<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Agostinis, Chiara</style></author><author><style face="normal" font="default" size="100%">Vidergar, Romana</style></author><author><style face="normal" font="default" size="100%">Belmonte, Beatrice</style></author><author><style face="normal" font="default" size="100%">Mangogna, Alessandro</style></author><author><style face="normal" font="default" size="100%">Amadio, Leonardo</style></author><author><style face="normal" font="default" size="100%">Geri, Pietro</style></author><author><style face="normal" font="default" size="100%">Borelli, Violetta</style></author><author><style face="normal" font="default" size="100%">Zanconati, Fabrizio</style></author><author><style face="normal" font="default" size="100%">Tedesco, Francesco</style></author><author><style face="normal" font="default" size="100%">Confalonieri, Marco</style></author><author><style face="normal" font="default" size="100%">Tripodo, Claudio</style></author><author><style face="normal" font="default" size="100%">Kishore, Uday</style></author><author><style face="normal" font="default" size="100%">Bulla, Roberta</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Complement Protein C1q Binds to Hyaluronic Acid in the Malignant Pleural Mesothelioma Microenvironment and Promotes Tumor Growth.</style></title><secondary-title><style face="normal" font="default" size="100%">Front Immunol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Front Immunol</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2017</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2017</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">8</style></volume><pages><style face="normal" font="default" size="100%">1559</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;C1q is the first recognition subcomponent of the complement classical pathway, which acts toward the clearance of pathogens and apoptotic cells. C1q is also known to modulate a range of functions of immune and non-immune cells, and has been shown to be involved in placental development and sensorial synaptic pruning. We have recently shown that C1q can promote tumor by encouraging their adhesion, migration, and proliferation in addition to angiogenesis and metastasis. In this study, we have examined the role of human C1q in the microenvironment of malignant pleural mesothelioma (MPM), a rare form of cancer commonly associated with exposure to asbestos. We found that C1q was highly expressed in all MPM histotypes, particularly in epithelioid rather than in sarcomatoid histotype. C1q avidly bound high and low molecular weight hyaluronic acid (HA)  its globular domain. C1q bound to HA was able to induce adhesion and proliferation of mesothelioma cells (MES)  enhancement of ERK1/2, SAPK/JNK, and p38 phosphorylation; however, it did not activate the complement cascade. Consistent with the modular organization of the globular domain, we demonstrated that C1q may bind to HA through ghA module, whereas it may interact with human MES through the ghC. In conclusion, C1q highly expressed in MPM binds to HA and enhances the tumor growth promoting cell adhesion and proliferation. These data can help develop novel diagnostic markers and molecular targets for MPM.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/29209316?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Bulla, Roberta</style></author><author><style face="normal" font="default" size="100%">Tripodo, Claudio</style></author><author><style face="normal" font="default" size="100%">Rami, Damiano</style></author><author><style face="normal" font="default" size="100%">Ling, Guang Sheng</style></author><author><style face="normal" font="default" size="100%">Agostinis, Chiara</style></author><author><style face="normal" font="default" size="100%">Guarnotta, Carla</style></author><author><style face="normal" font="default" size="100%">Zorzet, Sonia</style></author><author><style face="normal" font="default" size="100%">Durigutto, Paolo</style></author><author><style face="normal" font="default" size="100%">Botto, Marina</style></author><author><style face="normal" font="default" size="100%">Tedesco, Francesco</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">C1q acts in the tumour microenvironment as a cancer-promoting factor independently of complement activation.</style></title><secondary-title><style face="normal" font="default" size="100%">Nat Commun</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Nat Commun</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Apoptosis</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Line, Tumor</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Movement</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Proliferation</style></keyword><keyword><style  face="normal" font="default" size="100%">Complement Activation</style></keyword><keyword><style  face="normal" font="default" size="100%">Complement C1q</style></keyword><keyword><style  face="normal" font="default" size="100%">Complement C3</style></keyword><keyword><style  face="normal" font="default" size="100%">Complement C5</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice, Inbred C57BL</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice, Knockout</style></keyword><keyword><style  face="normal" font="default" size="100%">Neoplasms</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2016</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2016</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">7</style></volume><pages><style