PECAM-1 (CD31) expression in the central nervous system and its role in experimental allergic encephalomyelitis in the rat

Williams, Kenneth C.; Zhao, Richard W; Ueno, Keisuke; Hickey, William F.

doi:10.1002/(sici)1097-4547(19960915)45:6<747::aid-jnr11>3.0.co;2-t

Cited by 55 publications

(18 citation statements)

References 27 publications

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“…For single staining of c-Fos protein or IL-1R1, free-floating sections were pretreated with 0.3% H2O2 in PBS for 30 min, followed by 1% bovine serum albumin in PBS for 2 h, and then incubated in goat anti-IL-1R1 antibody (AF771; 1:1000; R&D Systems, Minneapolis, MN) or rabbit anti-c-Fos antibody (PC38 (Ab-5); 1:10,000; Millipore) in 0.3% Triton X-100 in PBS (PBST) at 4°C for 60 h, washed three times with 0.03% PBST, and processed using a Vectastain ABC kit (Vector Labs, Burlingame, CA). For dual-or triple-labeling immunofluorescence, free-floating sections were treated with rat anti-CD31 antibody (MCA2388GA; 1:1000; Serotec, Düsseldorf, Germany) as a marker for endothelial cells (Williams et al, 1996) or rat anti-CD206 antibody (MCA2235; 1:1000; Serotec) as a marker for perivascular macrophages (Galea et al, 2005), together with the antibodies against GFP (ab13970, made in chicken; 1:1000; Abcam, Cambridge, UK) or IL-1R1 and Cox-2 (sc-1747-R, made in rabbit; 1:1000; Santa Cruz Biotechnology, Santa Cruz, CA). Bound primary antibody was then detected with Alexa Fluor Dyes-conjugated secondary antibodies (405 donkey anti-rat IgG, 488 donkey anti-goat IgG, and 555 donkey anti-rabbit IgG; 1:1000; Invitrogen, Carlsbad, CA).…”

Section: Hormone Assaysmentioning

confidence: 99%

Interleukin-1β induced activation of the hypothalamus–pituitary–adrenal axis is dependent on interleukin-1 receptors on non-hematopoietic cells

Matsuwaki

Eskilsson

Kugelberg

et al. 2014

Brain, Behavior, and Immunity

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The proinflammatory cytokine interleukin-1β (IL-1β) plays a major role in the signal transduction of immune stimuli from the periphery to the central nervous system, and has been shown to be an important mediator of the immune-induced stress hormone release. The signaling pathway by which IL-1β exerts this function involves the bloodbrain-barrier and induced central prostaglandin synthesis, but the identity of the bloodbrain-barrier cells responsible for this signal transduction has been unclear, with both endothelial cells and perivascular macrophages suggested as critical components. Here, using an irradiation and transplantation strategy, we generated mice expressing IL-1 type 1 receptors (IL-1R1) either in hematopoietic or non-hematopoietic cells and subjected these mice to peripheral immune challenge with IL-1β. Following both intraperitoneal and intravenous administration of IL-1β, mice lacking IL-1R1 in hematopoietic cells showed induced expression of the activity marker c-Fos in the paraventricular hypothalamic nucleus, and increased plasma levels of ACTH and corticosterone. In contrast, these responses were not observed in mice with IL-1R1 expression only in hematopoietic cells. Immunoreactivity for IL-1R1 was detected in brain vascular cells that displayed induced expression of the prostaglandin synthesizing enzyme cyclooxygenase-2 and that were immunoreactive for the endothelial cell marker CD31, but was not seen in cell positive for the brain macrophage marker CD206. These results imply that activation of the HPA-axis by IL-1β is dependent on IL-1R1s on nonhematopoietic cells, such as brain endothelial cells, and that IL-1R1 on perivascular macrophages are not involved. Matsuwaki et al., p. 3

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Section: Hormone Assaysmentioning

confidence: 99%

Interleukin-1β induced activation of the hypothalamus–pituitary–adrenal axis is dependent on interleukin-1 receptors on non-hematopoietic cells

Matsuwaki

Eskilsson

Kugelberg

et al. 2014

Brain, Behavior, and Immunity

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“…The TA-2, WT.3 and TLD-3A12 mAbs have been shown to inhibit leukocyte migration to arthritic joints and dermal inflammation or to decrease T-cell proliferation (Issekutz & Issekutz, 1995;Issekutz AC et al, 1996;Issekutz TB et al, 1996;Williams et al, 1996). The TA-2 mAb is directed against the a 4 subunit and therefore recognizes two integrins sharing this subunit, a 4 /b 1 and a 4 /b 7 .…”

