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Article ; Online: Small G-Protein Rheb Gates Mammalian Target of Rapamycin Signaling to Regulate Morphine Tolerance in Mice.

Wang, Wenying / Ma, Xiaqing / Du, Wenjie / Lin, Raozhou / Li, Zhongping / Jiang, Wei / Wang, Lu-Yang / Worley, Paul F / Xu, Tao

Anesthesiology

2023 Volume 140, Issue 4, Page(s) 786–802

MeSH term(s)	Female ; Male ; Mice ; Animals ; Monomeric GTP-Binding Proteins/genetics ; Monomeric GTP-Binding Proteins/metabolism ; Morphine/pharmacology ; Sirolimus/pharmacology ; Mice, Inbred C57BL ; Signal Transduction ; TOR Serine-Threonine Kinases/metabolism ; Mechanistic Target of Rapamycin Complex 1/metabolism ; Pain ; Mammals/metabolism
Chemical Substances	Monomeric GTP-Binding Proteins (EC 3.6.5.2) ; Morphine (76I7G6D29C) ; Sirolimus (W36ZG6FT64) ; TOR Serine-Threonine Kinases (EC 2.7.11.1) ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1)
Language	English
Publishing date	2023-12-26
Publishing country	United States
Document type	Journal Article
ZDB-ID	269-0
ISSN	1528-1175 ; 0003-3022
ISSN (online)	1528-1175
ISSN	0003-3022
DOI	10.1097/ALN.0000000000004885
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Zs.MO 199: Show issues

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Article ; Online: Psychological distress, multimorbidity and health services among older adults in rural South Australia.

Asante, Dennis / Rio, Josephien / Stanaway, Fiona / Worley, Paul / Isaac, Vivian

Journal of affective disorders

2022 Volume 309, Page(s) 453–460

Abstract: Objective: Psychological distress may relate to higher health services use. However, data on psychological distress and health services use among rural older adults are limited. This study investigates psychological distress in older adults (aged ≥60) ... ...

Abstract	Objective: Psychological distress may relate to higher health services use. However, data on psychological distress and health services use among rural older adults are limited. This study investigates psychological distress in older adults (aged ≥60) and evaluates the relationship between psychological distress, multimorbidity and health services utilization. Design: A cross-sectional design was adopted using data on older adults (≥60) (n = 5920) from the South Australia's 2013-2017 population health survey. The Modified Monash Model MM2-7 was used to designate rural areas. The dataset provides information on reported physical health conditions, psychological distress, and patterns of health services use. The Kessler Psychological Distress Scale (K10) was used to compute scores for reported mental health disorders in this population. Results: The mean (SD) age of the study participants was 72.1 (8.1) years. Women constituted 58.8% of the sample. The mean (SD) score for psychological distress was 12.5 (3.6). One-fourth (33.7%) report one-chronic condition, 20.4% reported 2 chronic conditions and 13% had more than 3 chronic conditions. High psychological distress was associated with female gender (χ Conclusion/implication: Psychological distress and multimorbidity were independently associated with health services use. Thus, psychological distress, particularly in the presence of multimorbidity, presents an opportunity for intervention by clinicians that may reduce the demand on rural health services.
MeSH term(s)	Aged ; Chronic Disease ; Cross-Sectional Studies ; Female ; Health Services ; Humans ; Multimorbidity ; Psychological Distress ; South Australia/epidemiology
Language	English
Publishing date	2022-04-28
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	135449-8
ISSN	1573-2517 ; 0165-0327
ISSN (online)	1573-2517
ISSN	0165-0327
DOI	10.1016/j.jad.2022.04.140
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Zs.A 1485: Show issues

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Article ; Online: Upregulation of the long non-coding RNA, LIPCAR promotes proliferation, migration, and metastasis of hepatocellular carcinoma.

Bongolo, Christian Cedric / Thokerunga, Erick / Fidele, Nyimi Bushabu / Souraka, Tapara Dramani Maman / Kisembo, Peter / Rugera, Simon Peter / Worley, Paul F / Tu, Jian-Cheng

Cancer biomarkers : section A of Disease markers

2022 Volume 35, Issue 3, Page(s) 245–256

Abstract: Background: Hepatocellular carcinoma (HCC) early diagnosis remains a challenge to date. Alpha-feto protein, though less sensitive remains widely used for both diagnosis and prognosis. Recently however, a number of molecular biomarkers have been ... ...

