Butyrate inhibits cytokine-induced VCAM-1 and ICAM-1 expression in cultured endothelial cells: the role of NF-κB and PPARα

Zapolska-Downar, Danuta; Siennicka, Aldona; Kaczmarczyk, Mariusz; Kołodziej, Blanka; Naruszewicz, Marek

doi:10.1016/j.jnutbio.2003.11.008

Cited by 126 publications

(90 citation statements)

References 46 publications

(51 reference statements)

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“…It was shown before that endothelial cells from various origins might be a target for butyrate [13][14][15]. Here we show that SPB affects the expression of genes that are relevant to the SCD pathophysiology by cells from a bone marrow microcirculation cell line.…”

Section: Discussionsupporting

confidence: 51%

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Sodium phenyl butyrate downregulates endothelin‐1 expression in cultured human endothelial cells: Relevance to sickle‐cell disease

et al. 2007

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As hydroxyurea (HU), sodium phenyl butyrate (SPB) is known to induce fetal hemoglobin (HbF) expression and thus shows potentials for sickle-cell disease (SCD) treatment. More recently, few studies suggested that endothelial cells (ECs), a major pathophysiological actor of SCD, are also a target of SPB. Here, we show that SPB, as HU, reduces endothelin-1 mRNA expression and peptide release by human ECs in culture. SPB increases VCAM-1 and ICAM-1 mRNAs and soluble ICAM-1 release. Both drugs have a cumulative effect on ICAM-1 expression. We conclude that SPB, as HU, also affects the expression of molecules important to the pathophysiology of SCD, in addition to its effect on HbF. Its potential as an alternative or adjuvant drug in SCD treatment warrants further investigations. Am. J. Hematol. 82:357-362, 2007. V V C 2007 Wiley-Liss, Inc.

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Section: Discussionsupporting

confidence: 51%

“…In other contexts, it has been reported that butyrate can also alter the expression of some adhesion molecules in various endothelial cell cultures such as HUVEC [13,14], intestinal microvascular cells [15], or in acute myeloid leukemia cells [16].…”

Section: Introductionmentioning

confidence: 99%

Sodium phenyl butyrate downregulates endothelin‐1 expression in cultured human endothelial cells: Relevance to sickle‐cell disease

et al. 2007

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“…ICAM-1 plays an important role in cell adhesion to the vascular endothelium and may have a role in tumor cell dissemination or metastasis [18,19]. Suppressed expression of VCAM-1 and ICAM-1 is associated with reduced adhesion of monocytes and lymphocytes to human umbilical vein endothelial cell stimulated by cytokine [20]. ICAM-1 plays a crucial role in Trypanosoma cruzi recruitment to the cardiac tissue and host susceptibility during T. cruzi infection [21].…”

Section: Discussionmentioning

confidence: 99%

Lipoprotein p37 from Mycoplasma hyorhinis inhibiting mammalian cell adhesion

et al. 2005

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Summaryp37 protein is a membrane lipoprotein of Mycoplasma hyorhinis, and our previous work showed that there was high ratio of M. hyorhinis infection in human gastric carcinoma. To investigate the possible functions of p37 in cancer development, the nucleotide sequence of p37 gene was modified and expressed well in transfected cells. We found that p37 localized at the Golgi apparatus and could be secreted out of the cell. Human gastric cancer cells AGS, after being transfected with the p37 gene, were smaller, more spherical and easy to detach from each other. Their adhesion to matrix was also diminished and cytoskeleton in these stable p37 AGS cell was rearranged and transcription co-factor b-actin was transferred to nucleolus with down-regulation of ICAM-1 and integrin b1. These findings will be helpful for us to elucidate the effects of p37 on eukaryotic cells as well as to better understand the potential relationship between cancer and mycoplasma infection.

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“…Increasing evidence indicates that the NF-κB pathway contributes to inflammatory diseases and to the overexpression of pro-inflammatory cytokines, such as TNF-α, IL-6 and IL-1β (Moynagh, 2005). Butyrate reduced production of proinflammatory cytokines by modulating the activity of NF-κB (Zapolska-Downar et al, 2004) and it has been proposed that, through targeting NF-κB, it may thus be possible to suppress inflammation in the mammary gland. Moreover, some studies (Aveleira et al, 2010;Kamekura et al, 2010;Tang et al, 2010;Choi et al, 2012) have indicated that the activation of the NF-κB pathway increases tight junction permeability.…”

Section: Figurementioning

confidence: 99%

Butyrate protects against disruption of the blood‐milk barrier and moderates inflammatory responses in a model of mastitis induced by lipopolysaccharide

Wang

Wei

Zhang

et al. 2017

British J Pharmacology

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Short-chain fatty acids are fermentation end products produced by gut bacteria, which have been shown to ameliorate inflammatory bowel diseases and allergic asthma. However, the mechanism involved remains largely unknown. Here, we investigate the protective effects and mechanisms of sodium butyrate (SB) on LPS-induced mastitis model. EXPERIMENTAL APPROACHEffects of increasing doses of SB on blood-milk barrier function and inflammation are studied in BALB/c mice with LPS-induced mastitis. The underlying mechanisms of anti-inflammatory effects of SB were further investigated in LPS-stimulated mouse mammary epithelial cells (mMECs). KEY RESULTSThe results show that SB decreased LPS-induced disruption in mammary tissues, infiltration of inflammatory cells and the levels of TNF-α, IL-6 and IL-1β. SB up-regulated the tight junction proteins occludin and claudin-3 and reduced blood-milk barrier permeability in LPS-induced mastitis. Studies in vitro revealed that SB inhibited LPS-induced inflammatory response by inhibition of the NF-κB signalling pathway and histone deacetylases in LPS-stimulated mMECs. CONCLUSIONS AND IMPLICATIONSIn our model, SB protected against LPS-induced mastitis by preserving blood-milk barrier function and depressing proinflammatory responses, suggesting the potential use of SB as a prophylactic agent to protect blood-milk barrier function in mastitis.

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Butyrate inhibits cytokine-induced VCAM-1 and ICAM-1 expression in cultured endothelial cells: the role of NF-κB and PPARα

Cited by 126 publications

References 46 publications

Sodium phenyl butyrate downregulates endothelin‐1 expression in cultured human endothelial cells: Relevance to sickle‐cell disease

Sodium phenyl butyrate downregulates endothelin‐1 expression in cultured human endothelial cells: Relevance to sickle‐cell disease

Lipoprotein p37 from Mycoplasma hyorhinis inhibiting mammalian cell adhesion

Butyrate protects against disruption of the blood‐milk barrier and moderates inflammatory responses in a model of mastitis induced by lipopolysaccharide

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