Anti-Inflammatory Functions of Protein C Require RAGE and ICAM-1 in a Stimulus-Dependent Manner

Braach, Natascha; Buschmann, Kirsten; Pflaum, Johanna; Hudalla, Hannes; Koch, Lutz; Ryschich, Eduard; Poeschl, Johannes; Frommhold, David

doi:10.1155/2014/743678

Cited by 5 publications

(4 citation statements)

References 51 publications

(104 reference statements)

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“…The main differentially expressed gene involved in the AGE-RAGE signaling pathway was intercellular adhesion molecule-1 ( ICAM-1 ), as illustrated by the volcano plot in Fig. 5 C. The receptor for advanced glycation end products (RAGE) acts in concert with ICAM-1 to mediate pathological processes [ 32 , 33 ]. Next, we verified that the ICAM-1 mRNA level in MLE-12 cells indeed increased after stimulation with low-dose sTN-C (Fig.…”

Section: Resultsmentioning

confidence: 99%

Tenascin-C modulates alveolarization in bronchopulmonary dysplasia

Liu,

Mao,

et al. 2024

Inflamm Regener

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Bronchopulmonary dysplasia (BPD) is a chronic lung disease characterized by retarded alveolarization. Tenascin-C (TN-C), an extracellular matrix glycoprotein and soluble molecule, is involved in tissue morphogenesis. In the present study, we demonstrated that the level of TN-C in lung tissues was greater in a mouse model of BPD induced by 85% oxygen. TN-C deficiency, however, impaired alveolarization in the hyperoxia-induced BPD model. In contrast, a functional TN-C blocking antibody ameliorated alveolar dysplasia in BPD-like mice. Mechanistically, hyperoxia increased the soluble TN-C (sTN-C) released from respiratory epithelial cells. On one hand, low-dose sTN-C promoted lung epithelial cell proliferation and migration, which was mediated by ICAM-1. On the other hand, high-dose sTN-C hindered the proliferation and migration of epithelial cells. Overall, this study revealed that TN-C plays a dual role in lung alveolarization and that TN-C may be a target in BPD therapy.

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Section: Resultsmentioning

confidence: 99%

Tenascin-C modulates alveolarization in bronchopulmonary dysplasia

Liu,

Mao,

et al. 2024

Inflamm Regener

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“…Lethal endotoxemia was induced by a single i.p. injection of 40 mg/kg LPS ( Escherichia coli ; serotype 055:B5 Sigma, Taufkirchen, Germany) which was reconstituted in 100 μ L of sterile PBS, as reported previously [ 35 ]. Clinoleic, Smoflipid, Lipofundin, or equivalent volume of normal saline was administered i.v.…”

Section: Methodsmentioning

confidence: 99%

The Olive Oil‐Based Lipid Clinoleic Blocks Leukocyte Recruitment and Improves Survival during Systemic Inflammation: A Comparative In Vivo Study of Different Parenteral Lipid Emulsions

Buschmann

Poeschl

Braach

et al. 2015

Mediators of Inflammation

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Although fish oil-based and olive oil-based lipid emulsions have been shown to exert anti-inflammatory functions, the immunomodulating properties of lipids are still controversial. Therefore, we investigated the anti-inflammatory effect of three different parenterally administered lipid emulsions in vivo: olive oil-based Clinoleic, fish oil-based Smoflipid, and soybean oil-based Lipofundin. We observed leukocyte recruitment in inflamed murine cremaster muscle using intravital microscopy and survival in a murine model of LPS-induced systemic inflammation and analyzed expression of leukocyte and endothelial adhesion molecules. Olive oil-based Clinoleic and fish oil-based Smoflipid profoundly inhibited leukocyte adhesion compared to Lipofundin during LPS-induced inflammation of the murine cremaster muscle. In the trauma model of cremaster muscle inflammation, Lipofundin was the only lipid emulsion that even augmented leukocyte adhesion. In contrast to Smoflipid and Lipofundin, Clinoleic effectively blocked leukocyte recruitment and increased survival during lethal endotoxemia. Flow chamber experiments and analysis of adhesion molecule expression suggest that both endothelial and leukocyte driven mechanisms might contribute to anti-inflammatory effects of Clinoleic. We conclude that the anti-inflammatory properties of Clinoleic are superior to those of Smoflipid and Lipofundin even during systemic inflammation. Thus, these results should stimulate further studies investigating parenteral lipids as an anti-inflammatory strategy in critically ill patients.

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“…Administration of sRAGE decreases inflammation under various experimental conditions [ 136 ]. Another interesting still unexplored contribution of AECI to the inflammatory network may come from the known co-operation of ICAM-1 with RAGE in pulmonary endothelial cells to mediate leukocyte recruitment after LPS-mediated lung injury [ 137 ]. Since AECI selectively expresses both ICAM-1 [ 138 ] and RAGE, interactions of both inflammatory proteins are possible and should come into the experimental focus of AECs.…”

Section: Putative Signaling Pathways Connected With Aeci Cellsmentioning

confidence: 99%

Potential contribution of alveolar epithelial type I cells to pulmonary fibrosis

Kasper

Barth

2017

Bioscience Reports

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Pulmonary fibrosis (PF) is characterized by inflammation and fibrosis of the interstitium and destruction of alveolar histoarchitecture ultimately leading to a fatal impairment of lung function. Different concepts describe either a dominant role of inflammatory pathways or a disturbed remodeling of resident cells of the lung parenchyma during fibrogenesis. Further, a combination of both the mechanisms has been postulated. The present review emphasizes the particular involvement of alveolar epithelial type I cells in all these processes, their contribution to innate immune/inflammatory functions and maintenance of proper alveolar barrier functions. Amongst the different inflammatory and repair events the purinergic receptor P2X7, an ATP-gated cationic channel that regulates not only apoptosis, necrosis, autophagy, and NLPR3 inflammosome activation, but also the turnover of diverse tight junction (TJ) and water channel proteins, seems to be essential for the stability of alveolar barrier integrity and for the interaction with protective factors during lung injury.

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Anti-Inflammatory Functions of Protein C Require RAGE and ICAM-1 in a Stimulus-Dependent Manner

Cited by 5 publications

References 51 publications

Tenascin-C modulates alveolarization in bronchopulmonary dysplasia

Tenascin-C modulates alveolarization in bronchopulmonary dysplasia

The Olive Oil‐Based Lipid Clinoleic Blocks Leukocyte Recruitment and Improves Survival during Systemic Inflammation: A Comparative In Vivo Study of Different Parenteral Lipid Emulsions

Potential contribution of alveolar epithelial type I cells to pulmonary fibrosis

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