LPS-induced expression of a novel chemokine receptor (L-CCR) in mouse glial cells in vitro and in vivo

Mike W. Zuurman; Joost Heeroma; Nieske Brouwer; Hendrikus W.G.M. Boddeke; Knut Biber

doi:10.1002/glia.10156

Molecular cloning of two human cellular retinoic acid-binding proteins (CRABP). Retinoic acid-induced expression of CRABP-II but not CRABP-I in adult human skin in vivo and in skin fibroblasts in vitro.

Journal of Biological Chemistry ◽

10.1016/s0021-9258(19)47422-x ◽

1991 ◽

Vol 266 (26) ◽

pp. 17662-17666 ◽

Cited By ~ 3

Author(s):

A. Aström ◽

A. Tavakkol ◽

U. Pettersson ◽

M. Cromie ◽

J.T. Elder ◽

...

Keyword(s):

Retinoic Acid ◽

Molecular Cloning ◽

Human Skin ◽

Induced Expression ◽

Crabp I ◽

Retinoic Acid Binding Proteins ◽

Crabp Ii ◽

Adult Human Skin

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Neuroprotective Effects of the FGF21 Analogue LY2405319

Journal of Alzheimer s Disease ◽

10.3233/jad-200837 ◽

2021 ◽

pp. 1-13

Author(s):

Claire Rühlmann ◽

David Dannehl ◽

Marcus Brodtrück ◽

Andrew C. Adams ◽

Jan Stenzel ◽

...

Keyword(s):

Glial Cells ◽

Neuroprotective Effect ◽

Amyloid Β ◽

Fibroblast Growth Factor 21 ◽

Neuroprotective Effects ◽

Organotypic Brain Slice ◽

Brain Slice Cultures ◽

Abca1 Mrna

Background: To date, there are no effective treatments for Alzheimer’s disease (AD). Thus, a significant need for research of therapies remains. Objective: One promising pharmacological target is the hormone fibroblast growth factor 21 (FGF21), which is thought to be neuroprotective. A clinical candidate for medical use could be the FGF21 analogue LY2405319 (LY), which has a specificity and potency comparable to FGF21. Methods: The present study investigated the potential neuroprotective effect of LY via PPARγ/apoE/abca1 pathway which is known to degrade amyloid-β (Aβ) plaques by using primary glial cells and hippocampal organotypic brain slice cultures (OBSCs) from 30- and 50-week-old transgenic APPswe/PS1dE9 (tg) mice. By LY treatment of 52-week-old tg mice with advanced Aβ deposition, we further aimed to elaborate the effect of LY on AD pathology in vivo. Results: LY application to primary glial cells caused an upregulation of pparγ, apoE, and abca1 mRNA expression and significantly decreased number and area of Aβ plaques in OBSCs. LY treatment in tg mice increased cerebral [18F] FDG uptake and N-acetylaspartate/creatine ratio indicating enhanced neuronal activity and integrity. Although LY did not reduce the number of Aβ plaques in tg mice, the number of iba1-positive cells was significantly decreased indicating reduced microgliosis. Conclusion: These data identified LY in vitro as an activator of Aβ degrading genes leading to cerebral Aβ load amelioration in early and late AD pathology. Although Aβ plaque reduction by LY failed in vivo, LY may be used as therapeutic agent to treat AD-related neuroinflammation and impaired neuronal integrity.

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Carbon Monoxide Inhibits Tenascin-C Mediated Inflammation via IL-10 Expression in a Septic Mouse Model

Mediators of Inflammation ◽

10.1155/2015/613249 ◽

2015 ◽

Vol 2015 ◽

pp. 1-14 ◽

Cited By ~ 7

Author(s):

Md. Jamal Uddin ◽

Chun-shi Li ◽

Yeonsoo Joe ◽

Yingqing Chen ◽

Qinggao Zhang ◽

...

