Articoli di riviste: "Macrophage inhibitory cytokine"

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Colon-Echevarria, Claudia B., Tatiana Ortiz, Lizette Maldonado, Melanie J. Hidalgo-Vargas, Jaileene Pérez-Morales, Alexandra N. Aquino-Acevedo, Roberto Herrera-Noriega, Margarita Bonilla-Claudio, Eida M. Castro e Guillermo N. Armaiz-Pena. "Zoledronic Acid Abrogates Restraint Stress-Induced Macrophage Infiltration, PDGF-AA Expression, and Ovarian Cancer Growth". Cancers 12, n. 9 (18 settembre 2020): 2671. http://dx.doi.org/10.3390/cancers12092671.

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Multiple studies suggest that chronic stress accelerates the growth of existing tumors by activating the sympathetic nervous system. Data suggest that sustained adrenergic signaling can induce tumor growth, secretion of pro-inflammatory cytokines, and macrophage infiltration. Our goal was to study the role of adrenergic-stimulated macrophages in ovarian cancer biology. Cytokine arrays were used to assess the effect of adrenergic stimulation in pro-tumoral cytokine networks. An orthotopic model of ovarian cancer was used to assess the in vivo effect of daily restraint stress on tumor growth and adrenergic-induced macrophages. Cytokine analyses showed that adrenergic stimulation modulated pro-inflammatory cytokine secretion in a SKOV3ip1 ovarian cancer cell/U937 macrophage co-culture system. Among these, platelet-derived growth factor AA (PDGF-AA), epithelial cell-derived neutrophil-activating peptide (ENA-78), Angiogenin, vascular endothelial growth factor (VEGF), granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-5 (IL-5), Lipocalin-2, macrophage migration inhibitory factor (MIF), and transferrin receptor (TfR) were upregulated. Enriched biological processes included cytokine-mediated signaling pathways and positive regulation of cell proliferation. In addition, daily restraint stress increased ovarian cancer growth, infiltration of CD68+ macrophages, and expression of PDGF-AA in orthotopic models of ovarian cancer (SKOV3ip1 and HeyT30), while zoledronic acid, a macrophage-depleting agent, abrogated this effect. Furthermore, in ovarian cancer patients, high PDGFA expression correlated with worse outcomes. Here, it is shown that the adrenergic regulation of macrophages and PDGFA might play a role in ovarian cancer progression.

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Lu, Chunxia, P. Anil Kumar, Yong Fan, Mark A. Sperling e Ram K. Menon. "A Novel Effect of Growth Hormone on Macrophage Modulates Macrophage-Dependent Adipocyte Differentiation". Endocrinology 151, n. 5 (25 febbraio 2010): 2189–99. http://dx.doi.org/10.1210/en.2009-1194.

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The GH receptor (GHR) is expressed on macrophages. However, the precise role of GH in regulation of macrophage function is unclear. We hypothesized that soluble factors including cytokines produced by macrophages in a GH-dependent manner regulate adipogenesis. We confirmed expression and functional integrity of the GHR in the J774A.1 macrophage cells. Conditioned medium (CM) from macrophages inhibited adipogenesis in a 3T3-L1 adipogenesis assay. CM from GH-treated macrophages decreased the inhibitory effect of CM from macrophages on adipogenesis. This effect on preadipocyte differentiation was active only during the first (early) phase of adipocyte differentiation. CM from stromal vascular compartment macrophages of mice with macrophage-specific deletion of the GHR exhibited more inhibitory effect on 3T3-L1 preadipocyte differentiation compared with CM from stromal vascular compartment macrophages of control mice, indicating that intact GH action in primary macrophages also increases preadipocyte differentiation. GH did not increase IGF-1 expression in macrophages. PCR array analysis identified IL-1β as a candidate cytokine whose expression was altered by GH in macrophages. Levels of IL-1β mRNA and protein were significantly decreased in GH-treated J774A.1 macrophages. Nuclear factor-κB stimulates IL-1β gene expression, and GH induced a significant decrease in the levels of phosphorylated nuclear factor-κB in macrophages. IL-1β is a known inhibitor of adipogenesis, and these results support GH-dependent down-regulation of macrophage IL-1β expression as one mechanism for the observed increase in adipogenesis with CM from GH-treated macrophages. We conclude that GH decreases secretion of IL-1β by the macrophage and thus in a paracrine manner increases adipocyte differentiation. These results provide a novel mechanism for GH’s actions in the control of adipogenesis.

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Borsini, Alessandra, Maria Grazia Di Benedetto, Juliette Giacobbe e Carmine M. Pariante. "Pro- and Anti-Inflammatory Properties of Interleukin in Vitro: Relevance for Major Depression and Human Hippocampal Neurogenesis". International Journal of Neuropsychopharmacology 23, n. 11 (29 luglio 2020): 738–50. http://dx.doi.org/10.1093/ijnp/pyaa055.

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Abstract Background Although the pro-inflammatory cytokine interleukin (IL)6 has been generally regarded as “depressogenic,” recent research has started to question this assumption in light of the fact that this cytokine can also have anti-inflammatory properties. This bimodal action seems to be dependent on its concentration levels and on the concomitant presence of other pro-inflammatory cytokines. Methods We exposed a human hippocampal progenitor cell line, HPC0A07/03C, to cytokine levels described in depressed patients (IL6 5 pg/mL with IL1β 10 pg/mL or Macrophage Migration Inhibitory Factor (300 pg/mL) in healthy individuals (IL6 with IL1β, 1 pg/mL or Macrophage Migration Inhibitory Factor 10 pg/mL), as well as to the potentially anti-inflammatory, much higher concentrations of IL6 (50 000 pg/mL). Results Treatment with high concentrations of IL6 with IL1β or Macrophage Migration Inhibitory Factor (resembling depressed patients) decreases neurogenesis compared with low concentrations of the same cytokines (healthy individuals) and that this is mediated via production of, respectively, IL8 and IL1β in cell supernatant. Instead, treatment with very high, anti-inflammatory concentration of IL6 (50 000 pg/mL) together with high IL1β or Macrophage Migration Inhibitory Factor prevents decrease in neurogenesis and reduces both IL8 and IL1β. When high concentrations of both IL1β and Macrophage Migration Inhibitory Factor were used in co-treatment, as a model of treatment-resistant depression, we also demonstrated a reduction in neurogenesis and that this is mediated via a decrease in IL4; moreover, co-treatment with high IL1β and Macrophage Migration Inhibitory Factor and the very high concentration of IL6 prevented the reduction in neurogenesis and increased IL4. Conclusions Our results demonstrate that IL6 can exert both pro- and anti-inflammatory (potentially antidepressant) properties, depending on its concentrations and combinations with other inflammatory cytokines.

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Kasama, Tsuyoshi, Kumiko Ohtsuka, Michihito Sato, Ryo Takahashi, Kuninobu Wakabayashi e Kazuo Kobayashi. "Macrophage Migration Inhibitory Factor: A Multifunctional Cytokine in Rheumatic Diseases". Arthritis 2010 (3 gennaio 2010): 1–10. http://dx.doi.org/10.1155/2010/106202.

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Macrophage migration inhibitory factor (MIF) was originally identified in the culture medium of activated T lymphocytes as a soluble factor that inhibited the random migration of macrophages. MIF is now recognized to be a multipotent cytokine involved in the regulation of immune and inflammatory responses. Moreover, the pivotal nature of its involvement highlights the importance of MIF to the pathogenesis of various inflammatory disorders and suggests that blocking MIF may be a useful therapeutic strategy for treating these diseases. This paper discusses the function and expressional regulation of MIF in several rheumatic diseases and related conditions.

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Huh, Sung Jin, Chin-Ying Chung, Arati Sharma e Gavin P. Robertson. "Macrophage Inhibitory Cytokine-1 Regulates Melanoma Vascular Development". American Journal of Pathology 176, n. 6 (giugno 2010): 2948–57. http://dx.doi.org/10.2353/ajpath.2010.090963.

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Calandra, T., J. Bernhagen, R. A. Mitchell e R. Bucala. "The macrophage is an important and previously unrecognized source of macrophage migration inhibitory factor." Journal of Experimental Medicine 179, n. 6 (1 giugno 1994): 1895–902. http://dx.doi.org/10.1084/jem.179.6.1895.

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For over 25 years, the cytokine known as macrophage migration inhibitory factor (MIF) has been considered to be a product of activated T lymphocytes. We recently identified the murine homolog of human MIF as a protein secreted by the pituitary in response to endotoxin administration. In the course of these studies, we also detected MIF in acute sera obtained from endotoxin-treated, T cell-deficient (nude), and hypophysectomized mice, suggesting that still more cell types produce MIF. Here, we report that cells of the monocyte/macrophage lineage are an important source of MIF in vitro and in vivo. We observed high levels of both preformed MIF protein and MIF mRNA in resting, nonstimulated cells. In the murine macrophage cell line RAW 264.7, MIF secretion was induced by as little as 10 pg/ml of lipopolysaccharide (LPS), peaked at 1 ng/ml, and was undetectable at LPS concentrations > 1 microgram/ml. A similar stimulation profile was observed in LPS-treated peritoneal macrophages; however, higher LPS concentrations were necessary to induce peak MIF production unless cells had been preincubated with interferon gamma (IFN-gamma). In RAW 264.7 macrophages, MIF secretion also was induced by tumor necrosis factor alpha (TNF-alpha) and IFN-gamma, but not by interleukins 1 beta or 6. Of note, MIF-stimulated macrophages were observed to secrete bioactive TNF-alpha. Although previously overlooked, the macrophage is both an important source and an important target of MIF in vivo. The activation of both central (pituitary) and peripheral (macrophage) sources of MIF production by inflammatory stimuli provides further evidence for the critical role of this cytokine in the systemic response to tissue invasion.

