Variability Among Human Umbilical Vein Endothelial Cultures

Watson, Campbell D.; Camera-Benson, Louise; Palmer-Crocker, Rebecca; Pober, Jordan S.

doi:10.1126/science.7716553

Cited by 46 publications

(27 citation statements)

References 3 publications

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“…However, Orai1 was involved in regulating SOCE in HUVECs, consistent with evidence on the importance of Orai1 in mediating Ca 2ϩ entry in these cells (Abdullaev et al, 2008). The difference with HUVECs may reflect the specialized nature and uniqueness of these cells, which are often, and perhaps incorrectly, used as a surrogate for ECs (Watson et al, 1995).…”

Section: Discussionmentioning

confidence: 54%

The Ca²⁺ Sensor Stromal Interaction Molecule 1 (STIM1) Is Necessary and Sufficient for the Store-Operated Ca²⁺ Entry Function of Transient Receptor Potential Canonical (TRPC) 1 and 4 Channels in Endothelial Cells

et al. 2011

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Section: Discussionmentioning

confidence: 54%

The Ca²⁺ Sensor Stromal Interaction Molecule 1 (STIM1) Is Necessary and Sufficient for the Store-Operated Ca²⁺ Entry Function of Transient Receptor Potential Canonical (TRPC) 1 and 4 Channels in Endothelial Cells

et al. 2011

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“…It is unclear why we have not observed such an effect. Our HUVEC are devoid of CD45 ϩ contaminants, mostly monocytes, present in some other culture systems (76). Thus a possible explanation is that HMGB1 effects on HUVEC cultures may depend on monocyte contamination.…”

Section: Discussionmentioning

confidence: 99%

IL-1α and IL-1β Are Endogenous Mediators Linking Cell Injury to the Adaptive Alloimmune Response

Rao¹,

Tracey

Pober

2007

The Journal of Immunology

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Preoperative or perioperative ischemic injury of allografts predisposes to graft arteriosclerosis, the major cause of late graft failure. We hypothesize that injured tissues release mediators that increase the production of pathogenic cytokines by alloreactive T cells. We find that freeze-thaw lysates of human endothelial cells (EC) increase both IFN-γ and IL-17 production by human CD4+ T cells activated by HLA-DR+ allogeneic EC. Immunoadsorption of high-mobility group box 1 protein (HMGB1) reduces this activity in the lysates by about one-third, and recombinant HMGB1 increases T cell cytokine production. HMGB1 acts by inducing IL-1β secretion from contaminating monocytes via TLR4 and CD14. Upon removal of contaminating monocytes, the remaining stimulatory activity of EC lysates is largely attributable to IL-1α. Recombinant IL-1 directly augments IFN-γ and IL-17 production by activated memory CD4+ T cells, which express IL-1R1. Furthermore, IL-1 increases the frequency of alloreactive memory CD4+ T cells that produce IL-17, but not those that produce IFN-γ, in secondary cultures. Our results suggest that IL-1, released by injured EC or by HMGB1-stimulated monocytes, is a key link between injury and enhanced alloimmunity, offering a new therapeutic target for preventing late graft failure.

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“…In preliminary experiments, we have been able to detect the expression of IL-2R␣ and ␤ on ECs in some cultures, but we have not found consistent expression or a consistent increase in expression in response to IFN-␣ or IFN-␥. It is also possible that IL-2-induced responses require the mediation of an additional contaminating cell type (e.g., a T cell or monocyte) that may be more abundant in some endothelial culture systems than others (42).…”

Section: Resultsmentioning

confidence: 99%

IL-4 and IL-13 activate the JAK2 tyrosine kinase and Stat6 in cultured human vascular endothelial cells through a common pathway that does not involve the gamma c chain.

