Monocyte Chemotactic Protein-3 Is a Myocardial Mesenchymal Stem Cell Homing Factor

Schenk, Soren; Mal, Niladri; Finan, Amanda; Zhang, Ming; Kiedrowski, Matt; Popović, Zoran B.; McCarthy, Patrick M.; Penn, Marc S.

doi:10.1634/stemcells.2006-0293

Cited by 252 publications

(201 citation statements)

References 39 publications

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“…5 MSCs can migrate to sites of tissue damage, 6,7 where they are activated by inflammatory cytokines (such as IFN-c) and several chemokines, which can recruit or suppress lymphocytes. [8][9][10][11] Interleukin-1b (IL-1b) is an important inflammatory factor that is expressed abundantly during the active phase of UC. [12][13][14] The UC mice induced by DSS treatment exhibit many symptoms similar to human UC, such as diarrhea, bloody feces, body weight loss, mucosal ulceration and shortening of the large intestine.…”

Section: Introductionmentioning

confidence: 99%

Pre-treatment with IL-1β enhances the efficacy of MSC transplantation in DSS-induced colitis

et al. 2012

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Mesenchymal stem cells (MSCs) have been used experimentally for treating inflammatory disorders, partly due to their immunosuppressive properties. Although interleukin-1b (IL-1b) is one of the most important inflammatory mediators, growing evidence indicates that IL-1b signaling elicits the immunosuppressive properties of MSCs. However, it remains unclear how IL-1b signaling accomplishes this activity. Here, we focus on the therapeutic efficacy of IL-1b-primed MSCs in the dextran sulfate sodium (DSS)-induced colitis model, in addition to the underlining mechanisms. We first found that IL-1b-primed MSCs, without any observable phenotype change in vitro, significantly attenuated the development of DSS-induced murine colitis. Moreover, IL-1b-primed MSCs modulated the balance of immune cells in the spleen and the mesenteric lymph nodes (MLNs) through elevating cyclooxygenase-2 (COX-2), IL-6 and IL-8 expression and influencing the polarization of peritoneal macrophages. Importantly, IL-1b-primed MSCs possessed an enhanced ability to migrate to the inflammatory site of the gut via upregulation of chemokine receptor type 4 (CXCR4) expression. In summary, IL-1b-primed MSCs have improved efficacy in treating DSS-induced colitis, which at least partly depends on their increased immunosuppressive capacities and enhanced migration ability.

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Section: Introductionmentioning

confidence: 99%

Pre-treatment with IL-1β enhances the efficacy of MSC transplantation in DSS-induced colitis

et al. 2012

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“…MCP-3, another potent mononuclear cell chemoattractant, is also transiently induced in mouse myocardial infarcts [137]. Transplantation of MCP-3-expressing cardiac fibroblasts into the infarct border zone one month after coronary ligation resulted in enhanced homing of injected mesenchymal stem cells in the infarcted myocardium [137].…”

mentioning

confidence: 99%

“…Transplantation of MCP-3-expressing cardiac fibroblasts into the infarct border zone one month after coronary ligation resulted in enhanced homing of injected mesenchymal stem cells in the infarcted myocardium [137]. However, the exact role of MCP-3-mediated interactions in ischemic tissues remains poorly understood.…”

