CD154-stimulated GM-CSF release by vascular smooth muscle cells elicits monocyte activation—role in atherogenesis

Stojakovic, Milica; Krzesz, Robert; Wagner, Andreas H.; Hecker, Markus

doi:10.1007/s00109-007-0225-y

Cited by 15 publications

(8 citation statements)

References 24 publications

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“…Microarray expression studies showed that CD40 ligation of non-hematopoietic cells, such as endothelial cells (Pluvinet et al , 2008), pancreatic cells (Klein et al , 2008), renal proximal tubule ECs (Li and Nord, 2005), smooth muscle cells (Stojakovic et al , 2007), microglia (Ait-Ghezala et al , 2005), and ECs (this report), generally results in the upregulation of genes involved in immunity and inflammatory responses, cell fate, and cell adhesion. The response of ECs to CD40 stimulation is alike that of muscle cells and pancreatic cells.…”

Section: Discussionmentioning

confidence: 77%

CD40-Mediated Amplification of Local Immunity by Epithelial Cells Is Impaired by HPV

Tummers

Goedemans

Jha

et al. 2014

Journal of Investigative Dermatology

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The interaction between the transmembrane glycoprotein surface receptor CD40 expressed by skin epithelial cells (ECs) and its T-cell–expressed ligand CD154 was suggested to exacerbate inflammatory skin diseases. However, the full spectrum of CD40-mediated effects by ECs underlying this observation is unknown. Therefore, changes in gene expression after CD40 ligation of ECs were studied by microarrays. CD40-mediated activation for 2 hours stimulated the expression of a coordinated network of immune-involved genes strongly interconnected by IL8 and TNF, whereas after 24 hours anti-proliferative and anti-apoptotic genes were upregulated. CD40 ligation was associated with the production of chemokines and the attraction of lymphocytes and myeloid cells from peripheral blood mononuclear cells (PBMCs). Thus, CD40-mediated activation of ECs resulted in a highly coordinated response of genes required for the local development and sustainment of adaptive immune responses. The importance of this process was confirmed by a study on the effects of human papilloma virus (HPV) infection to the EC's response to CD40 ligation. HPV infection clearly attenuated the magnitude of the response to CD40 ligation and the EC's capacity to attract PBMCs. The fact that HPV attenuates CD40 signaling in ECs indicates the importance of the CD40-CD154 immune pathway in boosting cellular immunity within epithelia.

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Section: Discussionmentioning

confidence: 77%

CD40-Mediated Amplification of Local Immunity by Epithelial Cells Is Impaired by HPV

Tummers

Goedemans

Jha

et al. 2014

Journal of Investigative Dermatology

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“…The CSF2 gene encodes granulocyte-macrophage colony-stimulating factor (GM-CSF). CSF2 plays an important role in smooth muscle cell-dependent monocyte activation [32]. The ADFP gene encodes adipose differentiation-related protein (ADRP).…”

Section: Discussionmentioning

confidence: 99%

Consumption of oat β‐glucan with or without plant stanols did not influence inflammatory markers in hypercholesterolemic subjects

Theuwissen

Plat

Mensink³

2009

Molecular Nutrition Food Res

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We have earlier demonstrated that muesli enriched with oat beta-glucan effectively lowered serum LDL cholesterol. Addition of plant stanols further lowered LDL cholesterol. Besides these hypocholesterolemic effects, beta-glucan and plant stanol esters (PSE) may also affect inflammatory processes. Forty-two mildly hypercholesterolemic subjects randomly consumed for 4 wk (crossover design) control muesli (4.8 g control fiber), beta-glucan muesli (4.8 g oat beta-glucan), or combination muesli (4.8 g oat beta-glucan plus 1.4 g stanol as PSE). Changes in cytokine production (IL-6, IL-8, and TNF-alpha) of LPS-stimulated peripheral blood mononuclear cells (PBMC) and whole blood were evaluated, as well as changes in plasma high-sensitivity (hs)-CRP. Additionally, changes in expression profiles of 84 genes involved in atherosclerosis metabolism were assessed in isolated PBMC. IL-6, IL-8, and TNF-alpha production by PBMC and whole blood after LPS stimulation did not differ between the treatments. Also high-sensitivity C-reactive protein (hs-CRP) levels were similar. beta-Glucan consumption did not change gene expression, while only 3 genes (ADFP, CDH5, CSF2) out of the 84 genes from the atherosclerotic risk panel were differentially expressed (p < 0.05) after consumption of PSE. Consumption of beta-glucan with or without PSE did not influence inflammatory parameters in mildly hypercholesterolemic subjects.

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“…The complexity of GM-CSF biology is evident, because it is implicated in inflammatory conditions, such as rheumatoid arthritis and crescentic GN, 33 but also, as an inducer of M2 markers in microglia/macrophages surrounding glioblastoma tumor cells. 34 Nonhematopoietic cells, such as vascular smooth muscle cells and colon epithelial cells, have been reported to be important sources of GM-CSF, mediating atherogenic monocyte activation 35 and promoting colonic epithelial cell proliferation in colitis, 36 respectively. In addition, GM-CSF has been associated to Th2 immune responses in allergic lung inflammation.…”

Section: Discussionmentioning

confidence: 99%

GM-CSF Promotes Macrophage Alternative Activation after Renal Ischemia/Reperfusion Injury

Huen¹,

Huynh

Marlier³

et al. 2015

Journal of the American Society of Nephrology

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After kidney ischemia/reperfusion (I/R) injury, monocytes home to the kidney and differentiate into activated macrophages. Whereas proinflammatory macrophages contribute to the initial kidney damage, an alternatively activated phenotype can promote normal renal repair. The microenvironment of the kidney during the repair phase mediates the transition of macrophage activation from a proinflammatory to a reparative phenotype. In this study, we show that macrophages isolated from murine kidneys during the tubular repair phase after I/R exhibit an alternative activation gene profile that differs from the canonical alternative activation induced by IL-4-stimulated STAT6 signaling. This unique activation profile can be reproduced in vitro by stimulation of bone marrow-derived macrophages with conditioned media from serum-starved mouse proximal tubule cells. Secreted tubular factors were found to activate macrophage STAT3 and STAT5 but not STAT6, leading to induction of the unique alternative activation pattern. Using STAT3-deficient bone marrow-derived macrophages and pharmacologic inhibition of STAT5, we found that tubular cell-mediated macrophage alternative activation is regulated by STAT5 activation. Both in vitro and after renal I/R, tubular cells expressed GM-CSF, a known STAT5 activator, and this pathway was required for in vitro alternative activation of macrophages by tubular cells. Furthermore, administration of a neutralizing antibody against GM-CSF after renal I/R attenuated kidney macrophage alternative activation and suppressed tubular proliferation. Taken together, these data show that tubular cells can instruct macrophage activation by secreting GM-CSF, leading to a unique macrophage reparative phenotype that supports tubular proliferation after sterile ischemic injury.

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CD154-stimulated GM-CSF release by vascular smooth muscle cells elicits monocyte activation—role in atherogenesis

Cited by 15 publications

References 24 publications

CD40-Mediated Amplification of Local Immunity by Epithelial Cells Is Impaired by HPV

CD40-Mediated Amplification of Local Immunity by Epithelial Cells Is Impaired by HPV

Consumption of oat β‐glucan with or without plant stanols did not influence inflammatory markers in hypercholesterolemic subjects

GM-CSF Promotes Macrophage Alternative Activation after Renal Ischemia/Reperfusion Injury

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