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Baer, Mark, Allan Dillner, Richard C. Schwartz, Constance Sedon, Sergei Nedospasov e Peter F. Johnson. "Tumor Necrosis Factor Alpha Transcription in Macrophages Is Attenuated by an Autocrine Factor That Preferentially Induces NF-κB p50". Molecular and Cellular Biology 18, n. 10 (1 ottobre 1998): 5678–89. http://dx.doi.org/10.1128/mcb.18.10.5678.

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ABSTRACT Macrophages are a major source of proinflammatory cytokines such as tumor necrosis factor alpha (TNF-α), which are expressed during conditions of inflammation, infection, or injury. We identified an activity secreted by a macrophage tumor cell line that negatively regulates bacterial lipopolysaccharide (LPS)-induced expression of TNF-α. This activity, termed TNF-α-inhibiting factor (TIF), suppressed the induction of TNF-α expression in macrophages, whereas induction of three other proinflammatory cytokines (interleukin-1β [IL-1β], IL-6, and monocyte chemoattractant protein 1) was accelerated or enhanced. A similar or identical inhibitory activity was secreted by IC-21 macrophages following LPS stimulation. Inhibition of TNF-α expression by macrophage conditioned medium was associated with selective induction of the NF-κB p50 subunit. Hyperinduction of p50 occurred with delayed kinetics in LPS-stimulated macrophages but not in fibroblasts. Overexpression of p50 blocked LPS-induced transcription from a TNF-α promoter reporter construct, showing that this transcription factor is an inhibitor of the TNF-α gene. Repression of the TNF-α promoter by TIF required a distal region that includes three NF-κB binding sites with preferential affinity for p50 homodimers. Thus, the selective repression of the TNF-α promoter by TIF may be explained by the specific binding of inhibitory p50 homodimers. We propose that TIF serves as a negative autocrine signal to attenuate TNF-α expression in activated macrophages. TIF is distinct from the known TNF-α-inhibiting factors IL-4, IL-10, and transforming growth factor β and may represent a novel cytokine.

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Bozza, Marcelo T., Yuri C. Martins, Letícia A. M. Carneiro e Claudia N. Paiva. "Macrophage Migration Inhibitory Factor in Protozoan Infections". Journal of Parasitology Research 2012 (2012): 1–12. http://dx.doi.org/10.1155/2012/413052.

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Macrophage migration inhibitory factor (MIF) is a cytokine that plays a central role in immune and inflammatory responses. In the present paper, we discussed the participation of MIF in the immune response to protozoan parasite infections. As a general trend, MIF participates in the control of parasite burden at the expense of promoting tissue damage due to increased inflammation.

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Nishi, Kosuke, Takako Ito, Ayumu Kadota, Momoko Ishida, Hisashi Nishiwaki, Naohiro Fukuda, Naoaki Kanamoto, Yoko Nagata e Takuya Sugahara. "Aqueous Extract from Leaves of Citrus unshiu Attenuates Lipopolysaccharide-Induced Inflammatory Responses in a Mouse Model of Systemic Inflammation". Plants 10, n. 8 (19 agosto 2021): 1708. http://dx.doi.org/10.3390/plants10081708.

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Inflammation is related to various life-threatening diseases including cancer, neurodegenerative diseases, and metabolic syndrome. Because macrophages are prominent inflammatory cells, regulation of macrophage activation is a key issue to control the onset of inflammation-associated diseases. In this study, we aimed to evaluate the potential anti-inflammatory activity of Citrus unshiu leaf extract (CLE) and to elucidate the mechanism underlying its anti-inflammatory effect. We found the inhibitory activity of CLE on the secretion of proinflammatory cytokines and a chemokine from mouse macrophage-like RAW 264.7 cells and mouse peritoneal macrophages. The inhibitory activity of CLE was attributed to downregulated JNK, p38 MAPK, and NF-κB signaling pathways, leading to suppressed gene expression of inflammation-associated proteins. Oral administration of CLE significantly decreased the serum level of proinflammatory cytokines IL-6 and TNFα and increased that of anti-inflammatory cytokine IL-10 in lipopolysaccharide-induced systemic inflammation mice. In addition, oral administration of CLE decreased secretion and gene expression of several proinflammatory proteins in the liver and spleen of the model mice. Overall results revealed that C. unshiu leaf is effective to attenuate inflammatory responses in vitro and in vivo.

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Lemay, Serge, Tatiana V. Lebedeva e Ajay K. Singh. "Inhibition of Cytokine Gene Expression by Sodium Salicylate in a Macrophage Cell Line through an NF-κB-Independent Mechanism". Clinical Diagnostic Laboratory Immunology 6, n. 4 (1 luglio 1999): 567–72. http://dx.doi.org/10.1128/cdli.6.4.567-572.1999.

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ABSTRACT Macrophage-derived cytokines and chemokines are involved at multiple steps of immune and inflammatory responses, and the transcriptional factor NF-κB appears to play a pivotal role in their coordinated upregulation. The anti-inflammatory agents salicylates have been proposed to act in part by inhibiting NF-κB. We have therefore studied the effects of sodium salicylate on lipopolysaccharide (LPS)-induced κB-binding activity and on cytokine and chemokine gene expression in the RAW264.7 murine macrophage cell line and compared them to those of an established NF-κB inhibitor, pyrrolidine dithiocarbamate (PDTC). PDTC (100 μM) completely abrogated LPS-induced κB-binding activity and also profoundly inhibited the induction of interleukin 1α (IL-1α), IL-1β, IL-6, IL-10, granulocyte colony-stimulating factor, granulocyte-macrophage colony-stimulating factor, and MCP-1 and, to a lesser extent, leukemia inhibitory factor, RANTES, and IL-1Ra. In contrast, sodium salicylate (15 to 20 mM) had no effect on NF-κB activation but, nevertheless, suppressed several LPS-induced cytokine and chemokine genes to a degree similar to that obtained with PDTC. However, compared to PDTC, sodium salicylate caused significantly less inhibition of IL-1Ra and IL-10 gene expression after LPS stimulation. Neither LPS-induced MIP-1α, MIP-1β, nor MIP-2 was significantly affected by PDTC or sodium salicylate, demonstrating that NF-κB is dispensable for the transcriptional regulation of these genes by LPS. In summary, these results suggest that both NF-κB-dependent and NF-κB-independent pathways are necessary for the induction by LPS of a complex cytokine and chemokine response. In the RAW264.7 macrophage cell line, suprapharmacological concentrations of sodium salicylate exert a potent inhibitory effect on LPS-induced cytokine gene induction but appear to accomplish this by interfering with NF-κB-independent pathways of activation.

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Deftu, Alexandru F., Paolo Fiorenzani, Ilaria Ceccarelli, Jessica Pinassi, Martina Gambaretto, Violeta Ristoiu, Luana R. Paulesu e Anna-Maria Aloisi. "Macrophage migration inhibitory factor modulates formalin induced behaviors in rats". Animal Biology 66, n. 3-4 (2016): 249–58. http://dx.doi.org/10.1163/15707563-00002502.

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Cytokine proteins are involved in different signaling pathways throughout the central nervous system. To study the efficacy of an inflammatory cytokine, the macrophage migration inhibitory factor (MIF), which acts via several receptor molecules including the receptor CXCR2, male rats’ behaviors were determined after intracerebroventricular (ICV) administration of MIF. There were three treatments: One group received only the cytokine, a second group received MIF and an CXCR2 antagonist (SB265610), and a third, control group received only the carrier medium saline. All rats were subjected to a subcutaneous injection of formalin in the hind paw after the ICV administration. Pain behaviors induced after formalin injection showed increased values in the MIF group of licking in the first phase and increased values of flexing, licking and paw-jerk in the second phase. On the contrary, spontaneous behaviors induced by formalin injection changed alternatively between the two groups compared with saline. These results suggest a possible effect of cytokine MIF on central nervous processes implicated in pain modulation mediated by the receptor CXCR2.

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Vujicic, Milica, Ivana Nikolic, Tamara Krajnovic, Kai-Fan Cheng, Sonya VanPatten, Mingzhu He, Stanislava Stosic-Grujicic, Ivana Stojanovic, Yousef Al-Abed e Tamara Saksida. "Novel inhibitors of macrophage migration inhibitory factor prevent cytokine-induced beta cell death". European Journal of Pharmacology 740 (ottobre 2014): 683–89. http://dx.doi.org/10.1016/j.ejphar.2014.06.009.

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Crabtree, Traves D., Long Jin, Daniel P. Raymond, Shawn J. Pelletier, C. Webster Houlgrave, Thomas G. Gleason, Timothy L. Pruett e Robert G. Sawyer. "Preexposure of Murine Macrophages to CpG Oligonucleotide Results in a Biphasic Tumor Necrosis Factor Alpha Response to Subsequent Lipopolysaccharide Challenge". Infection and Immunity 69, n. 4 (1 aprile 2001): 2123–29. http://dx.doi.org/10.1128/iai.69.4.2123-2129.2001.