Keyword(s):

Carbon Monoxide ◽

Proinflammatory Cytokines ◽

Tissue Injury ◽

Inflammatory Diseases ◽

Septic Mouse ◽

Induced Expression ◽

Tenascin C ◽

Co Gas

Tenascin-C (TN-C), an extracellular matrix (ECM) glycoprotein, is specifically induced upon tissue injury and infection and during septic conditions. Carbon monoxide (CO) gas is known to exert various anti-inflammatory effects in various inflammatory diseases. However, the mechanisms underlying the effect of CO on TN-C-mediated inflammation are unknown. In the present study, we found that treatment with LPS significantly enhanced TN-C expression in macrophages. CO gas, or treatment with the CO-donor compound, CORM-2, dramatically reduced LPS-induced expression of TN-C and proinflammatory cytokines while significantly increased the expression of IL-10. Treatment with TN-C siRNA significantly suppressed the effects of LPS on proinflammatory cytokines production. TN-C siRNA did not affect the CORM-2-dependent increase of IL-10 expression. In cells transfected with IL-10 siRNA, CORM-2 had no effect on the LPS-induced expression of TN-C and its downstream cytokines. These data suggest that IL-10 mediates the inhibitory effect of CO on TN-C and the downstream production of proinflammatory cytokines. Additionally, administration of CORM-2 dramatically reduced LPS-induced TN-C and proinflammatory cytokines production while expression of IL-10 was significantly increased. In conclusion, CO regulated IL-10 expression and thus inhibited TN-C-mediated inflammationin vitroandin vivo.

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Gonadotropin-Induced Expression of Messenger Ribonucleic Acid for Cyclooxygenase-2 and Production of Prostaglandins E and F2α in Bovine Preovulatory Follicles Are Regulated by the Progesterone Receptor

Endocrinology ◽

10.1210/en.2005-1575 ◽

2006 ◽

Vol 147 (10) ◽

pp. 4713-4722 ◽

Cited By ~ 43

Author(s):

P. J. Bridges ◽

C. M. Komar ◽

J. E. Fortune

Keyword(s):

Granulosa Cells ◽

Medroxyprogesterone Acetate ◽

Cyclooxygenase 2 ◽

Induced Expression ◽

Messenger Ribonucleic Acid ◽

Preovulatory Follicles ◽

Gonadotropin Surge ◽

Induced Changes

Follicular production of prostaglandins (PGs) is essential for ovulation, but the factors mediating gonadotropin-induced secretion of PGE and PGF2α remain largely unknown. We tested the hypothesis that gonadotropin-induced changes in progesterone and its receptor (PR) mediate the increase in periovulatory PGs. Heifers were treated with PGF2α and GnRH to induce luteolysis and the LH/FSH surge (ovulation occurs ∼30 h after GnRH). Because there are two increases in intrafollicular progesterone/PR mRNA during the bovine periovulatory period, we first examined the temporal pattern of PG production by follicles collected at 0, 3.5, 6, 12, 18, and 24 h after GnRH. Although PGs did not increase in the follicular fluid until 24 h after GnRH, acute secretion of PGs by follicle wall (theca + granulosa cells) was initiated by 18 h and had increased manyfold by 24 h after GnRH. In vitro, FSH and LH induced dramatic transient increases in PG production by follicle wall and granulosa, but not theca, cells isolated from preovulatory follicles (0 h after GnRH). PG accumulation peaked on d 2 of culture, mimicking the secretion pattern after a gonadotropin surge in vivo. In cultures of follicle wall and granulosa cells, the PR antagonist mifepristone (MIFE, 1 μm) inhibited LH-induced PG secretion and the progestin medroxyprogesterone acetate (1 or 10 μm), but not the glucocorticoid dexamethasone (1 or 10 μm), overcame the effect of MIFE on PGs. Semiquantitative RT-PCR revealed that MIFE inhibited LH-induced expression of cyclooxygenase-2 mRNA in granulosa cells in vitro. Again, treatment with medroxyprogesterone acetate overcame the effect of MIFE. Together these results provide strong evidence that periovulatory increases in cyclooxygenase-2 mRNA, PGE, and PGF2α are mediated by gonadotropin-induced increases in progesterone/PR, indicating that in some species there is an important functional relationship between these pathways in the ovulatory cascade.

