Caveolae and caveolin in immune cells: distribution and functions

Harris, James; Werling, Dirk; Hope, Jayne; Taylor, Geraldine; Howard, Chris

doi:10.1016/s1471-4906(01)02161-5

Cited by 135 publications

(140 citation statements)

References 68 publications

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“…Thus, adhesion to the endothelium does not only regulate genes that are required for subsequent transendothelial migration but might also initiate the differentiation program of monocytes. This would be in agreement with the finding that HUVEC-attached monocytes showed an up-regulation of CD74 (35), caveolin-1 (36,37), and CD64 (40). CD74 (invariant chain) is required for antigen presentation on major histocompatibility complex class II molecules (35).…”

Section: Il-8 (4)supporting

confidence: 91%

“…Regulated genes in HUVEC-attached monocytes belonging to the phagocytic lineage include MCP-1 (16), MMP-1 (33), tTG-2 (34), CD74 (35), and caveolin-1 (36,37). The upregulation of MCP-1 by monocytes cocultured with endothelial cells was already reported by other groups (15,38) and was therefore used as a positive control.…”

Section: Il-8 (4)mentioning

confidence: 81%

“…CD74 (invariant chain) is required for antigen presentation on major histocompatibility complex class II molecules (35). Caveolin-1 and caveolin-2 have been identified as providing a novel route by which several pathogens are internalized by antigen-presenting cells (36,37). CD64 (Fc-␥-RI) is constitutively expressed on monocytes and represents a high-affinity Fc-␥ receptor that plays a pivotal role in the immune response (40).…”

Section: Il-8 (4)mentioning

confidence: 99%

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Alteration in the gene expression pattern of primary monocytes after adhesion to endothelial cells

Thomas-Ecker¹,

Lindecke

Hatzmann

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

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Monocytes originate from precursors made in the bone and remain in the circulation for nearly 24 h. Much effort has been done to identify the molecules regulating transendothelial migration of monocytes during inflammatory conditions. In contrast, considerably less is known about the process of constitutive monocyte emigration although nearly 340 million monocytes leave the circulation each day in healthy individuals. Previous studies indicated that chemokines were up-regulated in monocytes cocultured with endothelial cells that induce the retraction of the latter cell type, thereby increasing vascular permeability. Thus, we hypothesized that the utilities required for efficient constitutive monocyte extravasation are generated by monocytes themselves because of adhesion to naïve endothelial cells. To test this hypothesis, cDNA microarray analysis was performed to determine the changes in the gene expression pattern of primary monocytes that have been attached to endothelial cells compared with monocytes that were held in suspension, and we were able to identify three major groups of genes. The first group includes genes such as matrix metalloproteinase 1, monocyte chemoattractant protein 1, and tissue transglutaminase 2, which are likely required for monocyte extravasation. The second group consists of genes that are expressed in phagocytes such as caveolin-1 and CD74. Finally, the third group comprises genes that are expressed in cells of endothelial tissue and cartilage including E-selectin, fibronectin-1, matrix Gla protein, and aggrecanase-2. In summary, we conclude that adhesion of peripheral blood monocytes to naïve endothelial cells has two effects: mandatory extravasation-specific genes are regulated, and the differentiation program of monocytes is initiated. differentiation ͉ cDNA microarray

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Section: Il-8 (4)supporting

confidence: 91%

Section: Il-8 (4)mentioning

confidence: 81%

Section: Il-8 (4)mentioning

confidence: 99%

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Alteration in the gene expression pattern of primary monocytes after adhesion to endothelial cells

Thomas-Ecker¹,

Lindecke

Hatzmann

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

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“…However, as suggested (Le et al, 2002;Thomsen et al, 2002), caveolae may exist in lymphocytes too, but may be rapidly converted into endocytic vesicles. It is possible that the enhanced CCR5 trafficking during immune cell activation is due in part to up regulation of caveolin (reviewed in Harris et al, 2002), which may disrupt rafts. Alternatively, lipid remodeling, which occurs during immune cell activation and is known to redistribute several raft-embedded receptors (Alonso and Millan, 2001;Sedwick and Altman, 2002), may facilitate agonist-mediated CCR5 internalization by clathrin-dependent or other noncoated vesicular transport.…”

Section: Discussionmentioning

confidence: 99%

Distinct Mechanisms of Agonist-induced Endocytosis for Human Chemokine Receptors CCR5 and CXCR4