Palmer-Crocker

Hughes²,

Pober³

1996

J. Clin. Invest.

101

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1 and markedly augments VCAM-1 expression induced by TNF or IL-1 (1-6). These changes favor the binding of eosinophils and T cells to endothelial cells (ECs). In addition, IL-4-treated ECs secrete the chemokine MCP-1 (7) and selectively stimulate transendothelial migration of eosinophils in vitro (8). The effects of IL-4 on EC differ from those on hematopoietic cell types in that IL-4 is not an endothelial mitogen or survival factor.IL-13 is another pleiotropic immunoregulatory cytokine (9, 10) that shares a number of biological properties with IL-4 (11-16). IL-13, like IL-4, selectively induces VCAM-1 in cultured human ECs (17, 18). IL-13 has been shown recently to stimulate tyrosine phosphorylation of the IL-4-binding subunit of the 140-kD IL-4 receptor (IL-4R) in a number of hematopoietic cell types (19), suggesting that IL-4 and IL-13 may activate a common tyrosine kinase. Two recent findings further suggest that the IL-13-binding subunit of the IL-13 receptor (IL-13R) may share at least one subunit with the IL-4R: ( a ) the IL-4 mutant protein Y124D, which inhibits IL-4-dependent reactions (20) also inhibits effects of IL-13 (21, 22); and ( b ) IL-13 competes with radiolabeled IL-4 for binding to some cells (21-24).The IL-2 receptor (IL-2R) ␥ chain is a functional component of the IL-4R in lymphocytes, required for tyrosine phosphorylation of the insulin receptor substrate-1 in response to IL-4 (25) and for IL-4-induced cell proliferation (26). The (IL-2R) ␥ chain, recently renamed the common ␥ chain ( ␥ c chain), is also a common receptor component of many other members of the cytokine receptor superfamily including , [30][31][32]34). It is not known if IL-13 can signal through ␥ c , but some cell lines of hematopoietic origin are known to respond to IL-4 and IL-13 in the absence of ␥ c (24,35). This evidence suggests two distinct signaling pathways for IL-4, one involving ␥ c , and an alternate pathway, shared with IL-13, that does not use ␥ c .Previous work by our laboratory has shown that IL-4 activates a protein tyrosine kinase that phosphorylates the IL-4R binding subunit in cultured human ECs and that activation of this protein tyrosine kinase may play a part in the signaling pathway leading to increased VCAM-1 expression in response to . We now show that IL-13, like IL-4, causes the activation of a protein tyrosine kinase in ECs that phosphorylates IL-4R, that both cytokines activate JAK2 and the Stat6 transcription factor, and that these responses cannot involve ␥ c , since this protein is not expressed in ECs. MethodsCell isolation and culture. ECs were isolated and cultured as described previously (37,38). ECs used in these experiments were of passage levels 2 to 5 and were free of detectable CD45 ϩ leukocytes. PHA- 1. Abbreviations used in this paper: EC, endothelial cell; JAK, Janus kinase; RT, reverse transcription; Stat, signal transducer and activator of transcription; VCAM-1, vascular cell adhesion molecule-1.

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Variability Among Human Umbilical Vein Endothelial Cultures

Cited by 46 publications

References 3 publications

The Ca²⁺ Sensor Stromal Interaction Molecule 1 (STIM1) Is Necessary and Sufficient for the Store-Operated Ca²⁺ Entry Function of Transient Receptor Potential Canonical (TRPC) 1 and 4 Channels in Endothelial Cells

The Ca²⁺ Sensor Stromal Interaction Molecule 1 (STIM1) Is Necessary and Sufficient for the Store-Operated Ca²⁺ Entry Function of Transient Receptor Potential Canonical (TRPC) 1 and 4 Channels in Endothelial Cells

IL-1α and IL-1β Are Endogenous Mediators Linking Cell Injury to the Adaptive Alloimmune Response

IL-4 and IL-13 activate the JAK2 tyrosine kinase and Stat6 in cultured human vascular endothelial cells through a common pathway that does not involve the gamma c chain.

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Variability Among Human Umbilical Vein Endothelial Cultures

Cited by 46 publications

References 3 publications

The Ca2+ Sensor Stromal Interaction Molecule 1 (STIM1) Is Necessary and Sufficient for the Store-Operated Ca2+ Entry Function of Transient Receptor Potential Canonical (TRPC) 1 and 4 Channels in Endothelial Cells

The Ca2+ Sensor Stromal Interaction Molecule 1 (STIM1) Is Necessary and Sufficient for the Store-Operated Ca2+ Entry Function of Transient Receptor Potential Canonical (TRPC) 1 and 4 Channels in Endothelial Cells

IL-1α and IL-1β Are Endogenous Mediators Linking Cell Injury to the Adaptive Alloimmune Response

IL-4 and IL-13 activate the JAK2 tyrosine kinase and Stat6 in cultured human vascular endothelial cells through a common pathway that does not involve the gamma c chain.

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The Ca²⁺ Sensor Stromal Interaction Molecule 1 (STIM1) Is Necessary and Sufficient for the Store-Operated Ca²⁺ Entry Function of Transient Receptor Potential Canonical (TRPC) 1 and 4 Channels in Endothelial Cells

The Ca²⁺ Sensor Stromal Interaction Molecule 1 (STIM1) Is Necessary and Sufficient for the Store-Operated Ca²⁺ Entry Function of Transient Receptor Potential Canonical (TRPC) 1 and 4 Channels in Endothelial Cells