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ABSTRACT Bacterial DNA and synthetic oligonucleotides containing CpG sequences (CpG-DNA and CpG-ODN) provoke a proinflammatory cytokine response (tumor necrosis factor alpha [TNF-α], interleukin-12 [IL-12], and IL-6) and increased mortality in lipopolysaccharide (LPS)-challenged mice via a TNF-α-mediated mechanism. It was hypothesized that preexposure of macrophages to CpG-ODN would result in an increased TNF-α response to subsequent LPS challenge in vitro. Using the murine macrophage cell line RAW 264.7, we demonstrated both a rapid proinflammatory cytokine response (TNF-α) and a delayed inhibitory cytokine response (IL-10) with CpG-ODN. Preexposure of macrophages to CpG-ODN for brief periods (1 to 3 h) augmented TNF-α secretion and mRNA accumulation following subsequent LPS challenge (1 μg/ml). However, prolonged preexposure to CpG-ODN (6 to 9 h) resulted in suppression of the TNF-α protein and mRNA response to LPS. The addition of anti-IL-10 antibody to CpG-ODN during preexposure resulted in an increase in the LPS-induced TNF-α response over that induced by CpG-ODN preexposure alone. Thus, while brief preexposure of macrophages to CpG-ODN augments the proinflammatory cytokine response to subsequent LPS challenge, prolonged preexposure elicits IL-10 production, which inhibits the TNF-α response. Although the initial proinflammatory effects of CpG-DNA are well established, the immune response to CpG-DNA may also include autocrine or paracrine feedback mechanisms, leading to a complex interaction of proinflammatory and inhibitory cytokines.

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Wong, Louisa Y. F., Bernard M. Y. Cheung, Yuk-Yin Li e Fai Tang. "Adrenomedullin Is Both Proinflammatory and Antiinflammatory: Its Effects on Gene Expression and Secretion of Cytokines and Macrophage Migration Inhibitory Factor in NR8383 Macrophage Cell Line". Endocrinology 146, n. 3 (1 marzo 2005): 1321–27. http://dx.doi.org/10.1210/en.2004-1080.

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Adrenomedullin (ADM) is a potent vasorelaxant peptide that plays important roles in cardiovascular homeostasis and inflammatory response. ADM derived from macrophages is one of the major sources of ADM that is produced in the inflammatory process. To assess the functions of ADM in inflammation, we studied the temporal changes in ADM production and its effect on secretion of macrophage migration inhibitory factor (MIF) and cytokine response of NR8383 rat macrophages activated by lipopolysaccharide (LPS). NR8383 cells were stimulated by LPS in the absence and presence of exogenous ADM, and the concentrations of ADM, MIF, and proinflammatory cytokines (IL-6, TNF-α, and IL-1β) in the culture media and gene expressions of the cells were measured. We confirmed that the secretion and mRNA expression of ADM in the macrophages were markedly increased by LPS. ADM increased initial secretion of MIF and IL-1β from both nonstimulated and LPS-stimulated cells, and it also increased basal and LPS-induced IL-6 secretion of the cells by 2- to 15-fold. However, it reduced secretion of TNF-α from LPS-stimulated cells by 34–56%. Our results suggest that ADM modulates MIF secretion and cytokine production and plays important roles in both the initiation and propagation of the inflammatory response.

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Pastrana, Diana V., Nithyakalyani Raghavan, Peter FitzGerald, Stephen W. Eisinger, Christine Metz, Richard Bucala, Robert P. Schleimer, Carol Bickel e Alan L. Scott. "Filarial Nematode Parasites Secrete a Homologue of the Human Cytokine Macrophage Migration Inhibitory Factor". Infection and Immunity 66, n. 12 (1 dicembre 1998): 5955–63. http://dx.doi.org/10.1128/iai.66.12.5955-5963.1998.

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ABSTRACT Filarial nematode parasites establish long-term chronic infections in the context of an antiparasite immunity that is strongly biased toward a Th2 response. The mechanisms that lead to this Th2 bias toward filarial antigens are not clear, but one possibility is that the parasites produce molecules that have the capacity to proactively modify their immunological environment. Here we report that filarial parasites of humans secrete a homologue of the human proinflammatory cytokine macrophage migration inhibitory factor (MIF) that has the capability of modifying the activity of human monocytes/macrophages. A cDNA clone isolated from a Brugia malayi infective-stage larva expression library encoded a 12.5-kDa protein product (Bm-MIF) with 42% identity to human and murine MIF. MIF homologues were also found to be expressed in the related filarial species Wuchereria bancrofti and Onchocerca volvulus. Bm-mif was transcribed by adult and larval parasites, and the protein product was found in somatic extracts and in the parasite’s excretory-secretory products. Immunohistocytochemistry revealed that Bm-MIF was localized to cells of the hypodermis/lateral chord, the uterine wall, and larvae developing in utero. Unexpectedly, the activities of recombinant Bm-MIF and human MIF on human monocytes/macrophages were found to be similar. When placed with monocytes/macrophages in a cell migration assay,Bm-MIF inhibited random migration. When placed away from cells, Bm-MIF induced an increase in monocyte/macrophage migration that was specifically inhibited by neutralizing anti-Bm-MIF antibodies. Bm-MIF is the first demonstration that helminth parasites produce cytokine homologues that have the potential to modify host immune responses to promote parasite survival.

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Huang, Mingguo, Shintaro Narita, Takamitsu Inoue, Norihiko Tsuchiya, Shigeru Satoh, Hiroshi Nanjo, Takehiko Sasaki e Tomonori Habuchi. "Diet-induced macrophage inhibitory cytokine 1 promotes prostate cancer progression". Endocrine-Related Cancer 21, n. 1 (febbraio 2014): 39–50. http://dx.doi.org/10.1530/erc-13-0227.

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Recent studies have indicated that a high-fat diet (HFD) plays an important role in prostate cancer (PCa) progression. Palmitic acid (PA) is one of the most abundant saturated free fatty acids (FAs) and is associated with carcinogenesis. In this study, we investigated the mechanism underlying the association of dietary fat, including PA, with PCa progression. In four PCa cell lines,in vitroPA administration stimulated the expression of macrophage inhibitory cytokine 1 (MIC1), which is a divergent member of the transforming growth factor-β family.In vivo, LNCaP xenograft tumor growth, serum MIC1 levels, and FA levels in xenograft tumors were significantly higher in mice receiving an HFD containing high amounts of PA than in those receiving a low-fat diet (LFD). In addition, tumor cells with high MIC1 expression invaded to venules and lymph vessels in the LNCaP xenograft.In vitrostudies showed that proliferation and invasive capacity were significantly higher in PCa cells cultured with serum from HFD-fed mice than in those cultured with the serum from LFD-fed mice. This effect was attenuated by the addition of neutralizing antibodies against MIC1, but not by isotype control antibodies. Clinically, serum MIC1 levels were significantly higher in PCa patients than in healthy controls, and higher levels were associated with higher pathological grade and obesity. In conclusion, our results indicate that an HFD containing PA may promote growth and invasiveness of PCa cells through the upregulation of MIC1 expression.

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Yamashita, Toshiharu, Akihiro Yoneta e Tokimasa Hida. "Macrophage Inhibitory Cytokine-1: A New Player in Melanoma Development". Journal of Investigative Dermatology 129, n. 2 (febbraio 2009): 262–64. http://dx.doi.org/10.1038/jid.2008.366.

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Soumoy, Laura, Nadège Kindt, Ghanem Ghanem, Sven Saussez e Fabrice Journe. "Role of Macrophage Migration Inhibitory Factor (MIF) in Melanoma". Cancers 11, n. 4 (12 aprile 2019): 529. http://dx.doi.org/10.3390/cancers11040529.

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Macrophage migration inhibitory factor (MIF) is an inflammatory cytokine involved in the carcinogenesis of many cancer types. Here, we review the published experimental and clinical data for MIF and its involvement in melanoma. All reported data show that MIF is overexpressed in melanoma cells, especially in case of metastatic disease. Clinical studies also indicate that high MIF expression is positively associated with aggressiveness of the disease. Some data also highlight the implication of MIF in angiogenesis, immunity and metastasis in melanoma cell lines, as well as the availability of different therapeutic options targeting MIF for the treatment of metastatic melanoma. Indeed, the main problem in metastatic melanoma is the lack of long-term effective treatment. This is linked to the capacity of melanoma cells to mutate very quickly and/or activate alternative signaling pathways. Thus, MIF targeting therapies could provide a new effective way of treating melanoma. Moreover, cell sensitivity to MIF depletion does not correlate with the BRAF mutational status. Regarding the fact that many melanoma patients carry a BRAF mutation, and that they develop resistance to BRAF inhibitors, this observation is very interesting as MIF inhibitors could be used to treat many patients in relapse after treatment with an inhibitor of the mutant BRAF protein.

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Andreone, Teresa, Gordon P. Meares, Katherine J. Hughes, Polly A. Hansen e John A. Corbett. "Cytokine-mediated β-cell damage in PARP-1-deficient islets". American Journal of Physiology-Endocrinology and Metabolism 303, n. 2 (15 luglio 2012): E172—E179. http://dx.doi.org/10.1152/ajpendo.00055.2012.

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Poly(ADP)-ribose polymerase (PARP) is an abundant nuclear protein that is activated by DNA damage; once active, it modifies nuclear proteins through attachment of poly(ADP)-ribose units derived from β-nicotinamide adenine dinucleotide (NAD+). In mice, the deletion of PARP-1 attenuates tissue injury in a number of animal models of human disease, including streptozotocin-induced diabetes. Also, inflammatory cell signaling and inflammatory gene expression are attenuated in macrophages isolated from endotoxin-treated PARP-1-deficient mice. In this study, the effects of PARP-1 deletion on cytokine-mediated β-cell damage and macrophage activation were evaluated. There are no defects in inflammatory mediator signaling or inflammatory gene expression in macrophages and islets isolated from PARP-1-deficient mice. While PARP-1 deficiency protects islets against cytokine-induced islet cell death as measured by biochemical assays of membrane polarization, the genetic absence of PARP-1 does not effect cytokine-induced inhibition of insulin secretion or cytokine-induced DNA damage in islets. While PARP-1 deficiency appears to provide protection from cell death, it fails to provide protection against the inhibitory actions of cytokines on insulin secretion or the damaging actions on islet DNA integrity.