Venkatesan

Rose

Lodge

et al. 2003

MBoC

102

109

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Here we demonstrate that the rate of ligand-induced endocytosis of CCR5 in leukocytes and expression systems is significantly slower than that of CXCR4 and requires prolonged agonist treatment, suggesting that these two receptors use distinct mechanisms. We show that the C-terminal domain of CCR5 is the determinant of its slow endocytosis phenotype. When the C-tail of CXCR4 was exchanged for that of CCR5, the resulting CXCR4-CCR5 (X4-R5) chimera displayed a CCR5-like trafficking phenotype. We found that the palmitoylated cysteine residues in this domain anchor CCR5 to plasma membrane rafts. CXCR4 and a C-terminally truncated CCR5 mutant (CCR5-KRFX) lacking these cysteines are not raft associated and are endocytosed by a clathrin-dependent pathway. Genetic inhibition of clathrin-mediated endocytosis demonstrated that a significant fraction of ligand-occupied CCR5 trafficked by clathrin-independent routes into caveolin-containing vesicular structures. Thus, the palmitoylated C-tail of CCR5 is the major determinant of its raft association and endocytic itineraries, differentiating it from CXCR4 and other chemokine receptors. This novel feature of CCR5 may modulate its signaling potential and could explain its preferential use by HIV for person-to-person transmission of disease. INTRODUCTIONClathrin-mediated endocytosis has been the general paradigm and the most extensively studied mechanism of ligand-induced receptor internalization (Schmid, 1997). However, in recent years, alternative clathrin-independent mechanisms have been described for the uptake of viruses, toxins, and receptors that lack conventional endocytic signals ). Among the latter mechanisms, cholesterol-rich structures called caveolae (Anderson, 1998;Kurzchalia and Parton, 1999) and lipid rafts have been implicated in diverse membrane processes including the assembly of signaling receptor complexes (Simons and Toomre, 2000). Endocytosis of some receptors such as the ␣ subunit of the IL-2 receptor (Tac antigen) and MHC-I, which lack canonical endocytic signals, follow distinct itineraries regulated by the small GTP binding protein, ADP-ribosylation factor 6 (Arf6; Radhakrishna and Donaldson, 1997;Sugita et al., 1999). Clathrin-independent endocytic itineraries are slower than the clathrin-dependent pathway and are functionally relevant in that the long residence time of occupied receptors at the cell surface may enable coupling to multiple signaling pathways.Article published online ahead of print. Mol. Biol. Cell 10.1091/ mbc.E02-11-0714. Article and publication date are available at www.molbiolcell.org/cgi/doi/10.1091/mbc.E02-11-0714. † Corresponding author. E-mail address: aradhana@helix.nih.gov or sv1s@nih.gov. § Present address: INRS-Institut Armand-Frappier, Université du Québec, 531 des Prairies, Laval (Québec), Canada H7V 1B7. Abbreviations used: AOP-RANTES, aminooxypentane-regulated on activation, normal T-cell expressed and secreted; APC, allophycocyanin; Arf6, ADP-ribosylation factor 6; CCV, clathrin-coated vesicles; CHO, Chinese hamster o...

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“…Caveolin-1 is abundant in adipocytes, endothelial cells, and smooth muscle cells (14). Until recently, the presence of caveolae and caveolin-1 in immune cells was a controversial issue (16,17), and probably as a consequence of this, little information exists on its involvement in macrophage immune responses. Recently, however, caveolae have been shown to be involved in the internalization of pathogens (18).…”

mentioning

confidence: 99%

Altered Arachidonate Distribution in Macrophages from Caveolin-1 Null Mice Leading to Reduced Eicosanoid Synthesis

Astudillo

Pérez-Chacón

Meana

et al. 2011

Journal of Biological Chemistry

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Background:We have studied the effect of caveolin-1 deficiency on the mechanisms that regulate free arachidonic acid availability. Results: Macrophages from caveolin-1-deficient mice exhibit elevated fatty acid incorporation and remodeling and a constitutively increased CoA-independent transacylase activity. Conclusion: Macrophages from caveolin-1 null mice show decreased arachidonate mobilization and eicosanoid production upon cell stimulation. Significance: Caveolin-1 may play an important and previously unrecognized role in the eicosanoid biosynthetic response of macrophages.

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Caveolae and caveolin in immune cells: distribution and functions

Cited by 135 publications

References 68 publications

Alteration in the gene expression pattern of primary monocytes after adhesion to endothelial cells

Alteration in the gene expression pattern of primary monocytes after adhesion to endothelial cells

Distinct Mechanisms of Agonist-induced Endocytosis for Human Chemokine Receptors CCR5 and CXCR4

Altered Arachidonate Distribution in Macrophages from Caveolin-1 Null Mice Leading to Reduced Eicosanoid Synthesis

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