Review article: the effects of antitumour necrosis factor-α on bone metabolism in inflammatory bowel disease

Veerappan, Sundaram G.; O’Moráin, Colm; Daly, Jacqueline S.; Ryan, Barbara

doi:10.1111/j.1365-2036.2011.04667.x

Cited by 60 publications

(35 citation statements)

References 73 publications

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“…Previously it gained much attention for its role of inducing apoptosis of cells via activation of NF-κB and caspase pathways (MacFarlane, 2003). However, TNF-α could elicit complicated biological effects through binding to its receptors followed by activation of numerous intracellular signals ( Caminero et al, 2011, Rosenblum and Amital, 2011, Veerappan et al, 2011and Vujanovic, 2011. Since ETB2 receptors are not expressed in VSMC under normal conditions, but was impressively induced by short-term exposure to TNF-α during organ culture, which is also observed in patients with CVD, we were interested in the underlying mechanisms that may extend our knowledge of the toxic effects of TNF-α.…”

Section: Discussionmentioning

confidence: 99%

Activation of nuclear factor-κB pathway is responsible for tumor necrosis factor-α-induced up-regulation of endothelin B2 receptor expression in vascular smooth muscle cells in vitro

Zhang

Zeng

et al. 2012

Toxicology Letters

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. (2012). Activation of nuclear factorkappa B pathway is responsible for tumor necrosis factor-a-induced up-regulation of endothelin B2 receptor expression in vascular smooth muscle cells in vitro. Toxicology Letters, 209(2), 107-112. DOI: 10.1016DOI: 10. /j.toxlet.2011 General rights Copyright and moral rights for the publications made accessible in the public portal are retained by the authors and/or other copyright owners and it is a condition of accessing publications that users recognise and abide by the legal requirements associated with these rights.• Users may download and print one copy of any publication from the public portal for the purpose of private study or research.• You may not further distribute the material or use it for any profit-making activity or commercial gain • You may freely distribute the URL identifying the publication in the public portal Activation of nuclear factor-κB pathway is responsible for tumor necrosis factor-α-induced up-regulation of endothelin B2 receptor expression in vascular smooth muscle cells in vitro. AbstractThe endothelin B2 (ETB2) receptors are induced in vascular smooth muscle cells (VSMCs) in cardiovascular diseases. We tested if in vitro short-term exposure to the pro-inflammatory cytokine tumor necrosis factor-α (TNF-α) could up-regulate ETB2 receptors in rat mesenteric arteries, and if this effect is through activation of intracellular nuclear factor-κB (NF-κB) pathway. The mesenteric arteries were dissected from male Sprague-Dawley rats and the endothelium was removed. The arteries were co-incubated with TNF-α in serum-free Dulbecco's modified Eagle's medium. Real-time reverse transcription-PCR, Western blot and immunohistochemical staining were employed to assess the mRNA/protein expression of ETB2 receptors and activation of NF-κB pathway. The results showed that, during organ culture, TNF-α concentration-dependently enhanced ETB2 receptors expression at both mRNA and protein levels, paralleled with activation of NF-κB pathway in VSMC. The up-regulated ETB2 receptor expression and NF-κB activation could be effectively suppressed by general transcriptional inhibitor actinomycin D, or either of the selective IκB kinase inhibitors wedelolactone and IMD-0354. Conclusively, the activation of intracellular NF-κB pathway is responsible for the up-regulation of ETB2 receptors induced by short-term exposure to TNF-α. This could partly explain the toxic effects of TNF-α on VSMCs that account for cardiovascular diseases. HighlightsWe examined the mechanism of TNF-α on regulating ETB2 receptors during organ culture. TNF-α augmented ETB2 receptor expression and activated NF-κB pathway in VSMC. The inhibition of transcription or NF-κB abolished the ETB2 receptor up-regulation. NF-κB pathway is responsible for the ETB2 receptor up-regulation by TNF-α.