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Finucane, Orla M., Clare M. Reynolds, Fiona C. McGillicuddy e Helen M. Roche. "Insights into the role of macrophage migration inhibitory factor in obesity and insulin resistance". Proceedings of the Nutrition Society 71, n. 4 (23 agosto 2012): 622–33. http://dx.doi.org/10.1017/s0029665112000730.

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High-fat diet (HFD)-induced obesity has emerged as a state of chronic low-grade inflammation characterised by a progressive infiltration of immune cells, particularly macrophages, into obese adipose tissue. Adipose tissue macrophages (ATM) present immense plasticity. In early obesity, M2 anti-inflammatory macrophages acquire an M1 pro-inflammatory phenotype. Pro-inflammatory cytokines including TNF-α, IL-6 and IL-1β produced by M1 ATM exacerbate local inflammation promoting insulin resistance (IR), which consequently, can lead to type-2 diabetes mellitus (T2DM). However, the triggers responsible for ATM recruitment and activation are not fully understood. Adipose tissue-derived chemokines are significant players in driving ATM recruitment during obesity. Macrophage migration inhibitory factor (MIF), a chemokine-like inflammatory regulator, is enhanced during obesity and is directly associated with the degree of peripheral IR. This review focuses on the functional role of macrophages in obesity-induced IR and highlights the importance of the unique inflammatory cytokine MIF in propagating obesity-induced inflammation and IR. Given MIF chemotactic properties, MIF may be a primary candidate promoting ATM recruitment during obesity. Manipulating MIF inflammatory activities in obesity, using pharmacological agents or functional foods, may be therapeutically beneficial for the treatment and prevention of obesity-related metabolic diseases.

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Kim, Do-Hoon, Ji-Young Lee, Young-Jin Kim, Hyun-Ju Kim e Wansu Park. "Rubi Fructus Water Extract Alleviates LPS-Stimulated Macrophage Activation via an ER Stress-Induced Calcium/CHOP Signaling Pathway". Nutrients 12, n. 11 (22 novembre 2020): 3577. http://dx.doi.org/10.3390/nu12113577.

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Despite the availability of antibiotics and vaccines, many intractable infectious diseases still threaten human health across the globe. Uncontrolled infections can lead to systemic inflammatory response syndrome and the excessive production of inflammatory cytokines, known as a cytokine storm. As cytokines also play necessary and positive roles in fighting infections, it is important to identify nontoxic and anti-inflammatory natural products that can modulate cytokine production caused by infections. Rubi Fructus, the unripe fruits of Rubus coreanus Miquel, are known to possess antioxidative properties. In this study, the effect of the water extract of Rubi Fructus (RF) on the lipopolysaccharide (LPS)-induced inflammatory response in RAW 264.7 macrophages was investigated using biochemical and cell biology techniques. Our data indicated that RF inhibits p38 phosphorylation, intracellular calcium release, and the production of nitric oxide (NO), interleukin (IL)-6, monocyte chemotactic activating factor (MCP)-1, tumor necrosis factor (TNF)-α, leukemia inhibitory factor (LIF), lipopolysaccharide-induced CXC chemokine (LIX), granulocyte-colony stimulating factor (G-CSF), granulocyte macrophage colony-stimulating factor (GM-CSF), vascular endothelial growth factor (VEGF), macrophage colony-stimulating factor (M-CSF), macrophage inflammatory protein (MIP)-1α, MIP-1β, MIP-2, and regulated on activation, normal T cell expressed and secreted (RANTES) in LPS-treated macrophages. In addition, we observed decreasing mRNA expression of Chop, Camk2a, Stat1, Stat3, Jak2, Fas, c-Jun, c-Fos, Nos2, and Ptgs2 without cytotoxic effects. We concluded that RF demonstrated immunoregulatory activity on LPS-stimulated macrophages via an endoplasmic reticulum (ER) stress-induced calcium/CCAAT-enhancer-binding protein homologous protein (CHOP) pathway and the Janus kinase (JAK)/signal transducers and activators of transcription (STAT) pathway.

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Li, Lili, Maojia Xu, Simon C. Rowan, Katherine Howell, Adam Russell-Hallinan, Seamas C. Donnelly, Paul McLoughlin e John A. Baugh. "The effects of genetic deletion of Macrophage migration inhibitory factor on the chronically hypoxic pulmonary circulation". Pulmonary Circulation 10, n. 4 (ottobre 2020): 204589402094135. http://dx.doi.org/10.1177/2045894020941352.

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While it is well established that the haemodynamic cause of hypoxic pulmonary hypertension is increased pulmonary vascular resistance, the molecular pathogenesis of the increased resistance remains incompletely understood. Macrophage migration inhibitory factor is a pleiotropic cytokine with endogenous tautomerase enzymatic activity as well as both intracellular and extracellular signalling functions. In several diseases, macrophage migration inhibitory factor has pro-inflammatory roles that are dependent upon signalling through the cell surface receptors CD74, CXCR2 and CXCR4. Macrophage migration inhibitory factor expression is increased in animal models of hypoxic pulmonary hypertension and macrophage migration inhibitory factor tautomerase inhibitors, which block some of the functions of macrophage migration inhibitory factor, and have been shown to attenuate hypoxic pulmonary hypertension in mice and monocrotaline-induced pulmonary hypertension in rats. However, because of the multiple pathways through which it acts, the integrated actions of macrophage migration inhibitory factor during the development of hypoxic pulmonary hypertension were unclear. We report here that isolated lungs from adult macrophage migration inhibitory factor knockout ( MIF–/–) mice maintained in normoxic conditions showed greater acute hypoxic vasoconstriction than the lungs of wild type mice ( MIF+/+). Following exposure to hypoxia for three weeks, isolated lungs from MIF–/– mice had significantly higher pulmonary vascular resistance than those from MIF+/+ mice. The major mechanism underlying the greater increase in pulmonary vascular resistance in the hypoxic MIF–/– mice was reduction of the pulmonary vascular bed due to an impairment of the normal hypoxia-induced expansion of the alveolar capillary network. Taken together, these results demonstrate that macrophage migration inhibitory factor plays a central role in the development of the pulmonary vascular responses to chronic alveolar hypoxia.

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Bertholet, Sylvie, Harold L. Dickensheets, Faruk Sheikh, Albert A. Gam, Raymond P. Donnelly e Richard T. Kenney. "Leishmania donovani-Induced Expression of Suppressor of Cytokine Signaling 3 in Human Macrophages: a Novel Mechanism for Intracellular Parasite Suppression of Activation". Infection and Immunity 71, n. 4 (aprile 2003): 2095–101. http://dx.doi.org/10.1128/iai.71.4.2095-2101.2003.

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ABSTRACT Leishmania donovani protozoan parasites, the causative agent of visceral leishmaniasis, establish an infection partly by interfering with cytokine signaling in the host macrophages. Therefore, we investigated the expression of the suppressor of cytokine signaling (SOCS) genes in human macrophages infected with L. donovani. The expression of SOCS3 mRNA was induced transiently after exposure to live or heat-killed parasites, but not purified lipophosphoglycan, while that of other SOCS genes remained unchanged. SOCS3 gene expression was not dependent on phagocytosis or on cytokines released by L. donovani-infected macrophages, such as interleukin-1β or tumor necrosis factor alpha. In addition, Leishmania used a different signaling pathway(s) than bacterial lipopolysaccharide to induce SOCS3 mRNA, as indicated by the kinetics of induction and sensitivity to polymyxin B inhibition. Finally, phosphorylation of the STAT1 transcription factor was significantly reduced in L. donovani-infected macrophages and required de novo transcription. The induction of SOCS3 provides a potent inhibitory mechanism by which intracellular microorganisms may suppress macrophage activation and interfere with the host immune response.

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Kutsuna, Haruo, Kenichi Suzuki, Noriko Kamata, Takayuki Kato, Fumihiko Hato, Kensaku Mizuno, Hiromi Kobayashi, Masamitsu Ishii e Seiichi Kitagawa. "Actin reorganization and morphological changes in human neutrophils stimulated by TNF, GM-CSF, and G-CSF: the role of MAP kinases". American Journal of Physiology-Cell Physiology 286, n. 1 (gennaio 2004): C55—C64. http://dx.doi.org/10.1152/ajpcell.00131.2003.