Abstract	Background: Hepatocellular carcinoma (HCC) early diagnosis remains a challenge to date. Alpha-feto protein, though less sensitive remains widely used for both diagnosis and prognosis. Recently however, a number of molecular biomarkers have been suggested as alternatives to Alpha feto protein, especially for early diagnosis. Objective: To determine the role of the long non-coding RNA, LIPCAR in the pathogenesis and early diagnosis of hepatocellular carcinoma. Methods: Quantitative real-time PCR, and Fluorescence in situ hybridization assays were conducted to determine LIPCAR expression in HCC vs normal blood samples, and HCC cell lines vs normal liver cell lines. Transfection was done to upregulate LIPCAR in one HCC cell line, and used to study cell proliferation, migration, apoptosis and epithelial-mesenchymal transformation. Animal experiment was finally done to determine its effect on metastasis. Results: LIPCAR was significantly upregulated in HCC blood samples and HCC cell lines compared to their respective normal ones. Its overexpression promoted hepatocellular carcinoma cell proliferation, and migration, while inhibiting apoptosis. Its overexpression also promoted epithelial-mesenchymal transformation in hepatocellular carcinoma cells, and metastasis in vivo. Conclusion: The study demonstrated that the lncRNA, LIPCAR is significantly upregulated in hepatocellular carcinoma patients and that its upregulation promotes HCC proliferation, migration, and metastases.
MeSH term(s)	Humans ; Animals ; RNA, Long Noncoding/genetics ; Carcinoma, Hepatocellular/genetics ; Up-Regulation ; In Situ Hybridization, Fluorescence ; Liver Neoplasms/genetics ; Cell Proliferation/genetics
Chemical Substances	RNA, Long Noncoding
Language	English
Publishing date	2022-11-06
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2203517-5
ISSN	1875-8592 ; 1574-0153 ; 1875-8592
ISSN (online)	1875-8592 ; 1574-0153
ISSN	1875-8592
DOI	10.3233/CBM-220033
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Zs.A 6127: Show issues

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Article ; Online: Dynamic Regulation of Homer Binding to Group I Metabotropic Glutamate Receptors by Preso1 and Converging Kinase Cascades.

Hu, Jia-Hua / Worley, Paul F / Kammermeier, Paul J

The Journal of pharmacology and experimental therapeutics

2017 Volume 361, Issue 1, Page(s) 122–129

Abstract: In rat sympathetic neurons from the superior cervical ganglia (SCG) expressing metabotropic glutamate receptor mGluR1 or mGluR5, overexpression of scaffolding Homer proteins, which bind to a Homer ligand in their C termini, cause receptor clustering and ... ...

Abstract	In rat sympathetic neurons from the superior cervical ganglia (SCG) expressing metabotropic glutamate receptor mGluR1 or mGluR5, overexpression of scaffolding Homer proteins, which bind to a Homer ligand in their C termini, cause receptor clustering and uncoupling from ion channel modulation. In the absence of recombinant Homer protein overexpression, uncoupling of mGluRs from voltage-dependent channels can be induced by expression of Preso1, an adaptor of proline-directed kinases that phosphorylates the Homer ligand and recruits binding of endogenous Homer proteins. Here we show that in SCG neurons expressing mGluR1 and the tyrosine receptor kinase B, treatment with brain-derived neurotrophic factor (BDNF) produces a similar uncoupling of the receptors from calcium channels. We investigated the pathways that mediate this uncoupling and compared it with uncoupling observed with Preso1 expression. Both BDNF- and Preso1-induced uncoupling require residues T1151 and S1154 in the mGluR1 Homer ligand (TPPSPF). Uncoupling via Preso1 but not BDNF was prevented by expression of a dominant negative Cdk5, suggesting that endogenous Cdk5 mediates Preso1-dependent phosphorylation of mGluR1. Dominant negative Cdk5 did not block the BDNF effect but this was sensitive to inhibitors of the mitogen-activated protein kinase kinase/extracellular signal-regulated kinase cascade. Interestingly, the BDNF pathway appeared to require native Preso1 binding to mGluR, because overexpression of the Preso1 FERM domain, which mediates the Preso1-mGluR interaction, prevented BDNF-induced uncoupling. These data suggest that the BDNF/tyrosine receptor kinase B and Cdk5 pathways converge at the level of mGluR to similarly induce Homer ligand phosphorylation, recruit Homer binding, and uncouple mGluRs from channel regulation.
MeSH term(s)	Animals ; Brain-Derived Neurotrophic Factor/pharmacology ; Homer Scaffolding Proteins/metabolism ; MAP Kinase Signaling System/drug effects ; MAP Kinase Signaling System/physiology ; Male ; Nerve Tissue Proteins/biosynthesis ; Protein Binding/drug effects ; Protein Binding/physiology ; Rats ; Rats, Wistar ; Receptors, Metabotropic Glutamate/metabolism
Chemical Substances	Brain-Derived Neurotrophic Factor ; FRMPD4 protein, rat ; Homer Scaffolding Proteins ; Nerve Tissue Proteins ; Receptors, Metabotropic Glutamate ; metabotropic glutamate receptor type 1
Language	English
Publishing date	2017-02-08
Publishing country	United States
Document type	Journal Article
ZDB-ID	3106-9
ISSN	1521-0103 ; 0022-3565
ISSN (online)	1521-0103
ISSN	0022-3565
DOI	10.1124/jpet.116.238394
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Article: Homer2 and Homer3 Act as Novel Biomarkers in Diagnosis of hepatitis B virus-induced Hepatocellular Carcinoma.

