Connexins in leukocytes: shuttling messages?

Wong, Cindy; Christen, Thomas; Kwak, Brenda R.

doi:10.1016/j.cardiores.2003.12.015

Cited by 41 publications

(40 citation statements)

References 78 publications

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“…Connexins may regulate leukocyte trafficking into inflamed tissues. 131 Connexins form gap junctions that connect adjacent cells and permit intercellular communication. 132 Gap junctions may form between leukocytes and leukocytes, or leukocytes and endothelial cells.…”

Section: Connexinsmentioning

confidence: 99%

Vascular Adhesion Molecules in Atherosclerosis

Galkina

Ley

2007

ATVB

687

513

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Abstract-Numerous reports document the role of vascular adhesion molecules in the development and progression of atherosclerosis. Recent novel findings in the field of adhesion molecules require an updated summary of current research. In this review, we highlight the role of vascular adhesion molecules including selectins, vascular cell adhesion molecule (VCAM)-1, intercellular adhesion molecule1 (ICAM-1), PECAM-1, JAMs, and connexins in atherosclerosis. The immune system is important in atherosclerosis, and significant efforts are under way to understand the vascular adhesion molecule-dependent mechanisms of immune cell trafficking into healthy and atherosclerosis-prone arterial walls. This review focuses on the role of vascular adhesion molecules in the regulation of immune cell homing during atherosclerosis and discusses future directions that will lead to better understanding of this disease. (Arterioscler

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Section: Connexinsmentioning

confidence: 99%

Vascular Adhesion Molecules in Atherosclerosis

Galkina

Ley

2007

ATVB

687

513

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“…This process, termed gap junction-mediated intercellular communication (GJIC), is a widespread mechanism for the maintenance of homeostasis in tissues and organs. In the immune system, the existence and physiological role of GJIC between several types of immune cells have been reported (12,13). Indeed, many immune cells (e.g., T cells, B cells, macrophages, mast cells, and follicular DCs) have been found to form homotypic interactions with themselves or heterotypic interactions with other cell types via gap junctions (12,13).…”

Section: Endritic Cells (Dc)mentioning

confidence: 99%

“…Indeed, many immune cells (e.g., T cells, B cells, macrophages, mast cells, and follicular DCs) have been found to form homotypic interactions with themselves or heterotypic interactions with other cell types via gap junctions (12,13). With respect to functional aspects of GJIC, it is considered to be involved in hematopoiesis (14), T cell development in the thymus (15), inflammation (13), transendothelial migration of macrophages (16) and neutrophils (17), and Ab formation in the germinal center (18,19). Very recently, Neijssen et al (20) have revealed a novel mechanism of cross-presentation via GJIC.…”

Section: Endritic Cells (Dc)mentioning

confidence: 99%

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Gap Junction-Mediated Intercellular Communication between Dendritic Cells (DCs) Is Required for Effective Activation of DCs

Matsue

Yao

Matsue³

et al. 2006

The Journal of Immunology

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Gap junctions, formed by members of the connexin (Cx) family, are intercellular channels allowing direct exchange of signaling molecules. Gap junction-mediated intercellular communication (GJIC) is a widespread mechanism for homeostasis in organs. GJIC in the immune system is not yet fully understood. Although dendritic cells (DC) reportedly form cell-to-cell contact between DCs in nonlymphoid and lymphoid organs, GJIC between DCs remains unknown. In this study we examined whether DCs form GJIC. XS52 and bone marrow-derived DCs (BMDCs) were tested for GJIC by counting intercellular transfer of Lucifer Yellow microinjected into a cell. Either DC became effectively dye-coupled when activated with LPS plus IFN-γ or TNF-α plus IFN-γ. LPS- plus IFN-γ-induced dye-coupling was mediated by DC-derived TNF-α. In addition, CpG plus IFN-γ induced dye-coupling in BMDCs, which was also mediated by DC-derived TNF-α. LPS- plus IFN-γ-induced activation of DCs (assessed by CD40 expression) was observed when there was cell-to-cell contact and was significantly blocked by heptanol, a gap junction blocker. These results indicate that cell-to-cell contact and GJIC are required for effective DC activation. In addition, heptanol significantly inhibited the LPS- plus IFN-γ-induced up-regulation of the other costimulatory (i.e., CD80 and CD86) and MHC class II molecules expressed by BMDCs, and it significantly reduced their allostimulatory capacity. Among Cx members, Cx43 was up-regulated in dye-coupled BMDCs, and Cx mimetic peptide, a blocker of Cx-mediated GJIC, significantly inhibited the dye-coupling and activation, suggesting the involvement of Cx43. Thus, our study provides the first evidence for GJIC between DCs, which is required for effective DC activation.

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“…For example, inhibition of gap junctions increases neutrophil but decreases monocyte migration (Wong et al 2004). The inhibitory effect of gap junction expression on PMN migration appears to involve heterotypic (i.e.…”

Section: Sex Differences In Leukocyte Recruitmentmentioning

confidence: 99%

Sex differences in vascular function: implication of endothelium-derived hyperpolarizing factor

Villar¹,

Hobbs²,

Ahluwalia

2008

Journal of Endocrinology

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The vascular endothelium plays a crucial role in the regulation of vascular homeostasis by controlling vascular tone, coagulation, and inflammatory responses. These actions are exerted by endothelial factors including nitric oxide, prostacyclin, and endothelium-derived hyperpolarizing factor (EDHF). The greater incidence of cardiovascular disease (CVD) in men and postmenopausal women compared with premenopausal women implies a vasoprotective phenotype of females, which may be influenced by sex hormones. These hormones, particularly estrogen, have modulatory effects on the endothelium and circulating cells that have been implicated in vascular inflammation and in the development of CVD. EDHF seems to be the predominant endothelial factor in the resistance vasculature of females and this mediator could afford the beneficial cardiovascular risk profile observed in premenopausal woman. In this review, we discuss sex differences in EDHF biology and how sex hormones can modulate EDHF responses. We also review the implication of sex hormone-dependent regulation of EDHF in inflammatory processes, platelet function, and repair after vascular damage, each of which have a critical role in several aspects of the pathogenesis of CVD.

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Connexins in leukocytes: shuttling messages?

Cited by 41 publications

References 78 publications

Vascular Adhesion Molecules in Atherosclerosis

Vascular Adhesion Molecules in Atherosclerosis

Gap Junction-Mediated Intercellular Communication between Dendritic Cells (DCs) Is Required for Effective Activation of DCs

Sex differences in vascular function: implication of endothelium-derived hyperpolarizing factor

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