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Special Issue "Chemokines"

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A special issue of Pharmaceuticals (ISSN 1424-8247).

Deadline for manuscript submissions: closed (30 April 2013)

Special Issue Editor

Guest Editor
Dr. Mark Murphy

Research Immunology, Actelion Pharmaceuticals Ltd, Gewerbestrasse 16, CH- 4123 Allschwil, Switzerland
Website | E-Mail
Interests: immunology; targeted therapies for inflammatory and autoimmune diseases; signal transduction pathways as innovative therapeutic targets; stem cells; protein-protein interactions; targeted therapies for cancer; cytokines/chemokines

Special Issue Information

Submission

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. Papers will be published continuously (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are refereed through a peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Pharmaceuticals is an international peer-reviewed Open Access quarterly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 800 CHF (Swiss Francs).

Published Papers (2 papers)

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Review

Open AccessReview Dynamic Cross Talk between S1P and CXCL12 Regulates Hematopoietic Stem Cells Migration, Development and Bone Remodeling
Pharmaceuticals 2013, 6(9), 1145-1169; doi:10.3390/ph6091145
Received: 28 June 2013 / Revised: 18 August 2013 / Accepted: 4 September 2013 / Published: 23 September 2013
Cited by 10 | PDF Full-text (690 KB) | HTML Full-text | XML Full-text
Abstract
Hematopoietic stem cells (HSCs) are mostly retained in a quiescent non-motile mode in their bone marrow (BM) niches, shifting to a migratory cycling and differentiating state to replenish the blood with mature leukocytes on demand. The balance between the major chemo-attractants CXCL12, predominantly
[...] Read more.
Hematopoietic stem cells (HSCs) are mostly retained in a quiescent non-motile mode in their bone marrow (BM) niches, shifting to a migratory cycling and differentiating state to replenish the blood with mature leukocytes on demand. The balance between the major chemo-attractants CXCL12, predominantly in the BM, and S1P, mainly in the blood, dynamically regulates HSC recruitment to the circulation versus their retention in the BM. During alarm situations, stress-signals induce a decrease in CXCL12 levels in the BM, while S1P levels are rapidly and transiently increased in the circulation, thus favoring mobilization of stem cells as part of host defense and repair mechanisms. Myeloid cytokines, including G-CSF, up-regulate S1P signaling in the BM via the PI3K pathway. Induced CXCL12 secretion from stromal cells via reactive oxygen species (ROS) generation and increased S1P1 expression and ROS signaling in HSCs, all facilitate mobilization. Bone turnover is also modulated by both CXCL12 and S1P, regulating the dynamic BM stromal microenvironment, osteoclasts and stem cell niches which all functionally express CXCL12 and S1P receptors. Overall, CXCL12 and S1P levels in the BM and circulation are synchronized to mutually control HSC motility, leukocyte production and osteoclast/osteoblast bone turnover during homeostasis and stress situations. Full article
(This article belongs to the Special Issue Chemokines)
Open AccessReview Rationale and Means to Target Pro-Inflammatory Interleukin-8 (CXCL8) Signaling in Cancer
Pharmaceuticals 2013, 6(8), 929-959; doi:10.3390/ph6080929
Received: 9 May 2013 / Revised: 3 July 2013 / Accepted: 29 July 2013 / Published: 6 August 2013
Cited by 43 | PDF Full-text (611 KB) | HTML Full-text | XML Full-text
Abstract
It is well established that chronic inflammation underpins the development of a number of human cancers, with pro-inflammatory signaling within the tumor microenvironment contributing to tumor progression and metastasis. CXCL8 is an ELR+ pro-inflammatory CXC-chemokine which mediates its effects via signaling through
[...] Read more.
It is well established that chronic inflammation underpins the development of a number of human cancers, with pro-inflammatory signaling within the tumor microenvironment contributing to tumor progression and metastasis. CXCL8 is an ELR+ pro-inflammatory CXC-chemokine which mediates its effects via signaling through two G protein-coupled receptors, CXCR1 and CXCR2. Elevated CXCL8-CXCR1/2 signaling within the tumor microenvironment of numerous cancers is known to enhance tumor progression via activation of signaling pathways promoting proliferation, angiogenesis, migration, invasion and cell survival. This review provides an overview of established roles of CXCL8-CXCR1/2 signaling in cancer and subsequently, discusses the possible strategies of targeting CXCL8-CXCR1/2 signaling in cancer, covering indirect strategies (e.g., anti-inflammatories, NFκB inhibitors) and direct CXCL8 or CXCR1/2 inhibition (e.g., neutralizing antibodies, small molecule receptor antagonists, pepducin inhibitors and siRNA strategies). Reports of pre-clinical cancer studies and clinical trials using CXCL8-CXCR1/2-targeting strategies for the treatment of inflammatory diseases will be discussed. The future translational opportunities for use of such agents in oncology will be discussed, with emphasis on exploitation in stratified populations. Full article
(This article belongs to the Special Issue Chemokines)

Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.

Type of Paper: Review
Title: Orthosteric and Allosteric Ligand Interactions within the Chemokine System-­‐Implications for Future Drug Design
Authors: Stefanie Thiele and Mette M. Rosenkilde
Affiliation: The Laboratory of Molecular Pharmacology, Department of Neuroscience and Pharmacology, University of Copenhagen, The Panum Institute, Copenhagen, DK-2200, Denmark
Abstract: Chemokine receptors are class A 7TM receptors, thereby belonging to the largest protein group in the human genome. Together with their peptide ligands they control cell migration, and have been targets for drug development resulting in numerous small molecule drug candidates. Given the large size and extracellular receptor interaction of chemokines with their receptors, small molecules often act in an allosteric mode with a site within the transmembrane domain, and studies showing their probe-­‐dependent and receptor-­‐dependent character are accumulating. This mode of action is in clear contrast to prototype class A 7TM receptors, such as the adrenergic receptors, or class C 7TM receptors in which small molecule allosteric sites are often found in the extracellular domains. Here, the structural knowledge on chemokine and small-­‐molecule ligand interaction with chemokine receptors is reviewed, providing the basis for understanding the diversity of allosteric interactions in chemokine receptors.

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