Luo, Ping / Liang, Chunzi / Jing, Wei / Zhu, Man / Zhou, Hu / Chai, Hongyan / Worley, Paul F / Tu, Jiancheng

Journal of Cancer

2021 Volume 12, Issue 12, Page(s) 3439–3447

Abstract: Background: ...

Abstract	Background:
Language	English
Publishing date	2021-04-19
Publishing country	Australia
Document type	Journal Article
ZDB-ID	2573318-7
ISSN	1837-9664
ISSN	1837-9664
DOI	10.7150/jca.52118
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Article ; Online: Evidence for Phosphorylation-Dependent, Dynamic, Regulation of mGlu5 and Homer2 in Expression of Cocaine Aversion in Mice.

Szumlinski, Karen K / Beltran, Jacqueline / van Doren, Eliyana / Jimenez Chavez, C Leonardo / Domingo-Gonzalez, Racquel D / Reyes, Cindy M / Ary, Alexis W / Lang, Andrew / Guo, Weiruo / Worley, Paul F / Huber, Kimberly M

eNeuro

2023 Volume 10, Issue 4

Abstract: Cocaine-induced changes in the expression of the glutamate-related scaffolding protein Homer2 influence this drug's psychostimulant and rewarding properties. In response to neuronal activity, Homer2 is phosphorylated on S117/S216 by calcium-calmodulin ... ...

Abstract	Cocaine-induced changes in the expression of the glutamate-related scaffolding protein Homer2 influence this drug's psychostimulant and rewarding properties. In response to neuronal activity, Homer2 is phosphorylated on S117/S216 by calcium-calmodulin kinase IIα (CaMKIIα), which induces a rapid dissociation of mGlu5-Homer2 scaffolds. Herein, we examined the requirement for Homer2 phosphorylation in cocaine-induced changes in mGlu5-Homer2 coupling, to include behavioral sensitivity to cocaine. For this, mice with alanine point mutations at (S117/216)-Homer2 (
MeSH term(s)	Mice ; Animals ; Cocaine/pharmacology ; Mice, Knockout ; Phosphorylation ; Mice, Transgenic ; Conditioning, Psychological
Chemical Substances	Cocaine (I5Y540LHVR)
Language	English
Publishing date	2023-04-25
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2800598-3
ISSN	2373-2822 ; 2373-2822
ISSN (online)	2373-2822
ISSN	2373-2822
DOI	10.1523/ENEURO.0423-22.2023
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Article ; Online: Deficiency of SHANK3 isoforms impairs thermal hyperalgesia and dysregulates the expression of postsynaptic proteins in the spinal cord.

Huang, Min / Pu, Shaofeng / Jiang, Wei / Worley, Paul F / Xu, Tao

Neuroscience research

2020 Volume 163, Page(s) 26–33

Abstract: SHANK3 is one of the scaffolding proteins in the postsynaptic density (PSD). Pain perception and underlying mechanisms were investigated in Shank3 exon 21 deficient ( ... ...

