-12-04

Although systemic inflammation occurs in most pathological conditions that challenge the neural control of breathing, little is known concerning impact on respiratory motor plasticity. Here, we tested hypothesis low-grade induced by lipopolysaccharide (LPS, 100 μg/kg ip; 3 and 24 h postinjection) elicits spinal inflammatory gene expression attenuates a form spinal, plasticity: phrenic long-term facilitation (pLTF) acute intermittent hypoxia (AIH; 3, 5 min hypoxic episodes, intervals). pLTF...

10.1152/japplphysiol.01347.2012 article EN Journal of Applied Physiology 2013-01-18

Inflammation is characteristic of most clinical disorders that challenge the neural control breathing. Since inflammation modulates neuroplasticity, we studied impact caused by prolonged intermittent hypoxia on an important form respiratory plasticity, acute (three, 5 min hypoxic episodes, normoxic intervals) induced phrenic long-term facilitation (pLTF). Because chronic elicits neuroinflammation and pLTF undermined lipopolysaccharide-induced systemic inflammation, hypothesized one night...

10.1523/jneurosci.4539-14.2015 article EN cc-by-nc-sa Journal of Neuroscience 2015-04-29

Expression of the PRL gene is regulated by many factors, including cAMP, estradiol (E2), phorbol esters, epidermal growth factor (EGF), and TRH. The promoter region rat has been shown to contain DNA sequences that are thought support direct interaction estrogen receptors (ERs) with DNA. It this ER/DNA modulate expression PRL. We report here estrogen-induced requires an intact mitogen-activated protein kinase (MAPK) signal transduction pathway in cultured pituitary cells (PR1 lactotroph GH3...

10.1210/mend.14.11.0551 article EN Molecular Endocrinology 2000-11-01
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