CD55/decay accelerating factor is part of the lipopolysaccharide‐induced receptor complex

Heine, Holger; El-Samalouti, Volker T.; Nötzel, Corinna; Pfeiffer, Alexandra; Lentschat, Arnd; Kusumoto, Shoichi; Schmitz, Gerd; Hamann, Lutz; Ulmer, Artur J.

doi:10.1002/eji.200323381

Cited by 48 publications

(21 citation statements)

References 63 publications

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“…Therefore, the effect of LPS on the adipocyte cannot be directly related to the presence of CD14 on its membrane. However, it is possible that this effect occurs via the secretion of CD14 by the adipose cell (Su et al 1999), or possibly as a result of another receptor (Frleta et al 2003;Heine et al 2003). The expression of CD55 on the mature adipocyte would seem to agree with this hypothesis.…”

Section: Discussionmentioning

confidence: 61%

Surface protein expression between human adipose tissue-derived stromal cells and mature adipocytes

Festy¹,

Hoareau²,

Bès-Houtmann³

et al. 2005

Histochem Cell Biol

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Adipose tissue contains a stroma that can be easily isolated. Thus, human adipose tissue presents an source of multipotent stromal cells. In order to determine the implication of hematopoietic markers in adipocyte biology, we have defined part of the phenotype of the human adipose tissue-derived stromal cells, and compared this to fully differentiated adipocytes. Flow cytometry demonstrates that the protein expression phenotype of both cell types are similar and includes the expression of CD10, CD13, CD34, CD36, CD55, CD59 and CD65. No significant difference between subcutaneous and omental adipose tissue could be demonstrated concerning the expression of these markers. However, the expression of CD34, CD36 and CD65 is cell-dependent. While the expression of CD36 and CD65 doubled between stromal cells and mature adipocytes, the expression of CD34 decreased, despite this protein being present on the mature adipocyte. As CD34 is described as a stem cell marker and it being unlikely to be expressed on differentiated cells, this result was confirmed by immunostaining and western blot. The clear function of this protein on the adipocyte membrane remains to be determined. The characterization of new proteins on mature adipocytes could have broad implications for the comprehension of the biology of this tissue.

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Section: Discussionmentioning

confidence: 61%

Surface protein expression between human adipose tissue-derived stromal cells and mature adipocytes

Festy¹,

Hoareau²,

Bès-Houtmann³

et al. 2005

Histochem Cell Biol

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“…Signaling proteins at the cell surface, TLR4 and MD-2, which are involved in the perception of the stimulus, connect to several intracellular signaling cascades orchestrating the process of the cellular response. Recent investigations have revealed that the receptor complex is not a static structure but assembles upon stimulation with LPS by movement of the proteins into lipid raft domains of the cytoplasmic membrane, resulting in the formation of an active signaling complex (21)(22)(23). However, the molecular mechanisms of this receptor recruitment to specific membrane domains are not understood.…”

Section: Discussionmentioning

confidence: 99%

“…Only TLR2 has been shown to associate with other TLRs to build heteromeric receptors (10). TLR4/MD-2 as been found to associate in complexes that include CD11/CD18, CD55, CD81, hsp70, hsp90, GDF5, and CXCR4 (21)(22)(23). However, for most of these proteins, a functional participation in signal transduction is not clear, yet.…”

mentioning

confidence: 99%

MaxiK Blockade Selectively Inhibits the Lipopolysaccharide-Induced IκB-α/NF-κB Signaling Pathway in Macrophages

Papavlassopoulos¹,

Stamme²,

Thon³

et al. 2006

The Journal of Immunology

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Macrophages have a pivotal function in innate immunity against bacterial infections. They are present in all body compartments and able to detect invading microorganisms with high sensitivity. LPS (endotoxin) of Gram-negative bacteria is among the most potent stimuli for macrophages and initiates a wide panel of cellular activation responses. The release of mediators such as TNF-α and ILs is essential for the initiation of a proinflammatory antibacterial response. Here, we show that blockade of the large-conductance Ca2+-activated potassium channel MaxiK (BK) inhibited cytokine production from LPS-stimulated macrophages at the transcriptional level. This inhibitory effect of channel blockade was specific to stimulation with LPS and affected neither stimulation of macrophages with the cytokine TNF-α nor LPS-induced activation of cells that do not express MaxiK. Investigation of the upstream intracellular signaling pathways induced by LPS revealed that the blockade of MaxiK selectively inhibited signaling pathways leading to the activation of the transcription factor NF-κB and the MAPK p38, whereas activation of ERK was unaffected. We present data supporting that proximal regulation of the inhibitory factor IκB-α is critically involved in the observed inhibition of NF-κB translocation. Using alveolar macrophages from rats, we could show that the necessity of MaxiK function in activation of NF-κB and subsequent cytokine production is not restricted to in vitro-generated monocyte-derived macrophages but also can be observed in primary cells. Thus, MaxiK appears to be a central molecule in the NF-κB-dependent inflammatory response of macrophages to bacterial LPS.

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“…The possibility that additional receptor components such as integrins, 11,12 heat-shock proteins, 13,14 CXCR4, 14 or CD55 15 have been suggested to be part of this activation cluster, possibly acting as additional LPS transfer molecules. The involvement of K + channels in LPS signal transduction have also been suggested.…”

Section: Lps Recognitionmentioning

confidence: 97%

The dynamics of LPS recognition: complex orchestration of multiple receptors

Triantafilou¹,

Triantafilou²

2005

J. Endotoxin Res.

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The molecular mechanisms that have been designed to protect the host from invading pathogens are responsible for sepsis, an often fatal response of the immune system against microbial pathogens. In the past few years, intense research in the field of innate immunity has identified a plethora of pattern recognition receptors that are responsible for bacterial-induced activation. Recognition of bacterial lipopolysaccharide seems to involve a complex orchestration of protein-protein interactions that eventually leads to cellular activation. In this review, we attempt to unravel the dynamic interactions that occur among the different receptors involved and dictate the outcome of the innate immune response.

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CD55/decay accelerating factor is part of the lipopolysaccharide‐induced receptor complex

Cited by 48 publications

References 63 publications

Surface protein expression between human adipose tissue-derived stromal cells and mature adipocytes

Surface protein expression between human adipose tissue-derived stromal cells and mature adipocytes

MaxiK Blockade Selectively Inhibits the Lipopolysaccharide-Induced IκB-α/NF-κB Signaling Pathway in Macrophages

The dynamics of LPS recognition: complex orchestration of multiple receptors

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