Endothelial Cell Receptors for Histamine*

Simiónescu, N; Heltianu, Constantina; Antohe, Felicia; Simionescu, Maya

doi:10.1111/j.1749-6632.1982.tb25713.x

Cited by 29 publications

(11 citation statements)

References 59 publications

(20 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The demonstration that histamine-induced MARCKS phosphorylation is mediated by HI-type receptors is consistent with previous reports that elevations in TCa2+l, (Rotrosen and Gallin, 19861, VWF release (Hamilton and Sims, 19871, prostaglandin I, (Baenziger et al, 1980), and platelet-activating factor synthesis (McIntyre et al, 1985) are all blocked by HI-type receptor antagonists. Thus, despite the fact that endothelial cells possess both HI and Hz-type receptors (Simionescu et al, 1982), the HI receptor appears to be principally responsible for stimulusiresponse coupling in HUVEC.…”

Section: Discussionmentioning

confidence: 96%

Thrombin and histamine rapidly stimulate the phosphorylation of the myristoylated alanine‐rich C‐kinase substrate in human umbilical vein endothelial cells: Evidence for distinct patterns of protein kinase activation

Jacobson¹,

Pober

Fenton

et al. 1992

Journal Cellular Physiology

View full text Add to dashboard Cite

Human alpha-thrombin and histamine each stimulates protein phosphorylation in human umbilical vein endothelial cells (HUVEC). We have identified the most prominent of these phosphoproteins by immunoprecipitation as the human homolog of the widely distributed myristoylated alanine-rich C-kinase substrate (MARCKS). Stimulation by 0.1-10 U/ml of alpha-thrombin produces a time-dependent, sustained (plateau 3-5 min) level of MARCKS phosphorylation. MARCKS phosphorylation requires thrombin catalytic activity but not receptor binding and is also seen in response to stimulation by a peptide, TR (42-55), that duplicates a portion of the thrombin receptor tethered ligand created by thrombin proteolytic activity. One micromolar histamine, like alpha-thrombin, produces sustained phosphorylation of MARCKS (plateau 3-5 min). In contrast, 100 microM histamine results in rapid but transient MARCKS phosphorylation (peak 1-3 min). HUVEC treated with 100 microM histamine for 5 min can be restimulated by alpha-thrombin but not fresh histamine, suggesting that the histamine receptor was desensitized. MARCKS phosphorylation can also be induced by several exogenous protein kinase C (PKC) activators and both alpha-thrombin- and histamine-induced MARCKS phosphorylation are inhibited by the PKC antagonist staurosporine. However, while prolonged PMA pretreatment ablates histamine-induced MARCKS phosphorylation, the ability of thrombin to induce MARCKS phosphorylation is retained. These findings provide evidence for agonist-specific pathways of protein kinase activation in response to thrombin and histamine in HUVEC.

show abstract

Section: Discussionmentioning

confidence: 96%

Thrombin and histamine rapidly stimulate the phosphorylation of the myristoylated alanine‐rich C‐kinase substrate in human umbilical vein endothelial cells: Evidence for distinct patterns of protein kinase activation

Jacobson¹,

Pober

Fenton

et al. 1992

Journal Cellular Physiology

View full text Add to dashboard Cite

show abstract

“…We also found that ranitidine significantly decreased the elevated MPO activity in lung tissue by LPS in this model. These results suggest that endogenous histamine may be involved in the neutrophil infiltration in lung tissues via the H2 receptor, which is distributed most widely in the endothelial cells [13]. In the literature, the augmentation of neutrophil infiltration by histamine in the lung tissues, along with IL-8 administration, were blocked only by mepyramine, an H1 receptor antagonist [8], and the increased neutrophil activity by histamines was via the activation of the H2 receptor [10].…”

Section: Discussionmentioning

confidence: 71%

“…Because neutrophils should initially be recruited before participating in ALI, chemotactic factors that elicit neutrophil migration are important. Histamine is abundantly distributed in lung and increases the expression of P-selectin [13], which is involved in neutrophil migration to tissues at the surface of the vascular endothelial cells [14,15]. Furthermore, histamine has been reported to increase the release of IL-8 [16] and the chemokinesis of neutrophils via other pathways like phospholipase C and nitric oxide synthase isozymes [10].…”

Section: Discussionmentioning

confidence: 99%

“…It is involved in endothelial cell injury and the migration of neutrophils to tissues [8Y12]. Histamine reacts on its receptors on vascular endothelial cells [13] and increases the expression of Pselectin, which influences the migration of neutrophils to the tissues or endothelial cell surfaces [14,15]. In addition, histamine induces interleukin (IL)-8, a potent neutrophil chemoattractant secreted by endothelial cells [16], and increases the chemokinesis of neutrophils [9].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

The Role of Endogenous Histamine on the Pathogenesis of the Lipopolysaccharide (LPS)-Induced, Acute Lung Injury: A Pilot Study

et al. 2006

View full text Add to dashboard Cite

Histamine is widely distributed in the lungs and increases capillary permeability and P-selectin expression. To observe the role of histamine in acute lung injury (ALI), we measured the histamine and protein concentrations and cell numbers in the bronchoalveolar lavage (BAL) of LPS-induced ALI in rats. We instilled LPS (3 mg/kg) intratracheally, in conjunction with the intravenous histamine receptor antagonists (mepyramine, a H1-receptor antagonist, or ranitidine, a H2-receptor antagonist). LPS increased protein concentration and neutrophil numbers in the BAL as well as myeloperoxidase (MPO) activity in lungs after 6 h. LPS also increased histamine concentration in BAL after 2 h. Mepyramine and ranitidine attenuated the increased histamine concentrations. Total cell number in the BAL and MPO activity in the lungs were significantly decreased and neutrophil numbers and protein concentration in the BAL seemed to decrease with the administration of ranitidine at 6 h. In conclusion, endogenous histamine might be involved in the recruitment of neutrophils and protein leaks in LPS-induced ALI via the H2 receptors.

show abstract

“…Because of this complexity, it is difficult to define the contribution of each cell type and the exact mechanisms underlying each phase of the inflammatory response [Smedegârd, 1985]. For example, it is still debated whether the capability of the endothelial cells to contract and separate [Hammersen, 1980;Simionescu, 1979;Simionescu et al, 1982] is a pre requisite for macromolecular escape from the vessel lumen and the mechanism by which neutrophils increase leakage is still not fully understood [Wedmore and Wil liams, 1980;Williams et al, 1984;Smedegàrd. 1985],…”

Section: Inflammation O F the Microvascular Bedmentioning

confidence: 99%

Leukotriene B<sub>4</sub>, Platelet-Activating Factor and Substance P as Mediators of Acute Inflammation

Thureson‐Klein

Hedqvist

Öhlén³

et al. 1987

Path Immunopathol Res

View full text Add to dashboard Cite

Endothelial Cell Receptors for Histamine*

Cited by 29 publications

References 59 publications

Thrombin and histamine rapidly stimulate the phosphorylation of the myristoylated alanine‐rich C‐kinase substrate in human umbilical vein endothelial cells: Evidence for distinct patterns of protein kinase activation

Thrombin and histamine rapidly stimulate the phosphorylation of the myristoylated alanine‐rich C‐kinase substrate in human umbilical vein endothelial cells: Evidence for distinct patterns of protein kinase activation

The Role of Endogenous Histamine on the Pathogenesis of the Lipopolysaccharide (LPS)-Induced, Acute Lung Injury: A Pilot Study

Leukotriene B<sub>4</sub>, Platelet-Activating Factor and Substance P as Mediators of Acute Inflammation

Contact Info

Product

Resources

About