face="normal" font="default" size="100%">10346</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Complement C1q is the activator of the classical pathway. However, it is now recognized that C1q can exert functions unrelated to complement activation. Here we show that C1q, but not C4, is expressed in the stroma and vascular endothelium of several human malignant tumours. Compared with wild-type (WT) or C3- or C5-deficient mice, C1q-deficient (C1qa(-/-)) mice bearing a syngeneic B16 melanoma exhibit a slower tumour growth and prolonged survival. This effect is not attributable to differences in the tumour-infiltrating immune cells. Tumours developing in WT mice display early deposition of C1q, higher vascular density and an increase in the number of lung metastases compared with C1qa(-/-) mice. Bone marrow (BM) chimeras between C1qa(-/-) and WT mice identify non-BM-derived cells as the main local source of C1q that can promote cancer cell adhesion, migration and proliferation. Together these findings support a role for locally synthesized C1q in promoting tumour growth.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/26831747?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Bossi, Fleur</style></author><author><style face="normal" font="default" size="100%">Tripodo, Claudio</style></author><author><style face="normal" font="default" size="100%">Rizzi, Lucia</style></author><author><style face="normal" font="default" size="100%">Bulla, Roberta</style></author><author><style face="normal" font="default" size="100%">Agostinis, Chiara</style></author><author><style face="normal" font="default" size="100%">Guarnotta, Carla</style></author><author><style face="normal" font="default" size="100%">Munaut, Carine</style></author><author><style face="normal" font="default" size="100%">Baldassarre, Gustavo</style></author><author><style face="normal" font="default" size="100%">Papa, Giovanni</style></author><author><style face="normal" font="default" size="100%">Zorzet, Sonia</style></author><author><style face="normal" font="default" size="100%">Ghebrehiwet, Berhane</style></author><author><style face="normal" font="default" size="100%">Ling, Guang Sheng</style></author><author><style face="normal" font="default" size="100%">Botto, Marina</style></author><author><style face="normal" font="default" size="100%">Tedesco, Francesco</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">C1q as a unique player in angiogenesis with therapeutic implication in wound healing.</style></title><secondary-title><style face="normal" font="default" size="100%">Proc Natl Acad Sci U S A</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Proc. Natl. Acad. Sci. U.S.A.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Proliferation</style></keyword><keyword><style  face="normal" font="default" size="100%">Complement C1q</style></keyword><keyword><style  face="normal" font="default" size="100%">DNA Primers</style></keyword><keyword><style  face="normal" font="default" size="100%">Endothelial Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Enzyme-Linked Immunosorbent Assay</style></keyword><keyword><style  face="normal" font="default" size="100%">Human Umbilical Vein Endothelial Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Immunoblotting</style></keyword><keyword><style  face="normal" font="default" size="100%">Immunohistochemistry</style></keyword><keyword><style  face="normal" font="default" size="100%">In Situ Hybridization</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice, Inbred C57BL</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice, Knockout</style></keyword><keyword><style  face="normal" font="default" size="100%">Neovascularization, Physiologic</style></keyword><keyword><style  face="normal" font="default" size="100%">Rats</style></keyword><keyword><style  face="normal" font="default" size="100%">Rats, Wistar</style></keyword><keyword><style  face="normal" font="default" size="100%">Real-Time Polymerase Chain Reaction</style></keyword><keyword><style  face="normal" font="default" size="100%">Wound Healing</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2014</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2014 Mar 18</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">111</style></volume><pages><style face="normal" font="default" size="100%">4209-14</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;We have previously shown that C1q is expressed on endothelial cells (ECs) of newly formed decidual tissue. Here we demonstrate that C1q is deposited in wound-healing skin in the absence of C4 and C3 and that C1q mRNA is locally expressed as revealed by real-time PCR and in situ hybridization. C1q was found to induce permeability of the EC monolayer, to stimulate EC proliferation and migration, and to promote tube formation and sprouting of new vessels in a rat aortic ring assay. Using a murine model of wound healing we observed that vessel formation was defective in C1qa(-/-) mice and was restored to normal after local application of C1q. The mean vessel density of wound-healing tissue and the healed wound area were significantly increased in C1q-treated rats. On the basis of these results we suggest that C1q may represent a valuable therapeutic agent that can be used to treat chronic ulcers or other pathological conditions in which angiogenesis is impaired, such as myocardial ischemia.