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Section: Discussionmentioning

confidence: 99%

Activation of nuclear factor-κB pathway is responsible for tumor necrosis factor-α-induced up-regulation of endothelin B2 receptor expression in vascular smooth muscle cells in vitro

Zhang

Zeng

et al. 2012

Toxicology Letters

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“…Az ALP izoformái szerkezetben, kinetikus tulajdonságokban, molekulaméretben és izoelektromos pontban különböznek [2]. A rutinvizsgálatok során diagnosztizált hyperphosphatasaemiának számos oka lehet, amelyek dön-tően máj-vagy csonteredetűek.…”

Section: áBraunclassified

The role of intestinal alkaline phosphatase in pediatric inflammatory bowel and celiac diseases

et al. 2012

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Az intestinalis alkalikus foszfatáz enzim alapvető fontosságú a bélnyálkahártya épségének fenntartásában, mivel detoxifi kálni képes a lipopoliszacharidot, amely a Toll-like receptor-4 ligandja. A helytelen immunválasz, valamint a mucosalis barrier sérülése hozzájárulhat a gyulladásos bélbetegség és a coeliakia kialakulásához. Gyulladásos bél-betegségben szenvedő gyermekek gyulladt vastagbél-és újonnan diagnosztizált coeliakiás gyermekek duodenumnyálkahártyájában a csökkent intestinalis alkalikus foszfatáz és a Toll-like receptor-4 fehérjeexpresszió emelkedése következményesen fokozott lipopoliszacharid-aktivitással járhat, amely a szövetkárosító folyamatokat erősítheti. Az intestinalis alkalikus foszfatáz aktivitásának elősegítése colitises állatmodellben és terápiarezisztens colitis ulcerosás felnőtt betegekben csökkentette a bélgyulladás tüneteit. Ennek megfelelően a két vizsgált kórképben az enzim célzott intestinalis bejuttatása kiegészítő terápiás konzekvenciával is járhat a jövőben. Orv. Hetil., 2012Hetil., , 153, 1389Hetil., -1395

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“…DeBoer et al [126] have shown, using a dextran sodium sulfate induced colitis model, that mice treated with anti-TNF-α antibodies demonstrated a partial normalization of pubertal timing coincident with decreased systemic inflammation. Bone metabolism is also positively affected by infliximab, at least in the short-term, manifested by improved bone formation markers [127,128].…”

Section: Biologic Treatmentmentioning

confidence: 99%

Impact of Therapeutic Strategies on Growth in Pediatric Inflammatory Bowel Disease

Shamir¹

2014

J Clin Cell Immunol

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Growth retardation is a common complication of pediatric inflammatory bowel disease (IBD), which may have long term effects on final adult height and carries significant social and psychological implications. Etiology may be multifactorial including undernutrition, metabolic dysregulation, inflammatory impact on hormonal growth axis and the effect of drugs such as glucocorticoids. Control of disease activity and minimizing the need for corticosteroid therapy are necessary measures in order to facilitate normal growth. However, in many cases these strategies are not sufficient. Currently, there is inconsistent evidence regarding the efficacy of available therapeutic agents to induce long-term effect on growth. The new era of biologic therapies which carries a greater potential to achieve mucosal healing, holds promise for better growth even in children with severe growth impairment. It becomes apparent that prompt recognition of growth impairment combined with aggressive tailored therapeutic approach may offer the best chance for catch-up growth. This review will discuss the definition, prevalence and mechanism of growth retardation in children with IBD and highlight the specific benefits of current therapeutic strategies.

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Review article: the effects of antitumour necrosis factor-α on bone metabolism in inflammatory bowel disease

Abstract: SUMMARY BackgroundPatients with inflammatory bowel disease (IBD) are at increased risk of osteoporosis. A number of studies have emerged in recent years indicating that tumour necrosis factor (TNF) blockade appears to have a beneficial effect on bone mineral density (BMD) in IBD patients.

Cited by 60 publications

References 73 publications

Activation of nuclear factor-κB pathway is responsible for tumor necrosis factor-α-induced up-regulation of endothelin B2 receptor expression in vascular smooth muscle cells in vitro

Activation of nuclear factor-κB pathway is responsible for tumor necrosis factor-α-induced up-regulation of endothelin B2 receptor expression in vascular smooth muscle cells in vitro

The role of intestinal alkaline phosphatase in pediatric inflammatory bowel and celiac diseases

Impact of Therapeutic Strategies on Growth in Pediatric Inflammatory Bowel Disease

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