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Stimulation of human neutrophils with tumor necrosis factor-α (TNF), granulocyte-macrophage colony-stimulating factor (GM-CSF), or granulocyte CSF (G-CSF) resulted in decreased fluorescence intensity of FITC-phalloidin (actin depolymerization) and morphological changes. Cytokine-induced actin depolymerization was dependent on the concentration of cytokines used as stimuli. The maximal changes were detected at 10 min after stimulation with TNF or GM-CSF and at 20 min after stimulation with G-CSF. Cytokine-induced actin depolymerization was sustained for at least 30 min after stimulation. In contrast, N-formyl-methionyl-leucyl-phenylalanine (FMLP) rapidly (within 45 s) induced an increase in the fluorescence intensity of FITC-phalloidin (actin polymerization) and morphological changes. TNF- and GM-CSF-induced actin depolymerization and morphological changes, but not FMLP-induced responses, were partially inhibited by either PD-98059, an inhibitor of mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) kinase, or SB-203580, an inhibitor of p38 MAPK, and were almost completely abolished by these inhibitors in combination. G-CSF-induced responses were almost completely abolished by PD-98059 and were unaffected by SB-203580. These findings are consistent with the ability of these cytokines to activate the distinct MAPK subtype cascade in human neutrophils. Phosphorylated ERK and p38 MAPK were not colocalized with F-actin in neutrophils stimulated by cytokines or FMLP. Furthermore, FMLP-induced polarization and actin polymerization were prevented by cytokine pretreatment. These findings suggest that TNF, GM-CSF, and G-CSF induce actin depolymerization and morphological changes through activation of ERK and/or p38 MAPK and that cytokine-induced actin reorganization may be partly responsible for the inhibitory effect of these cytokines on neutrophil chemotaxis.

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Lyu, Qingkang, Magdalena Wawrzyniuk, Victor P. M. G. Rutten, Willem van Eden, Alice J. A. M. Sijts e Femke Broere. "Hsp70 and NF-kB Mediated Control of Innate Inflammatory Responses in a Canine Macrophage Cell Line". International Journal of Molecular Sciences 21, n. 18 (4 settembre 2020): 6464. http://dx.doi.org/10.3390/ijms21186464.

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Abstract (sommario):

The pathogenesis of many inflammatory diseases is associated with the uncontrolled activation of nuclear factor kappa B (NF-κB) in macrophages. Previous studies have shown that in various cell types, heat shock protein 70 (Hsp70) plays a crucial role in controlling NF-κB activity. So far, little is known about the role of Hsp70 in canine inflammatory processes. In this study we investigated the potential anti-inflammatory effects of Hsp70 in canine macrophages as well as the mechanisms underlying these effects. To this end, a canine macrophage cell line was stressed with arsenite, a chemical stressor, which upregulated Hsp70 expression as detected by flow cytometry and qPCR. A gene-edited version of this macrophage cell line lacking inducible Hsp70 was generated using CRISPR-Cas9 technology. To determine the effects of Hsp70 on macrophage inflammatory properties, arsenite-stressed wild-type and Hsp70 knockout macrophages were exposed to lipopolysaccharide (LPS), and the expression of the inflammatory cytokines IL-6, IL-1β and tumor necrosis factor-α (TNF-α) and levels of phosphorylated NF-κB were determined by qPCR and Western Blotting, respectively. Our results show that non-toxic concentrations of arsenite induced Hsp70 expression in canine macrophages; Hsp70 upregulation significantly inhibited the LPS-induced expression of the pro-inflammatory mediators TNF-α and IL-6, as well as NF-κB activation in canine macrophages. Furthermore, the gene editing of inducible Hsp70 by CRISPR-Cas9-mediated gene editing neutralized this inhibitory effect of cell stress on NF-κB activation and pro-inflammatory cytokine expression. Collectively, our study reveals that Hsp70 may regulate inflammatory responses through NF-κB activation and cytokine expression in canine macrophages.

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Casals, Cristina, Javier Arias-Díaz, Fernando Valiño, Alejandra Sáenz, Cruz García, José L. Balibrea e Elena Vara. "Surfactant strengthens the inhibitory effect of C-reactive protein on human lung macrophage cytokine release". American Journal of Physiology-Lung Cellular and Molecular Physiology 284, n. 3 (1 marzo 2003): L466—L472. http://dx.doi.org/10.1152/ajplung.00325.2002.

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In this study we investigated the effect of acute-phase levels of C-reactive protein (CRP) on cytokine production by pulmonary macrophages in the presence or absence of pulmonary surfactant. Both human alveolar and interstitial macrophages as well as human surfactant were obtained from multiple organ donor lungs. Precultured macrophages were stimulated with LPS alone or together with IFN-γ in the presence or absence of CRP, surfactant, and combinations. Releases of TNF-α and of IL-1β to the medium were determined. We found that CRP could modulate lung inflammation in humans by decreasing the production of proinflammatory cytokines by both alveolar and interstitial macrophages stimulated with LPS alone or together with IFN-γ. The potential interaction between CRP and surfactant phospholipids did not overcome the effect of either CRP or surfactant on TNF-α and IL-1β release by lung macrophages. On the contrary, CRP and pulmonary surfactant together had a greater inhibitory effect than either alone on the release of proinflammatory cytokines by lung macrophages.

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Müller, Ruth, Jörg Klug, Miriam Rodewald e Andreas Meinhardt. "Macrophage migration inhibitory factor suppresses transforming growth factor-β2 secretion in cultured rat testicular peritubular cells". Reproduction, Fertility and Development 17, n. 4 (2005): 435. http://dx.doi.org/10.1071/rd04061.

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Cytokines have direct effects on testicular cell functions and a number of cytokines are produced constitutively within the testis, even in the absence of immune-activation events. There is clear evidence that cytokines play a dual role as important regulatory factors in the normal function of the testis, as well as in testicular inflammation. The pro-inflammatory cytokine macrophage migration inhibitory factor (MIF) is expressed locally in the testis and has direct effects on peritubular cells, which, in turn, produce anti-inflammatory mediators, including transforming growth factor (TGF)-β2. In the present study, we investigated the function of MIF by examining its effect on the secretion of TGF-β2 in peritubular cells. Expression of TGF-β2 mRNA was shown by reverse transcription–polymerase chain reaction in peritubular cells isolated from 19-day-old rat testis. The addition of recombinant MIF to cultured peritubular cells resulted in a dose-dependent decrease in TGF-β2 secretion up to 52% of control levels after 48 h, which was significant for all doses investigated (10–100 ng mL−1 MIF). Inhibition of TGF-β2 secretion was sustained for 72 h for the highest dose of MIF used (100 ng mL−1). No effect of MIF was observed on TGF-β2 mRNA expression levels, as shown by real-time polymerase chain reaction. These results suggest that the pro-inflammatory cytokine MIF can shift the cytokine balance from the immunosuppressive state towards an inflammatory reaction, potentially through the inhibition of TGF-β2 secretion by peritubular cells.

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Xu, Lei, Youyong Li, Dan Li, Peng Xu, Sheng Tian, Huiyong Sun, Hui Liu e Tingjun Hou. "Exploring the binding mechanisms of MIF to CXCR2 using theoretical approaches". Physical Chemistry Chemical Physics 17, n. 5 (2015): 3370–82. http://dx.doi.org/10.1039/c4cp05095a.

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de Souza, Gabriela F., Stéfanie P. Muraro, Leonardo D. Santos, Ana Paula T. Monteiro, Amanda G. da Silva, Ana Paula D. de Souza, Renato T. Stein, Patrícia T. Bozza e Bárbara N. Porto. "Macrophage migration inhibitory factor (MIF) controls cytokine release during respiratory syncytial virus infection in macrophages". Inflammation Research 68, n. 6 (3 aprile 2019): 481–91. http://dx.doi.org/10.1007/s00011-019-01233-z.

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Mukherjee, Snigdha, Anindita Ukil e Pijush K. Das. "Immunomodulatory Peptide from Cystatin, a Natural Cysteine Protease Inhibitor, against Leishmaniasis as a Model Macrophage Disease". Antimicrobial Agents and Chemotherapy 51, n. 5 (5 marzo 2007): 1700–1707. http://dx.doi.org/10.1128/aac.01555-06.

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Abstract (sommario):

ABSTRACT Cystatin, a natural cysteine protease inhibitor, has strong antileishmanial activity, which is due to its potential to induce nitric oxide (NO) generation from macrophages. Cysteine protease-inhibitory activity and NO-up-regulatory activity correspond to different regions, as revealed by the dissection of cystatin cDNA into nonoverlapping fragments. By using synthetic overlapping peptides, the NO-up-regulatory activity was found to be confined to a 10-mer sequence. In addition to having reasonable inhibitory effects on amastigote multiplication within macrophages (50% inhibitory concentration, 5.2 μg/ml), 97 and 93% suppression, respectively, of liver and spleen parasite burdens was achieved with the 10-mer peptide at a dose of 0.5 mg/kg of body weight/day, given consecutively for 4 days along with a suboptimal dose of gamma interferon in a 45-day mouse model of visceral leishmaniasis. Peptide treatment modulated the levels of cytokine secretion by infected splenocytes, with increased levels of interleukin-12 and tumor necrosis factor alpha and increased inducible NO synthase production, and also resulted in resistance to reinfection. The generation of a natural peptide from cystatin with robust immunomodulatory potential may therefore provide a promising therapeutic agent for macrophage-associated diseases.

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Ietta, Francesca, Yuanhong Wu, Roberta Romagnoli, Nima Soleymanlou, Barbara Orsini, Stacy Zamudio, Luana Paulesu e Isabella Caniggia. "Oxygen regulation of macrophage migration inhibitory factor in human placenta". American Journal of Physiology-Endocrinology and Metabolism 292, n. 1 (gennaio 2007): E272—E280. http://dx.doi.org/10.1152/ajpendo.00086.2006.

