Mesenchymal stem cell adhesion to cardiac microvascular endothelium: activators and mechanisms

Segers, Vincent F.M.; Riet, Ivan Van; Andries, Luc; Lemmens, Katrien; Demolder, M.; Becker, Ann J. M. L. De; Kockx, Mark; Keulenaer, Gilles W. De

doi:10.1152/ajpheart.00523.2005

Cited by 189 publications

(146 citation statements)

References 32 publications

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“…Existing data suggest that the cytokines IL-1b and TNF-a activate adherence properties of the MSC including the upregulation of the VCAM-1-VLA-4 adhesion pathway. 48 Additional receptors known to be upregulated by TNF-a priming include CCR3 and CCR4; these findings correlate with the observation of increased in vitro migration to RANTES (a CCR3 ligand) and macrophage-derived cytokine (MDC (CCL22)-a CCR4 ligand). 3 Several growth factors have been shown to induce MSC migration.…”

Section: Activation Of Msc With Proinflammatory Cytokines (That Is Tmentioning

confidence: 53%

Inflammation and tumor microenvironments: defining the migratory itinerary of mesenchymal stem cells

et al. 2008

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Section: Activation Of Msc With Proinflammatory Cytokines (That Is Tmentioning

confidence: 53%

Inflammation and tumor microenvironments: defining the migratory itinerary of mesenchymal stem cells

et al. 2008

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“…2B, 18Co cells were treated overnight with TNF-␣ at varying concentrations (0 -80 ng/ml), followed by treatment with LPA (10 M) for 4 h. Increases in COX-2 protein expression were evident at a TNF-␣ concentration as low as 0.8 ng/ml, well within physiological levels, and persisted at a concentration of 80 ng/ml. Based on this data, subsequent experiments were performed using TNF-␣ at a concentration of 8 ng/ml, well within the range of concentrations used in other studies (12,26,41,61). In Fig.…”

Section: Lpa and Tnf-␣ Lead To Synergistic Cox-2 Expression In 18co Cmentioning

confidence: 88%

TNF-α potentiates lysophosphatidic acid-induced COX-2 expression via PKD in human colonic myofibroblasts

Perez

Nie

Sinnett‐Smith

et al. 2011

American Journal of Physiology-Gastrointestinal and Liver Physi

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The myofibroblast (MFB) has recently been identified as an important mediator of tumor necrosis factor-α (TNF-α)-associated colitis and cancer, but the mechanism(s) involved remains incompletely understood. Here, we show that treatment of 18Co cells, a model of human colonic MFBs, with TNF-α and lysophosphatidic acid (LPA) induced striking synergistic cyclooxygenase-2 (COX-2) protein expression and production of PGE2. This effect was prevented by the LPA1 receptor antagonist Ki16425, the Giα-specific inhibitor pertussis toxin, and by the preferential protein kinase (PK) C inhibitors GF109203X and Go6983. As a known downstream target of LPA and PKC, we tested whether PKD, recently implicated in the regulation of COX-2 expression in MFB, was involved in this response. TNF-α, while having no detectable effect on the activation of PKD when added alone, augmented PKD activation stimulated by LPA, as measured by PKD autophosphorylation at Ser910. LPA-induced PKD activation was also inhibited by Ki16425, pertussis toxin, GF109203X, and Go6983. Transfection of 18Co cells with short interfering RNA targeting PKD completely inhibited the synergistic increase in COX-2 protein, demonstrating a critical role of PKD in this response. Our results imply that cross talk between TNF-α and LPA results in the amplification of COX-2 protein expression via a conserved PKD-dependent signaling pathway that appears to involve the LPA1 receptor and the G protein Giα. PKD plays a critical role in the expression of COX-2 in human colonic MFBs and may contribute to an inflammatory microenvironment that promotes tumor growth.

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“…Electron microscopy revealed that, even after 30 min of perfusion, approximately 30% of the perfused MSC had transmigrated across the endothelium -this percentage rose to 50% after 60 min but remained constant thereafter (Schmidt et al, 2006). Elsewhere, transmigration across the endothelium into cardiac tissue of MSC injected into the ventricular cavity has been observed in rats pre-treated with TNF-a or in rats 24 h after ischaemia (30 min)-reperfusion injury (Segers et al, 2006). Whilst the adhesion molecules and mechanisms involved in MSC diapedesis are, as yet, unclear, the molecules identified to date that regulate the various other stages of MSC recruitment from the blood stream to the surrounding tissues, summarised in Fig 1, have furthered our understanding of this process and extended our appreciation of the ability to administer MSC systemically as a potential therapeutic strategy.…”

Section: +mentioning

confidence: 99%

“…. The process of MSC transendothelial migration appears to be similar to that of leucocytes and HSC, albeit under the control of specific adhesion molecules elucidated largely by Ruster et al (2006); Segers et al (2006) and Schmidt et al (2006). 1 Has been shown to be inhibited by: a neutralising P-selectin antibody, fucosidase or O-sialoglucoprotein-endopeptidase treatment of MSC, the absence of Ca 2+ /Mg…”

Section: Integrins and Their Role In Msc Firm-adhesion And Transendotmentioning

confidence: 99%

Recent advances into the understanding of mesenchymal stem cell trafficking

et al. 2007

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SummaryThe use of adult stem cells to regenerate damaged tissue circumvents the moral and technical issues associated with the use of those from an embryonic source. Mesenchymal stem cells (MSC) can be isolated from a variety of tissues, most commonly from the bone marrow, and, although they represent a very small percentage of these cells, are easily expandable. Recently, the use of MSC has provided clinical benefit to patients with osteogenesis imperfecta, graft-versushost disease and myocardial infarction. The cellular cues that enabled the MSC to be directed to the sites of tissue damage and the mechanisms by which MSC then exert their therapeutic effect are becoming clearer. This review discusses the relative therapeutic importance of the ability of MSC to differentiate into multiple cell lineages or stimulate resident or attracted cells via a paracrine mode of action. It also reviews recent findings that MSC home to damaged tissues in a similar, but somewhat distinct, manner to that of leucocytes via the utilisation of adhesion molecules, such as selectins and integrins, and chemokines and their receptors in a manner reminiscent of leucocytes trafficking from the blood stream to inflammatory sites.

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Mesenchymal stem cell adhesion to cardiac microvascular endothelium: activators and mechanisms

Abstract: . Mesenchymal stem cell adhesion to cardiac microvascular endothelium: activators and mechanisms.

Cited by 189 publications

References 32 publications

Inflammation and tumor microenvironments: defining the migratory itinerary of mesenchymal stem cells

Inflammation and tumor microenvironments: defining the migratory itinerary of mesenchymal stem cells

TNF-α potentiates lysophosphatidic acid-induced COX-2 expression via PKD in human colonic myofibroblasts

Recent advances into the understanding of mesenchymal stem cell trafficking

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