Section: Antibodiesmentioning

confidence: 99%

Selectins and integrins but not platelet–endothelial cell adhesion molecule‐1 regulate opioid inhibition of inflammatory pain

Machelska

Brack

Mousa

et al. 2004

British J Pharmacology

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1 Control of inflammatory pain can result from activation of opioid receptors on peripheral sensory nerves by opioid peptides secreted from leukocytes in response to stress (e.g. experimental swim stress or surgery). The extravasation of immunocytes to injured tissues involves rolling, adhesion and transmigration through the vessel wall, orchestrated by various adhesion molecules. 2 Here we evaluate the relative contribution of selectins, integrins a 4 and b 2 , and platelet-endothelial cell adhesion molecule-1 (PECAM-1) to the opioid-mediated inhibition of inflammatory pain. 3 We use flow cytometry, double immunofluorescence and nociceptive (paw pressure) testing in rats with unilateral hind paw inflammation induced by complete Freund's adjuvant. 4 In inflamed tissue, 43-58% of hematopoietic cells (CD45 þ ) expressed opioid peptides. L-selectin and b 2 were coexpressed by 7 and 98% of opioid-containing leukocytes, respectively. Alpha 4 integrin was expressed in low levels by the majority of leukocytes. Opioid-containing cells, vascular P-and E-selectin and PECAM-1 were simultaneously upregulated. 5 Swim stress produced potent opioid-mediated antinociception in inflamed tissue, unaffected by blockade of PECAM-1. However, blockade of L-and P-selectins by fucoidin, or of a 4 and b 2 by monoclonal antibodies completely abolished peripheral stress-induced antinociception. This coincided with a 40% decrease in the migration of opioid-containing leukocytes to inflamed tissue. 6 These findings establish selectins and integrins a 4 and b 2 , but not PECAM-1, as important molecules involved in stress-induced opioid-mediated antinociception in inflammation. They point to a cautious use of anti-inflammatory treatments applying anti-selectin, anti-a 4 and anti-b 2 strategies because they may impair intrinsic pain inhibition.

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“…Serial frozen sections (7 m) of subcutaneous tumor or whole brain were stained in the following ways: (1) hematoxylin and eosin for tumor cell volumes and infiltrating granulocytes; (2) indirect immunoperoxidase with the rat anti-mouse PECAM monoclonal antibody (MAB) (PharMingen, San Diego, CA, USA) or mouse anti-rat PECAM MAB (Endogen, Woburn, MA, USA) for vascular endothelial cells in mouse 7,37,42 or rat 43,44 tissue respectively; (3) indirect immunoperoxidase with the mouse anti-rat RT1.B class II MAB (HIS 19; Serotec, Oxford, UK), the mouse anti-rat RT1.A MHC class I MAB (Ox-18; Serotec), the rat anti-mouse IFN-␥ MAB (XMG1-2), the mouse anti-rat CD3 + /TcR MAB (453(MCA)), the mouse anti-rat CD4 + MAB (W3/25), the mouse anti-rat CD8 + MAB (Ox8) or the mouse anti-rat macrophage MAB (ED1) (gifts from P Motram, The University of Melbourne); (4) ␤-galactosidase staining for visualization of RPC and transduced cells. 24 Vascular density was calculated by counting the number of vessels in 10 random standard fields (0.55 × 0.4 mm) in five sections per tumor.…”

Section: Histological Analysis Of Tissuementioning

confidence: 99%

The treatment of established intracranial tumors by in situ retroviral IFN-γ transfer

et al. 2000

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Current treatments for malignant gliomas are still largely ineffective in significantly improving prognosis. We have investigated the efficacy of treating established rat C6 glioma by in situ retroviral delivery of IFN-␥ cDNA. Ecotropic retrovirus packaging cells were transfected with a retroviral vector containing the mouse IFN-␥ gene. The IFN-␥ packaging cells were stereotactically implanted into established intracranial C6 glioma in immunocompetent Wistar rats, resulting in the eradication of these tumors. All IFN-␥-treated rats survived to 92 days after C6 implantation (an arbitrary

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PECAM-1 (CD31) expression in the central nervous system and its role in experimental allergic encephalomyelitis in the rat

Cited by 55 publications

References 27 publications

Interleukin-1β induced activation of the hypothalamus–pituitary–adrenal axis is dependent on interleukin-1 receptors on non-hematopoietic cells

Interleukin-1β induced activation of the hypothalamus–pituitary–adrenal axis is dependent on interleukin-1 receptors on non-hematopoietic cells

Selectins and integrins but not platelet–endothelial cell adhesion molecule‐1 regulate opioid inhibition of inflammatory pain

The treatment of established intracranial tumors by in situ retroviral IFN-γ transfer

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