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10.1371/journal.pone.0151765 http://scihub22266oqcxt.onion/10.1371/journal.pone.0151765 C4801399!4801399 !26998906     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26998906 &cmd=llinks): Failed to open stream: HTTP request failed! 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Impact of a CXCL12/CXCR4 Antagonist in Bleomycin (BLM) Induced Pulmonary Fibrosis and Carbon Tetrachloride (CCl4) Induced Hepatic Fibrosis in Mice |pdf=|usr=}}{{26998906 }} gab.com Text Impact of a CXCL12/CXCR4 Antagonist in Bleomycin (BLM) Induced Pulmonary Fibrosis and Carbon Tetrachloride (CCl4) Induced Hepatic Fibrosis in Mice JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=26998906 #FOAvip Modulation of chemokine CXCL12 and its receptor CXCR4 has been implicated in attenuation of bleomycin (BLM)-induced pulmonary fibrosis and carbon tetrachloride (CCl4)-induced hepatic injury. In pulmonary fibrosis, published reports suggest that collagen production in the injured lung is derived from fibrocytes recruited from the circulation in response to release of pulmonary CXCL12. Conversely, in hepatic fibrosis, resident hepatic stellate cells (HSC), the key cell type in progression of fibrosis, upregulate CXCR4 expression in response to activation. Further, CXCL12 induces HSC proliferation and subsequent production of collagen I. In the current study, we evaluated AMD070, an orally bioavailable inhibitor of CXCL12/CXCR4 in alleviating BLM-induced pulmonary and CCl4-induced hepatic fibrosis in mice. Similar to other CXCR4 antagonists, treatment with AMD070 significantly increased leukocyte mobilization. However, in these two models of fibrosis, AMD070 had a negligible impact on extracellular matrix deposition. Interestingly, our results indicated that CXCL12/CXCR4 signaling has a role in improving mortality associated with BLM induced pulmonary injury, likely through dampening an early inflammatory response and/or vascular leakage. Together, these findings indicate that the CXCL12-CXCR4 signaling axis is not an effective target for reducing fibrosis. Twit Text FOAVip Impact of a CXCL12/CXCR4 Antagonist in Bleomycin (BLM) Induced Pulmonary Fibrosis and Carbon Tetrachloride (CCl4) Induced Hepatic Fibrosis in Mice ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=26998906 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26998906 #FOAvip English Wikipedia <ref>{{Cite pmid|26998906 }}</ref> Impact of a CXCL12/CXCR4 Antagonist in Bleomycin (BLM) Induced Pulmonary Fibrosis and Carbon Tetrachloride (CCl4) Induced Hepatic Fibrosis in Mice #MMPMID26998906 Chow LN ; Schreiner P ; Ng BY ; Lo B ; Hughes MR ; Scott RW ; Gusti V ; Lecour S ; Simonson E ; Manisali I ; Barta I ; McNagny KM ; Crawford J ; Webb M ; Underhill TM PLoS One 2016[]; 11 (3 ): e0151765 PMID26998906 show ga Modulation of chemokine CXCL12 and its receptor CXCR4 has been implicated in attenuation of bleomycin (BLM)-induced pulmonary fibrosis and carbon tetrachloride (CCl4)-induced hepatic injury. In pulmonary fibrosis, published reports suggest that collagen production in the injured lung is derived from fibrocytes recruited from the circulation in response to release of pulmonary CXCL12. Conversely, in hepatic fibrosis, resident hepatic stellate cells (HSC), the key cell type in progression of fibrosis, upregulate CXCR4 expression in response to activation. Further, CXCL12 induces HSC proliferation and subsequent production of collagen I. In the current study, we evaluated AMD070, an orally bioavailable inhibitor of CXCL12/CXCR4 in alleviating BLM-induced pulmonary and CCl4-induced hepatic fibrosis in mice. Similar to other CXCR4 antagonists, treatment with AMD070 significantly increased leukocyte mobilization. However, in these two models of fibrosis, AMD070 had a negligible impact on extracellular matrix deposition. Interestingly, our results indicated that CXCL12/CXCR4 signaling has a role in improving mortality associated with BLM induced pulmonary injury, likely through dampening an early inflammatory response and/or vascular leakage. Together, these findings indicate that the CXCL12-CXCR4 signaling axis is not an effective target for reducing fibrosis. |Aminoquinolines [MESH] |Animals [MESH] |Benzimidazoles [MESH] |Bleomycin [MESH] |Butylamines [MESH] |Carbon Tetrachloride [MESH] |Chemokine CXCL12/*antagonists & inhibitors/metabolism [MESH] |Disease Models, Animal [MESH] |Female [MESH] |Heterocyclic Compounds, 1-Ring/administration & dosage/pharmacokinetics/pharmacology/*therapeutic use [MESH] |Liver Cirrhosis/blood/chemically induced/complications/*drug therapy [MESH] |Lung/pathology [MESH] |Lymphocytes/drug effects [MESH] |Mice, Inbred C57BL [MESH] |Pneumonia/blood/complications/drug therapy [MESH] |Pulmonary Fibrosis/blood/chemically induced/complications/*drug therapy [MESH] |Receptors, CXCR4/*antagonists & inhibitors/metabolism [MESH]Impact of a CXCL12/CXCR4 Antagonist in Bleomycin (BLM) Induced Pulmona(epmc).pdf DeepDyve Pubget Overpricing