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Macrophage migration inhibitory factor (MIF) is an important proinflammatory cytokine involved in regulation of macrophage function. In addition, MIF may also play a role in murine and human reproduction. Although both first trimester trophoblast and decidua express MIF, the regulation and functional significance of this cytokine during human placental development remains unclear. We assessed MIF expression throughout normal human placental development, as well as in in vitro (chorionic villous explants) and in vivo (high altitude placentae) models of human placental hypoxia. Dimethyloxalylglycine (DMOG), which stabilizes hypoxia inducible factor-1 under normoxic conditions, was also used to mimic the effects of hypoxia on MIF expression. Quantitative real-time PCR and Western blot analysis showed high MIF protein and mRNA expression at 7–10 wk and lower levels at 11–12 wk until term. Exposure of villous explants to 3% O2 resulted in increased MIF expression and secretion relative to standard conditions (20% O2). DMOG treatment under 20% O2 increased MIF expression. In situ hybridization and immunohistochemistry showed elevated MIF expression in low oxygen-induced extravillous trophoblast cells. Finally, a significant increase in MIF transcript was observed in placental tissues from high-altitude pregnancies. Hence, three experimental models of placental hypoxia (early gestation, DMOG treatment, and high altitude) converge in stimulating increased MIF, supporting the conclusion that placental-derived MIF is an oxygen-responsive cytokine highly expressed in physiological in vivo and in in vitro low oxygen conditions.

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Wen, Yeshao, Jiali Gu, Shu-Lian Li, Marpadga A. Reddy, Rama Natarajan e Jerry L. Nadler. "Elevated Glucose and Diabetes Promote Interleukin-12 Cytokine Gene Expression in Mouse Macrophages". Endocrinology 147, n. 5 (1 maggio 2006): 2518–25. http://dx.doi.org/10.1210/en.2005-0519.

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Abstract (sommario):

Inflammation is emerging as an important mechanism for micro- and macrovascular complication of diabetes. The macrophage plays a key role in the chronic inflammatory response in part by generating particular cytokines. IL-1β, IL-6, IL12, IL-18, TNFα, and interferon-γ are produced primarily in macrophages and have been associated with accelerated atherosclerosis and altered vascular wall function. In this study, we evaluated the effect and mechanism of high glucose (HG) on gene expression of these cytokines in mouse peritoneal macrophages (MPM). HG led to a 2-fold increase in the mRNA expression of these cytokines, with IL-12 showing the highest activation (5.4-fold) in a time-dependent (3–12 h) and dose-dependent (10, 17.5, and 25 mmol/liter) manner. The effects were specific to HG because mannitol and 3-O-methyl-glucose had no effect on cytokine mRNA expression. HG also increased IL-12 protein accumulation from MPM. We also explored the role of induced and spontaneous diabetes on inflammatory cytokine expression in MPM. Increases in expression in MPM of multiple inflammatory cytokines, including a 20-fold increase in IL-12 mRNA, were observed in streptozotocin-induced type 1 diabetic mice as well as type 2 diabetic db/db mice, suggesting that cytokine gene expression is increased by hyperglycemia in vivo. We next explored potential mechanisms of HG-induced increases in IL-12 mRNA. HG increased the activity of protein kinase C, p38 MAPK (p38), c-Jun terminal kinase, and inhibitory-κB kinase in MPM. Furthermore, inhibitors of these signaling pathways significantly reduced HG-induced IL-12 mRNA expression in MPM. These results provide evidence for a potentially important mechanism linking elevated glucose and diabetes to inflammation.

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Lu, Hong, Yongyu Bai, Lianfeng Wu, Weilong Hong, Yong Liang, Bicheng Chen e Yongheng Bai. "Inhibition of Macrophage Migration Inhibitory Factor Protects against Inflammation and Matrix Deposition in Kidney Tissues after Injury". Mediators of Inflammation 2016 (2016): 1–12. http://dx.doi.org/10.1155/2016/2174682.

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Abstract (sommario):

Background. Macrophage migration inhibitory factor (MIF) is an important immunoregulatory cytokine involved in inflammation, which may be one important reason resulting in matrix deposition in renal tissues after injury. However, the underlying mechanisms have not yet been elucidated.Methods and Results. We uncovered a crucial role of MIF in inflammation and collagen depositionin vivoandin vitro. In rats, ureteral obstruction induced tubular injury, matrix accumulation, and inflammatory cell infiltration. Additionally, enhanced MIF levels in the obstructed kidneys were closely related to the increasing numbers of CD68-positive macrophages. These obstruction-induced injuries can be relieved by recanalization, consequently resulting in downregulated expression of MIF and its receptor CD74. Similarly, ischemia reperfusion induced renal injury, and it was accompanied by elevated MIF levels and macrophages infiltration. In cultured tubular epithelial cells (TECs), aristolochic acid (AA) promoted matrix production and increased MIF expression, as well as the release of macrophage-related factors. Inhibition of MIF with an antagonist ISO-1 resulted in the abolishment of these genotypes in AA-treated TECs.Conclusion. MIF plays an important role in macrophage-related inflammation and matrix deposition in kidney tissues following injury. MIF as a specific inhibitor may have therapeutic potential for patients with inflammatory and fibrotic kidney diseases.

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Hayes, V. M. "Macrophage Inhibitory Cytokine-1 H6D Polymorphism, Prostate Cancer Risk, and Survival". Cancer Epidemiology Biomarkers & Prevention 15, n. 6 (1 giugno 2006): 1223–25. http://dx.doi.org/10.1158/1055-9965.epi-06-0063.

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Brown, D. A., F. Lindmark, P. Stattin, K. Balter, H. O. Adami, S. L. Zheng, J. Xu et al. "Macrophage Inhibitory Cytokine 1: A New Prognostic Marker in Prostate Cancer". Clinical Cancer Research 15, n. 21 (20 ottobre 2009): 6658–64. http://dx.doi.org/10.1158/1078-0432.ccr-08-3126.

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Park, Jeong-Sook. "Pro-inflammatory Cytokine Production Inhibitory Effects of Frankincence in Murine Macrophage". Journal of the Korea Convergence Society 8, n. 1 (28 gennaio 2017): 239–43. http://dx.doi.org/10.15207/jkcs.2017.8.1.239.

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Nam, Tae Gyu, Tae-Gyu Lim, Bong Han Lee, Sol Lim, Hee Kang, Seok Hyun Eom, Miyoung Yoo, Hae Won Jang e Dae-Ok Kim. "Comparison of Anti-Inflammatory Effects of Flavonoid-Rich Common and Tartary Buckwheat Sprout Extracts in Lipopolysaccharide-Stimulated RAW 264.7 and Peritoneal Macrophages". Oxidative Medicine and Cellular Longevity 2017 (2017): 1–12. http://dx.doi.org/10.1155/2017/9658030.

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Abstract (sommario):

Buckwheat sprouts have been widely consumed all around world due to their great abundance of bioactive compounds. In this study, the anti-inflammatory effects of flavonoid-rich common buckwheat sprout (CBS) and tartary buckwheat sprout (TBS) extracts were evaluated in lipopolysaccharide- (LPS-) stimulated RAW 264.7 murine macrophages and primary peritoneal macrophages from male BALB/c mice. Based on the reversed-phase HPLC analysis, the major flavonoids in CBS were determined to beC-glycosylflavones (orientin, isoorientin, vitexin, and isovitexin), quercetin-3-O-robinobioside, and rutin, whereas TBS contained only high amounts of rutin. The TBS extract exhibited higher inhibitory activity as assessed by the production of proinflammatory mediators such as nitric oxide and cytokines including tumor necrosis factor-α, interleukin- (IL-) 6, and IL-12 in LPS-stimulated RAW 264.7 macrophages than CBS extract. In addition, TBS extract suppressed nuclear factor-kappa B activation by preventing inhibitor kappa B-alpha degradation and mitogen-activated protein kinase phosphorylation in LPS-stimulated RAW 264.7 macrophages. Moreover, the TBS extract markedly reduced LPS-induced cytokine production in peritoneal macrophages. Taken together, these findings suggest that TBS extract can be a potential source of anti-inflammatory agents that may influence macrophage-mediated inflammatory disorders.

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Tao, Tianzhu, Lulong Bo, Teng Li, Longbao Shi, Hui Zhang, Bo Ye, Yuhai Xu, Qingqing Ma, Xiaoming Deng e Guorong Zhang. "High-Affinity Anti-VISTA Antibody Protects against Sepsis by Inhibition of T Lymphocyte Apoptosis and Suppression of the Inflammatory Response". Mediators of Inflammation 2021 (28 luglio 2021): 1–9. http://dx.doi.org/10.1155/2021/6650329.

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Abstract (sommario):

Background. B7 family members and ligands have been identified as critical checkpoints in orchestrating the immune response during sepsis. V-domain Ig suppressor of T cell activation (VISTA) is a new inhibitory immune checkpoint involved in restraining T cell response. Previous studies demonstrated that VISTA engagement on T cells and myeloid cells could transmit inhibitory signals, resulting in reduced activation and function. The current study was designed to determine the potential therapeutic effects of a high-affinity anti-VISTA antibody (clone MH5A) in a murine model of sepsis. Methods. Polymicrobial sepsis was induced in male C57BL/6 mice via cecal ligation and puncture. Expression profiles of VISTA on T lymphocytes and macrophage were examined at 24 and 72 h postsurgery. The effects of anti-VISTA mAb on the 7-day survival, lymphocyte apoptosis, cytokine expression, bacterial burden, and vital organ damage were determined. Furthermore, the effects of anti-VISTA mAb on CD3+ T cell apoptosis and macrophage activation were determined in vitro. Results. VISTA was substantially expressed on T cells and macrophages in sham-operated mice; septic peritonitis did not induce significant changes in the expression profiles. Treatment with MH5A improved the survival of septic mice, accompanied by reduced lymphocyte apoptosis, decreased cytokine expression, and enhanced bacterial clearance. Engagement of VISTA receptor with MH5A mitigated CD3+ T cell apoptosis cultured from CLP mice and suppressed LPS-induced cytokine production by macrophage in vitro. Conclusion. The present study identified VISTA as a novel immune checkpoint in the regulation of T cell and macrophage response during sepsis. Modulation of the VISTA pathway might offer a promising opportunity in the immunotherapy for sepsis.