Abstract	SHANK3 is one of the scaffolding proteins in the postsynaptic density (PSD). Pain perception and underlying mechanisms were investigated in Shank3 exon 21 deficient (Shank3
MeSH term(s)	Animals ; Freund's Adjuvant ; Hyperalgesia/chemically induced ; Mice ; Microfilament Proteins ; Nerve Tissue Proteins/genetics ; Pain ; Protein Isoforms ; Spinal Cord
Chemical Substances	Microfilament Proteins ; Nerve Tissue Proteins ; Protein Isoforms ; Shank3 protein, mouse ; Freund's Adjuvant (9007-81-2)
Language	English
Publishing date	2020-03-05
Publishing country	Ireland
Document type	Journal Article
ZDB-ID	605842-5
ISSN	1872-8111 ; 0168-0102 ; 0921-8696
ISSN (online)	1872-8111
ISSN	0168-0102 ; 0921-8696
DOI	10.1016/j.neures.2020.03.001
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Zs.A 1993: Show issues

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Article ; Online: The neuronal pentraxin Nptx2 regulates complement activity and restrains microglia-mediated synapse loss in neurodegeneration.

Zhou, Jiechao / Wade, Sarah D / Graykowski, David / Xiao, Mei-Fang / Zhao, Binhui / Giannini, Lucia A A / Hanson, Jesse E / van Swieten, John C / Sheng, Morgan / Worley, Paul F / Dejanovic, Borislav

Science translational medicine

2023 Volume 15, Issue 689, Page(s) eadf0141

Abstract: Complement overactivation mediates microglial synapse elimination in neurological diseases such as Alzheimer's disease (AD) and frontotemporal dementia (FTD), but how complement activity is regulated in the brain remains largely unknown. We identified ... ...

Abstract	Complement overactivation mediates microglial synapse elimination in neurological diseases such as Alzheimer's disease (AD) and frontotemporal dementia (FTD), but how complement activity is regulated in the brain remains largely unknown. We identified that the secreted neuronal pentraxin Nptx2 binds complement C1q and thereby regulates its activity in the brain. Nptx2-deficient mice show increased complement activity, C1q-dependent microglial synapse engulfment, and loss of excitatory synapses. In a neuroinflammation culture model and in aged TauP301S mice, adeno-associated virus (AAV)-mediated neuronal overexpression of Nptx2 was sufficient to restrain complement activity and ameliorate microglia-mediated synapse loss. Analysis of human cerebrospinal fluid (CSF) samples from a genetic FTD cohort revealed reduced concentrations of Nptx2 and Nptx2-C1q protein complexes in symptomatic patients, which correlated with elevated C1q and activated C3. Together, these results show that Nptx2 regulates complement activity and microglial synapse elimination in the brain and that diminished Nptx2 concentrations might exacerbate complement-mediated neurodegeneration in patients with FTD.
MeSH term(s)	Humans ; Mice ; Animals ; Aged ; Microglia/metabolism ; Complement C1q/genetics ; Complement C1q/metabolism ; Frontotemporal Dementia/genetics ; Frontotemporal Dementia/metabolism ; Synapses/metabolism ; Complement System Proteins/metabolism
Chemical Substances	neuronal pentraxin ; Complement C1q (80295-33-6) ; Complement System Proteins (9007-36-7)
Language	English
Publishing date	2023-03-29
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2518854-9
ISSN	1946-6242 ; 1946-6234
ISSN (online)	1946-6242
ISSN	1946-6234
DOI	10.1126/scitranslmed.adf0141
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Article ; Online: Homer1a Is Required for Establishment of Contralateral Bias and Maintenance of Ocular Dominance in Mouse Visual Cortex.

Chokshi, Varun / Druciak, Brian / Worley, Paul F / Lee, Hey-Kyoung

The Journal of neuroscience : the official journal of the Society for Neuroscience

2019 Volume 39, Issue 20, Page(s) 3897–3905

Abstract: It is well established across many species that neurons in the primary visual cortex (V1) display preference for visual input from one eye or the other, which is termed ocular dominance (OD). In rodents, V1 neurons exhibit a strong bias toward the ... ...