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Cc Chemokine Receptor (Ccr)3/Eotaxin Is Followed by Ccr4/Monocyte-Derived Chemokine in Mediating Pulmonary T Helper Lymphocyte Type 2 Recruitment after Serial Antigen Challenge in Vivo

Journal of Experimental Medicine ◽

10.1084/jem.191.2.265 ◽

2000 ◽

Vol 191 (2) ◽

pp. 265-274 ◽

Cited By ~ 230

Author(s):

Clare M. Lloyd ◽

Tracy Delaney ◽

Trang Nguyen ◽

Jane Tian ◽

Carlos Martinez-A ◽

...

Keyword(s):

Chemokine Receptor ◽

Progressive Increase ◽

Allergic Airway Disease ◽

Antigen Challenge ◽

Th2 Cells ◽

T Helper ◽

Cc Chemokine

Isolated peripheral blood CD4 cells from allergic individuals express CC chemokine receptor (CCR)3 and CCR4 after expansion in vitro. In addition, human T helper type 2 (Th2) cells polarized in vitro selectively express CCR3 and CCR4 at certain stages of activation/differentiation and respond preferentially to the ligands eotaxin and monocyte-derived chemokine (MDC). However, controversy arises when the in vivo significance of this distinct expression is discussed. To address the functional role of CCR3/eotaxin and CCR4/MDC during the in vivo recruitment of Th2 cells, we have transferred effector Th cells into naive mice to induce allergic airway disease. Tracking of these cells after repeated antigen challenge has established that both CCR3/eotaxin and CCR4/MDC axes contribute to the recruitment of Th2 cells to the lung, demonstrating the in vivo relevance of the expression of these receptors on Th2 cells. We have shown that involvement of the CCR3/eotaxin pathway is confined to early stages of the response in vivo, whereas repeated antigen stimulation results in the predominant use of the CCR4/MDC pathway. We propose that effector Th2 cells respond to both CCR3/eotaxin and CCR4/MDC pathways initially, but that a progressive increase in CCR4-positive cells results in the predominance of the CCR4/MDC axis in the long-term recruitment of Th2 cells in vivo.

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Matrix metalloproteinase processing of monocyte chemoattractant proteins generates CC chemokine receptor antagonists with anti-inflammatory properties in vivo

Blood ◽

10.1182/blood.v100.4.1160.h81602001160_1160_1167 ◽

2002 ◽

Vol 100 (4) ◽

pp. 1160-1167 ◽

Cited By ~ 392

Author(s):

G. Angus McQuibban ◽

Jiang-Hong Gong ◽

Julie P. Wong ◽

John L. Wallace ◽

Ian Clark-Lewis ◽

...

Keyword(s):