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Crilly, Anne, Susan E. Robertson, James H. Reilly, J. Alastair Gracie, Wen-Qi Lai, Bernard P. Leung, Paul F. Life e Iain B. McInnes. "Phosphodiesterase 4 (PDE4) regulation of proinflammatory cytokine and chemokine release from rheumatoid synovial membrane". Annals of the Rheumatic Diseases 70, n. 6 (21 febbraio 2011): 1130–37. http://dx.doi.org/10.1136/ard.2010.134825.

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Abstract (sommario):

BackgroundThe cAMP-metabolising enzyme, phosphodiesterase 4 (PDE4), has been implicated in a number of immune responses, including tumour necrosis factor α (TNFα) production. To date, few data have directly addressed whether synovial cytokine and chemokine production is modified by PDE4.ObjectiveUsing specific PDE4 inhibitors, roflumilast plus two novel inhibitors, INH 0061 and INH 0062, the authors studied the effect of PDE4 inhibition on proinflammatory cytokine and chemokine release from primary rheumatoid arthritis (RA) synovial digest suspensions and in a macrophage T cell co-culture assay system.ResultsAll PDE4 inhibitors dose-dependently reduced the release of TNFα from primary synovial membrane cultures (n=5), half maximal inhibitory concentration (IC50) 300–30 nM, p<0.05. Similarly, a significant suppression in the release the proinflammatory chemokines, monocyte chemoattractant protein-1 (MCP-1), macrophage inflammatory protein (MIP)-1α, MIP-1β (IC50 300–30 nM) and regulated upon activation normal T-cell expressed and secreted (RANTES) (IC50 3 nM) was also observed, p<0.05. While interleukin 1β was also reduced, it did not achieve an IC50. These observations were further confirmed in a macrophage T cell co-culture system, demonstrating the importance of PDE4 pathways in regulating cytokine/chemokine release in a cellular interaction implicated in inflammatory synovitis. Subsequent studies using the human monocytic cell line U937 also demonstrated cytokine regulation with PDE4 knockdown utilising a small interfering RNA approach.ConclusionThese data provide direct evidence of PDE4-dependent pathways in human RA synovial inflammatory cytokine and chemokine release and may provide a novel approach in treating chronic autoimmune conditions such as RA.

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Jovanović Krivokuća, Milica, Ivana Stefanoska, Aleksandra Vilotić, Danica Ćujić, Svetlana Vrzić Petronijević e Ljiljana Vićovac. "Macrophage migration inhibitory factor modulates cytokine expression in the trophoblast cell line HTR-8/SVneo". Reproduction, Fertility and Development 32, n. 18 (2020): 1326. http://dx.doi.org/10.1071/rd20138.

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Abstract (sommario):

Extravillous trophoblasts are specific placental cells that invade the uterine stroma and spiral arteries modifying and adjusting them to pregnancy. Many pregnancy pathologies are associated with impairment of this process, including preeclampsia and intrauterine growth restriction, among others. Macrophage migration inhibitory factor (MIF) is a pleiotropic cytokine that is abundant at the fetomaternal interface. Previous results from our group showed that MIF participates in trophoblast invasion and modulates the expression of molecules known to mediate stromal and endovascular trophoblast invasion. In this study we investigated the possibility that MIF could act as a regulator of cytokines known to modulate trophoblast invasion using the normal extravillous trophoblast-derived cell line HTR-8/SVneo. Expression of trophoblast MIF was attenuated by MIF mRNA-specific small interfering RNAs. Cytokine expression was assessed at the mRNA and protein levels using real-time quantitative polymerase chain reaction and flow cytometry respectively. Knockdown of MIF led to a significant decrease in mRNA for IL-1β (IL1B) and IL-8 (CXCL8) and interleukin (IL)-8 protein. The addition of recombinant human MIF to cell culture medium increased IL-6 after 24h treatment and IL-6 and IL-8 after 72h treatment. Cell viability was not affected by MIF silencing or rhMIF treatment. The results of this study imply that at least some of the effects of MIF on trophoblast invasion could be mediated through autocrine or paracrine modulation of trophoblast cytokine production.

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Hirase, Tetsuaki, Hiromitsu Hara, Yoshiyuki Miyazaki, Noriko Ide, Ai Nishimoto-Hazuku, Hirokazu Fujimoto, Christiaan J. M. Saris, Hiroki Yoshida e Koichi Node. "Interleukin 27 inhibits atherosclerosis via immunoregulation of macrophages in mice". American Journal of Physiology-Heart and Circulatory Physiology 305, n. 3 (1 agosto 2013): H420—H429. http://dx.doi.org/10.1152/ajpheart.00198.2013.

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Abstract (sommario):

Chronic inflammation in arterial wall that is driven by immune cells and cytokines plays pivotal roles in the development of atherosclerosis. Interleukin 27 (IL-27) is a member of the IL-12 family of cytokines that consists of IL-27p28 and Epstein-Barr virus induced gene 3 (EBI3) and has anti-inflammatory properties that regulate T cell polarization and cytokine production. IL-27-deficient ( Ldlr−/− Ebi3−/−) and IL-27 receptor-deficient ( Ldlr−/− WSX-1−/−) Ldlr−/− mice were generated and fed with a high-cholesterol diet to induce atherosclerosis. Roles of bone marrow-derived cells in vivo and macrophages in vitro were studied using bone marrow reconstitution by transplantation and cultured peritoneal macrophages, respectively. We demonstrate that mice lacking IL-27 or IL-27 receptor are more susceptible to atherosclerosis compared with wild type due to enhanced accumulation and activation of macrophages in arterial walls. The number of circulating proinflammatory Ly6Chi monocytes showed no significant difference between wild-type mice and mice lacking IL-27 or IL-27 receptor. Administration of IL-27 suppressed the development of atherosclerosis in vivo and macrophage activation in vitro that was indicated by increased uptake of modified low-density lipoprotein and augmented production of proinflammatory cytokines. These findings define a novel inhibitory role for IL-27 in atherosclerosis that regulates macrophage activation in mice.

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Vazifeh, D., A. Bryskier e M. T. Labro. "Effect of Proinflammatory Cytokines on the Interplay between Roxithromycin, HMR 3647, or HMR 3004 and Human Polymorphonuclear Neutrophils". Antimicrobial Agents and Chemotherapy 44, n. 3 (1 marzo 2000): 511–21. http://dx.doi.org/10.1128/aac.44.3.511-521.2000.

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ABSTRACT Cytokines, the hallmarks of infectious and inflammatory diseases, modify phagocyte activities and thus may interfere with the immunomodulating properties of antibacterial agents. We have investigated whether various proinflammatory cytokines (interleukin 1 [IL-1], IL-6, IL-8, gamma interferon, tumor necrosis factor alpha [TNF-α], and granulocyte-macrophage colony-stimulating factor [GM-CSF]) modify two macrolide properties, i.e., inhibition of oxidant production by polymorphonuclear neutrophils (PMN) and cellular uptake. Roxithromycin and two ketolides, HMR 3647 and HMR 3004, were chosen as the test agents. TNF-α and GM-CSF (but not the other cytokines) decreased the inhibitory effect of HMR 3647 only on oxidant production by PMN. Fifty percent inhibitory concentrations were, however, in the same range in control and cytokine-treated cells (about 60 to 70 μg/ml), suggesting that HMR 3647 acts downstream of the priming effect of cytokines. In contrast, the impairment of oxidant production by roxithromycin and HMR 3004 was unchanged (or increased) in cytokine-treated cells. This result suggests that HMR 3004 (the strongest inhibitory drug, likely owing to its quinoline side chain) and roxithromycin act on a cellular target upstream of cytokine action. In addition, TNF-α and GM-CSF significantly (albeit moderately) impaired (by about 20%) the uptake of the three molecules by PMN. The inhibitory effect of these two cytokines seems to be related to activation of the p38 mitogen-activated protein kinase. Our data also illuminate the mechanism underlying macrolide uptake: protein kinase A- and tyrosine kinase-dependent phosphorylation seems to be necessary for optimal uptake, while protein kinase C activation impairs it. The relevance of our data to the clinical setting requires further investigations, owing to the complexity of the cytokine cascade during infection and inflammation.

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Moore, A. G., D. A. Brown, W. D. Fairlie, A. R. Bauskin, P. K. Brown, M. L. C. Munier, P. K. Russell, L. A. Salamonsen, E. M. Wallace e S. N. Breit. "The Transforming Growth Factor-β Superfamily Cytokine Macrophage Inhibitory Cytokine-1 Is Present in High Concentrations in the Serum of Pregnant Women1". Journal of Clinical Endocrinology & Metabolism 85, n. 12 (1 dicembre 2000): 4781–88. http://dx.doi.org/10.1210/jcem.85.12.7007.