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confidence: 99%

The immune system and cardiac repair

Frangogiannis

2008

Pharmacological Research

572

499

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Myocardial infarction is the most common cause of cardiac injury and results in acute loss of a large number of myocardial cells. Because the heart has negligible regenerative capacity, cardiomyocyte death triggers a reparative response that ultimately results in formation of a scar and is associated with dilative remodeling of the ventricle. Cardiac injury activates innate immune mechanisms initiating an inflammatory reaction. Toll Like Receptor-mediated pathways, the complement cascade and reactive oxygen generation induce Nuclear Factor (NF)-κB activation and upregulate chemokine and cytokine synthesis in the infarcted heart. Chemokines stimulate the chemotactic recruitment of inflammatory leukocytes into the infarct, while cytokines promote adhesive interactions between leukocytes and endothelial cells, resulting in transmigration of inflammatory cells into the site of injury. Monocyte subsets play distinct roles in phagocytosis of dead cardiomyocytes and in granulation tissue formation through the release of growth factors. Clearance of dead cells and matrix debris may be essential for resolution of inflammation and transition into the reparative phase. Transforming Growth Factor (TGF)-β plays a crucial role in cardiac repair by suppressing inflammation while promoting myofibroblast phenotypic modulation and extracellular matrix deposition. Myofibroblast proliferation and angiogenesis result in formation of highly vascularized granulation tissue. As the healing infarct matures, fibroblasts become apoptotic and a collagen-based matrix is formed, while many infarct neovessels acquire a muscular coat and uncoated vessels regress. Timely resolution of the inflammatory infiltrate and spatial containment of the inflammatory and reparative response into the infarcted area are essential for optimal infarct healing. Targeting inflammatory pathways following infarction may reduce cardiomyocyte injury and attenuate adverse remodeling. In addition, understanding the role of the immune system in cardiac repair is necessary in order to design optimal strategies for cardiac regeneration.

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“…CCL7, previously known as monocyte-specific CCL3/MCP-3, belongs to the MCP subfamily of CCLs. CCL7 binds to CCR1, CCR2, and CCR3, is expressed at multiple sites of inflammation, and is produced by monocytes, fibroblasts, endothelial cells, and mast cells (24)(25)(26). Several studies suggest that CCL7 may be involved in vascular pathologies in which proliferation of smooth muscle cells plays an important role (27).…”

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confidence: 99%

Role of CCL7 in Type I Hypersensitivity Reactions in Murine Experimental Allergic Conjunctivitis

Kuo

Collins

Boettner

et al. 2017

The Journal of Immunology

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Molecules that are necessary for ocular hypersensitivity reactions include the receptors CCR1 and CCR3; CCL7 is a ligand for these receptors. Therefore, we explored the role of CCL7 in mast cell activity and motility in vitro and investigated the requirement for CCL7 in a murine model of IgE-mediated allergic conjunctivitis. For mast cells treated with IgE and Ag, the presence of CCL7 synergistically enhanced degranulation and calcium influx. CCL7 also induced chemotaxis in mast cells. CCL7-deficient bone marrow–derived mast cells showed decreased degranulation following IgE and Ag treatment compared with wild-type bone marrow–derived mast cells, but there was no difference in degranulation when cells were activated via an IgE-independent pathway. In vivo, CCL7 was upregulated in conjunctival tissue during an OVA-induced allergic response. Notably, the early-phase clinical symptoms in the conjunctiva after OVA challenge were significantly higher in OVA-sensitized wild-type mice than in control challenged wild-type mice; the increase was suppressed in CCL7-deficient mice. In the OVA-induced allergic response, the numbers of conjunctival mast cells were lower in CCL7-deficient mice than in wild-type mice. Our results demonstrate that CCL7 is required for maximal OVA-induced ocular anaphylaxis, mast cell recruitment in vivo, and maximal FcεRI-mediated mast cell activation in vitro. A better understanding of the role of CCL7 in mediating ocular hypersensitivity reactions will provide insights into mast cell function and novel treatments for allergic ocular diseases.

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Monocyte Chemotactic Protein-3 Is a Myocardial Mesenchymal Stem Cell Homing Factor

Cited by 252 publications

References 39 publications

Pre-treatment with IL-1β enhances the efficacy of MSC transplantation in DSS-induced colitis

Pre-treatment with IL-1β enhances the efficacy of MSC transplantation in DSS-induced colitis

The immune system and cardiac repair

Role of CCL7 in Type I Hypersensitivity Reactions in Murine Experimental Allergic Conjunctivitis

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