Abstract	It is well established across many species that neurons in the primary visual cortex (V1) display preference for visual input from one eye or the other, which is termed ocular dominance (OD). In rodents, V1 neurons exhibit a strong bias toward the contralateral eye. Molecular mechanisms of how OD is established and later maintained by plastic changes are largely unknown. Here we report a novel role of an activity-dependent immediate early gene Homer1a (H1a) in these processes. Using both sexes of H1a knock-out (KO) mice, we found that there is basal reduction in the OD index of V1 neurons measured using intrinsic signal imaging. This was because of a reduction in the strength of inputs from the contralateral eye, which is normally dominant in mice. The abnormal basal OD index was not dependent on visual experience and is driven by postnatal expression of H1a. Despite this, H1a KOs still exhibited normal shifts in OD index following a short-term (2-3 d) monocular deprivation (MD) of the contralateral eye with lid suture. However, unlike wild-type counterparts, H1a KOs continued to shift OD index with a longer duration (5-6 d) of MD. The same phenotype was recapitulated in a mouse model that has reduced Homer1 binding to metabotropic glutamate receptor 5 (mGluR5). Our results suggest a novel role of H1a and its interaction with mGluR5 in strengthening contralateral eye inputs during postnatal development to establish normal contralateral bias in mouse V1 without much impact on OD shift with brief MD.
MeSH term(s)	Animals ; Dominance, Ocular/physiology ; Female ; Homer Scaffolding Proteins/genetics ; Homer Scaffolding Proteins/physiology ; Male ; Mice, Inbred C57BL ; Mice, Knockout ; Neurons/physiology ; Photic Stimulation ; Receptor, Metabotropic Glutamate 5/physiology ; Visual Cortex/physiology
Chemical Substances	Grm5 protein, mouse ; Homer Scaffolding Proteins ; Homer1 protein, mouse ; Receptor, Metabotropic Glutamate 5
Language	English
Publishing date	2019-03-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	604637-x
ISSN	1529-2401 ; 0270-6474
ISSN (online)	1529-2401
ISSN	0270-6474
DOI	10.1523/JNEUROSCI.3188-18.2019
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Zs.A 1668: Show issues

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Article ; Online: The calcium channel Orai1 is required for osteoblast development: Studies in a chimeric mouse with variable in vivo Runx-cre deletion of Orai-1.

Robinson, Lisa J / Soboloff, Jonathan / Tourkova, Irina L / Larrouture, Quitterie C / Onwuka, Kelechi M / Papachristou, Dionysios J / Gross, Scott / Hooper, Robert / Samakai, Elsie / Worley, Paul F / Liu, Peng / Tuckermann, Jan / Witt, Michelle R / Blair, Harry C

PloS one

2023 Volume 18, Issue 5, Page(s) e0264596

Abstract: The calcium-selective ion channel Orai1 has a complex role in bone homeostasis, with defects in both bone production and resorption detected in Orai1 germline knock-out mice. To determine whether Orai1 has a direct, cell-intrinsic role in osteoblast ... ...

Abstract	The calcium-selective ion channel Orai1 has a complex role in bone homeostasis, with defects in both bone production and resorption detected in Orai1 germline knock-out mice. To determine whether Orai1 has a direct, cell-intrinsic role in osteoblast differentiation and function, we bred Orai1 flox/flox (Orai1fl/fl) mice with Runx2-cre mice to eliminate its expression in osteoprogenitor cells. Interestingly, Orai1 was expressed in a mosaic pattern in Orai1fl/fl-Runx2-cre bone. Specifically, antibody labeling for Orai1 in vertebral sections was uniform in wild type animals, but patchy regions in Orai1fl/fl-Runx2-cre bone revealed Orai1 loss while in other areas expression persisted. Nevertheless, by micro-CT, bones from Orai1fl/fl-Runx2-cre mice showed reduced bone mass overall, with impaired bone formation identified by dynamic histomorphometry. Cortical surfaces of Orai1fl/fl-Runx2-cre vertebrae however exhibited patchy defects. In cell culture, Orai1-negative osteoblasts showed profound reductions in store-operated Ca2+ entry, exhibited greatly decreased alkaline phosphatase activity, and had markedly impaired substrate mineralization. We conclude that defective bone formation observed in the absence of Orai1 reflects an intrinsic role for Orai1 in differentiating osteoblasts.
MeSH term(s)	Animals ; Mice ; Calcium/metabolism ; Calcium Channels/genetics ; Calcium Channels/metabolism ; Core Binding Factor Alpha 1 Subunit/genetics ; Core Binding Factor Alpha 1 Subunit/metabolism ; Mice, Knockout ; ORAI1 Protein/genetics ; ORAI1 Protein/metabolism ; Osteoblasts/metabolism
Chemical Substances	Calcium (SY7Q814VUP) ; Calcium Channels ; Core Binding Factor Alpha 1 Subunit ; Cre recombinase (EC 2.7.7.-) ; ORAI1 Protein ; Orai1 protein, mouse ; Runx2 protein, mouse
Language	English
Publishing date	2023-05-11
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0264596
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