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Macrophage inhibitory cytokine-1 (MIC-1) is a recently described divergent member of the transforming growth factor-β superfamily. MIC-1 transcription up-regulation is associated with macrophage activation, and this observation led to its cloning. Northern blots indicate that MIC-1 is also present in human placenta. A sensitive sandwich enzyme-linked immunosorbent assay for the quantification of MIC-1 was developed and used to examine the role of this cytokine in pregnancy. High levels of MIC-1 are present in the sera of pregnant women. The level rises substantially with progress of gestation. MIC-1 can also be detected, in large amounts, in amniotic fluid and placental extracts. In addition, the BeWo placental trophoblastic cell line was found to constitutively express the MIC-1 transcript and secrete large amounts of MIC-1. These findings suggest that the placental trophoblast is a major source of the MIC-1 present in maternal serum and amniotic fluid. We suggest that MIC-1 may promote fetal survival by suppressing the production of maternally derived proinflammatory cytokines within the uterus.

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Chung, Fan. "Anti-inflammatory cytokines in asthma and allergy: interleukin-10, interleukin-12, interferon-γ". Mediators of Inflammation 10, n. 2 (2001): 51–59. http://dx.doi.org/10.1080/09629350120054518.

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Interleukin-10 (IL-10) is a cytokine derived fromCD4+T-helper type 2 (TH2) cells identified as a suppressor of cytokines from T-helper type 1(TH1) cells. Interleukin-12 (IL-12) is produced by B cells, macrophages and dendritic cells, and primarily regulates TH1cell differentiation, while suppressing the expansion of TH2cell clones. Interferon-γ (IFN-γ) is a product of TH1cells and exerts inhibitory effects on TH2cell differentiation. These cytokines have been implicated in the pathogenesis of asthma and allergies. In this context, IL-12 and IFN-γ production in asthma have been found to be decreased, and this may reduce their capacity to inhibit IgE synthesis and allergic inflammation. IL-10 is a potent inhibitor of monocyte/macrophage function, suppressing the production of many pro-inflammatory cytokines. A relative underproduction of IL-10 from alveolar macrophages of atopic asthmatics has been reported. Therapeutic modulation of TH1/TH2imbalance in asthma and allergy by mycobacterial vaccine, specific immunotherapy and cytoline-guanosine dinucleotide motif may lead to increases in IL-12 and IFN-γ production. Stimulation of IL-10 production by antigen-specific T-cells during immunotherapy may lead to anergy through inhibition of CD28-costimulatory molecule signalling by IL-10s anti-inflammatory effect on basophils, mast cells and eosinophils.

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45

Doroudian, Mohammad, Andrew O'Neill, Ciaran O'Reilly, Aisling Tynan, Leona Mawhinney, Aoife McElroy, Shanice S. Webster et al. "Aerosolized drug-loaded nanoparticles targeting migration inhibitory factors inhibit Pseudomonas aeruginosa-induced inflammation and biofilm formation". Nanomedicine 15, n. 30 (dicembre 2020): 2933–53. http://dx.doi.org/10.2217/nnm-2020-0344.

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Aim: Macrophage migration inhibitory factor (MIF) is a pro-inflammatory cytokine, which has been shown to promote disease severity in cystic fibrosis. Methods: In this study, aerosolized drug-loaded nanoparticles containing SCD-19, an inhibitor of MIF's tautomerase enzymatic activity, were developed and characterized. Results: The aerosolized nanoparticles had an optimal droplet size distribution for deep lung deposition, with a high degree of biocompatibility and significant cellular uptake. Conclusion: For the first time, we have developed an aerosolized nano-formulation against MIF's enzymatic activity that achieved a significant reduction in the inflammatory response of macrophages, and inhibited Pseudomonas aeruginosa biofilm formation on airway epithelial cells. This represents a potential novel adjunctive therapy for the treatment of P. aeruginosa infection in cystic fibrosis.

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Osawa, Y., H. T. Lee, C. A. Hirshman, D. Xu e C. W. Emala. "Lipopolysaccharide-induced sensitization of adenylyl cyclase activity in murine macrophages". American Journal of Physiology-Cell Physiology 290, n. 1 (gennaio 2006): C143—C151. http://dx.doi.org/10.1152/ajpcell.00171.2005.

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LPS is known to modulate macrophage responses during sepsis, including cytokine release, phagocytosis, and proliferation. Although agents that elevate cAMP reverse LPS-induced macrophage functions, whether LPS itself modulates cAMP and whether LPS-induced decreases in proliferation are modulated via a cAMP-dependent pathway are not known. Murine macrophages (RAW264.7 cells) were treated with LPS in the presence or absence of inhibitors of prostaglandin signaling, protein kinases, CaM, Giproteins, and NF-κB translocation or transcription/translation. LPS effects on CaMKII phosphorylation and the expression of relevant adenylyl cyclase (AC) isoforms were measured. LPS caused a significant dose (5–10,000 ng/ml)- and time (1–8 h)-dependent increase in forskolin-stimulated AC activity that was abrogated by pretreatment with SN50 (an NF-κB inhibitor), actinomycin D, or cycloheximide, indicating that the effect is mediated via NF-κB-dependent transcription and new protein synthesis. Furthermore, LPS decreased the phosphorylation state of CaMKII, and pretreatment with a CaM antagonist attenuated the LPS-induced sensitization of AC. LPS, cAMP, or PKA activation each independently decreased macrophage proliferation. However, inhibition of NF-κB had no effect on LPS-induced decreased proliferation, indicating that LPS-induced decreased macrophage proliferation can proceed via PKA-independent signaling pathways. Taken together, these findings indicate that LPS induces sensitization of AC activity by augmenting the stimulatory effect of CaM and attenuating the inhibitory effect of CaMKII on isoforms of AC that are CaMK sensitive.

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Savaskan, Nic E., Günter Fingerle-Rowson, Michael Buchfelder e Ilker Y. Eyüpoglu. "Brain Miffed by Macrophage Migration Inhibitory Factor". International Journal of Cell Biology 2012 (2012): 1–11. http://dx.doi.org/10.1155/2012/139573.

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Macrophage migration inhibitory factor (MIF) is a cytokine which also exhibits enzymatic properties like oxidoreductase and tautomerase. MIF plays a pivotal role in innate and acquired immunity as well as in the neuroendocrine axis. Since it is involved in the pathogenesis of acute and chronic inflammation, neoangiogenesis, and cancer, MIF and its signaling components are considered suitable targets for therapeutic intervention in several fields of medicine. In neurodegenerative and neurooncological diseases, MIF is a highly relevant, but still a hardly investigated mediator. MIF operates via intracellular protein-protein interaction as well as in CD74/CXCR2/CXCR4 receptor-mediated pathways to regulate essential cellular systems such as redox balance, HIF-1, and p53-mediated senescence and apoptosis as well as multiple signaling pathways. Acting as an endogenous glucocorticoid antagonist, MIF thus represents a relevant resistance gene in brain tumor therapies. Alongside this dual action, a functional homolog-annotated D-dopachrome tautomerase/MIF-2 has been uncovered utilizing the same cell surface receptor signaling cascade as MIF. Here we review MIF actions with respect to redox regulation in apoptosis and in tumor growth as well as its extracellular function with a focus on its potential role in brain diseases. We consider the possibility of MIF targeting in neurodegenerative processes and brain tumors by novel MIF-neutralizing approaches.

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Wu, Yaxian, Huiqiong He, Yunhe Ding, Sirui Liu, Depeng Zhang, Jun Wang, Hongchao Jiang et al. "MK2 mediates macrophage activation and acute lung injury by regulating let-7e miRNA". American Journal of Physiology-Lung Cellular and Molecular Physiology 315, n. 3 (1 settembre 2018): L371—L381. http://dx.doi.org/10.1152/ajplung.00019.2018.

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MAPK-activated protein kinase 2 (MK2) plays a critical role in the development of inflammation. However, the modulatory mechanisms in macrophage activation and acute lung injury (ALI) have not been completely defined. Here, we reported that MK2-deficient mice (MK2−/−) protected against sepsis-induced ALI. In response to lipopolysaccharide (LPS) challenge, MK2−/− mice and myeloid cell-specific MK2 conditional knockout mice (MK2Lyz2-KO) exhibited attenuated inflammatory response, especially producing fewer amounts of tumor necrosis factor-α (TNF-α), interleukin (IL)-6, and macrophage inflammatory protein 2 (MIP-2). LPS treatment in vitro resulted in reduced cytokine expression in MK2−/− bone marrow-derived macrophages (BMDMs). Furthermore, we found that LPS-induced microRNA lethal-7e ( let-7e) expression was significantly increased in MK2−/− macrophages. Transfection of let-7e antagomirs into MK2−/− BMDM rescued LPS-induced expression of TNF-α, IL-6, and MIP-2. In contrast, transfection of let-7e mimics into MK2+/+BMDM decreased cytokine expression. Meanwhile, LPS-induced phosphorylation of cAMP response element-binding (CREB) protein, a substrate of MK2, was downregulated in MK2−/− BMDMs. Lin28, an inhibitory molecule of let-7, was significantly reduced in MK2−/− macrophages. Our results suggested that MK2 boosts LPS-induced macrophage activation and ALI via increasing activation of CREB and consequently, the expression of Lin28 and downregulation of let-7e.

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Khaled, Yazan S., Eyad Elkord e Basil J. Ammori. "Macrophage Inhibitory Cytokine-1: A review of its pleiotropic actions in cancer". Cancer Biomarkers 11, n. 5 (29 novembre 2012): 183–90. http://dx.doi.org/10.3233/cbm-2012-00287.

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Takahashi, M. "Macrophage migration inhibitory factor as a redox-sensitive cytokine in cardiac myocytes". Cardiovascular Research 52, n. 3 (dicembre 2001): 438–45. http://dx.doi.org/10.1016/s0008-6363(01)00408-4.

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