Matrix Metalloproteinase ◽

Chemokine Receptor ◽

Chemokine Receptors ◽

Leukemic Cell ◽

Proteolytic Processing ◽

Cc Chemokine ◽

Monocyte Chemoattractant ◽

The Matrix

Monocyte chemoattractant protein (MCP)–3 is inactivated upon cleavage by the matrix metalloproteinase (MMP) gelatinase A (MMP-2). We investigated the susceptibility to proteolytic processing of the 4 human MCPs by 8 recombinant MMPs to determine whether MCP-3 is an isolated example or represents a general susceptibility of chemokines to proteolytic inactivation by these important inflammatory proteases. In addition to MMP-2, MCP-3 is efficiently cleaved by membrane type 1 (MT1)–MMP, the cellular activator of MMP-2, and by collagenase-1 and collagenase-3 (MMP-1, MMP-13) and stromelysin-1 (MMP-3). Specificity was shown by absence of cleavage by matrilysin (MMP-7) and the leukocytic MMPs neutrophil collagenase (MMP-8) and gelatinase B (MMP-9). The closely related chemokines MCP-1, MCP-2, and MCP-4 were not cleaved by MMP-2 or MT1-MMP, but were cleaved by MMP-1 and MMP-3 with varying efficiency. MCPs were typically cleaved between residues 4 and 5, but MCP-4 was further processed at Val7-Pro8. Synthetic MCP analogs corresponding to the MMP-cleaved forms bound CC chemokine receptor (CCR)–2 and CCR-3, but lacked chemoattractant activity in pre-B cells transfected with CCR-2 and CCR-3 or in THP-1 monocytic cells, a transformed leukemic cell line. Moreover, the truncated products of MCP-2 and MCP-4, like MCP-3, were potent antagonists of their cognate CC chemokine receptors in transwell cell migration assays in vitro. When they were injected 24 hours after the initiation of carrageenan-induced inflammation in rat paws, their in vivo antagonist activities were revealed by a greater than 66% reduction in inflammatory edema progression after 12 hours. We propose that MMPs have an important role in modulating inflammatory and immune responses by processing chemokines in wound healing and in disease.

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Chemokine receptor-mediated delivery directs self-tumor antigen efficiently into the class II processing pathway in vitro and induces protective immunity in vivo

Blood ◽

10.1182/blood-2004-02-0637 ◽

2004 ◽

Vol 104 (7) ◽

pp. 1961-1969 ◽

Cited By ~ 38

Author(s):

A. Biragyn

Keyword(s):

Chemokine Receptor ◽

Tumor Antigen ◽

Protective Immunity ◽

Class Ii

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Differential expression of interferon-γ receptor on human glial cells in vivo and in vitro

Journal of Neuroimmunology ◽

10.1016/j.jneuroim.2010.04.023 ◽

2010 ◽

Vol 225 (1-2) ◽

pp. 91-99 ◽

Cited By ~ 29

Author(s):

Sadayuki Hashioka ◽

Andis Klegeris ◽

Claudia Schwab ◽

Sheng Yu ◽

Patrick L. McGeer

Keyword(s):

Differential Expression ◽

Glial Cells ◽

Interferon Γ

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Mutation of the α-tubulin Tuba1a leads to straighter microtubules and perturbs neuronal migration

The Journal of Cell Biology ◽

10.1083/jcb.201607074 ◽

2017 ◽

Vol 216 (8) ◽

pp. 2443-2461 ◽

Cited By ~ 29

Author(s):

Richard Belvindrah ◽

Kathiresan Natarajan ◽

Preety Shabajee ◽

Elodie Bruel-Jungerman ◽

Jennifer Bernard ◽

...

Keyword(s):

Missense Mutation ◽

Glial Cells ◽

Neuronal Migration ◽

Cortical Malformations ◽

Tubulin Isotype ◽

Modeling Data ◽

Migratory Stream ◽

Β Tubulin

Brain development involves extensive migration of neurons. Microtubules (MTs) are key cellular effectors of neuronal displacement that are assembled from α/β-tubulin heterodimers. Mutation of the α-tubulin isotype TUBA1A is associated with cortical malformations in humans. In this study, we provide detailed in vivo and in vitro analyses of Tuba1a mutants. In mice carrying a Tuba1a missense mutation (S140G), neurons accumulate, and glial cells are dispersed along the rostral migratory stream in postnatal and adult brains. Live imaging of Tuba1a-mutant neurons revealed slowed migration and increased neuronal branching, which correlated with directionality alterations and perturbed nucleus–centrosome (N–C) coupling. Tuba1a mutation led to increased straightness of newly polymerized MTs, and structural modeling data suggest a conformational change in the α/β-tubulin heterodimer. We show that Tuba8, another α-tubulin isotype previously associated with cortical malformations, has altered function compared with Tuba1a. Our work shows that Tuba1a plays an essential, noncompensated role in neuronal saltatory migration in vivo and highlights the importance of MT flexibility in N–C coupling and neuronal-branching regulation during neuronal migration.

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