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">11</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/24591625?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Carlino, Claudia</style></author><author><style face="normal" font="default" size="100%">Trotta, Eleonora</style></author><author><style face="normal" font="default" size="100%">Stabile, Helena</style></author><author><style face="normal" font="default" size="100%">Morrone, Stefania</style></author><author><style face="normal" font="default" size="100%">Bulla, Roberta</style></author><author><style face="normal" font="default" size="100%">Soriani, Alessandra</style></author><author><style face="normal" font="default" size="100%">Iannitto, Maria Luisa</style></author><author><style face="normal" font="default" size="100%">Agostinis, Chiara</style></author><author><style face="normal" font="default" size="100%">Mocci, Carlo</style></author><author><style face="normal" font="default" size="100%">Minozzi, Massimo</style></author><author><style face="normal" font="default" size="100%">Aragona, Cesare</style></author><author><style face="normal" font="default" size="100%">Perniola, Giorgia</style></author><author><style face="normal" font="default" size="100%">Tedesco, Francesco</style></author><author><style face="normal" font="default" size="100%">Sozzani, Silvano</style></author><author><style face="normal" font="default" size="100%">Santoni, Angela</style></author><author><style face="normal" font="default" size="100%">Gismondi, Angela</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Chemerin regulates NK cell accumulation and endothelial cell morphogenesis in the decidua during early pregnancy.</style></title><secondary-title><style face="normal" font="default" size="100%">J Clin Endocrinol Metab</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J. Clin. Endocrinol. Metab.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Capillaries</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Movement</style></keyword><keyword><style  face="normal" font="default" size="100%">Chemokines</style></keyword><keyword><style  face="normal" font="default" size="100%">Decidua</style></keyword><keyword><style  face="normal" font="default" size="100%">Endothelial Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Killer Cells, Natural</style></keyword><keyword><style  face="normal" font="default" size="100%">MAP Kinase Signaling System</style></keyword><keyword><style  face="normal" font="default" size="100%">Neovascularization, Physiologic</style></keyword><keyword><style  face="normal" font="default" size="100%">Pregnancy</style></keyword><keyword><style  face="normal" font="default" size="100%">Pregnancy Trimester, First</style></keyword><keyword><style  face="normal" font="default" size="100%">Receptors, Chemokine</style></keyword><keyword><style  face="normal" font="default" size="100%">RNA, Messenger</style></keyword><keyword><style  face="normal" font="default" size="100%">Stromal Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Trophoblasts</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2012</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2012 Oct</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">97</style></volume><pages><style face="normal" font="default" size="100%">3603-12</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;CONTEXT: &lt;/b&gt;Although decidual natural killer (NK) cell accumulation and vascular remodeling are critical steps to ensure successful pregnancy, the molecular mechanisms controlling these events are poorly defined.&lt;/p&gt;&lt;p&gt;&lt;b&gt;OBJECTIVE: &lt;/b&gt;Herein we analyzed whether chemerin, a recently identified chemoattractant involved in many pathophysiological processes, could be expressed in the uterine compartment and could regulate events relevant for the good outcome of pregnancy.&lt;/p&gt;&lt;p&gt;&lt;b&gt;DESIGN: &lt;/b&gt;Chemerin expression in human primary culture of stromal (ST) cells, extravillous trophoblast cells, and decidual endothelial cells (DEC) was analyzed by RT-PCR, ELISA, and Western blot. Migration through ST or DEC of peripheral blood and decidual (d) NK cells from pregnant women was performed using a transwell assay. A DEC capillary-like tube formation assay was used to evaluate endothelial morphogenesis.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;Chemerin is differentially expressed by decidual cells during early pregnancy being present at high levels in ST and extravillous trophoblast cells but not in DEC. Notably, ST cells from pregnant women exhibit and release higher levels of chemerin as compared with ST cells from menopausal or fertile nonpregnant women. Chemerin can support peripheral blood NK cell migration through both DEC and ST cells. Although dNK cells exhibit lower chemerin receptor (CMKLR1) expression than their blood counterpart, CMKLR1 engagement on dNK cells resulted in both ERK activation and migration through decidual ST cells. Interestingly, DEC also express CMKLR1 and undergo ERK activation and capillary-like tube structure formation upon exposure to chemerin.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;Our data indicate that chemerin is up-regulated during decidualization and might contribute to NK cell accumulation and vascular remodeling during early pregnancy.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">10</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/22791765?dopt=Abstract</style></custom1></record></records></xml>