IL-1β, TNF-α, TGF-β, and bFGF expression in bone biopsies before and after parathyroidectomy

Santos, Francisco R. Lello; Moysés, Rosa Maria Affonso; Montenegro, Fábio Luiz de Menezes; Jorgetti, Vanda; Noronha, Irene L.

doi:10.1046/j.1523-1755.2003.00835.x

Cited by 44 publications

(9 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Bone marrow inflammatory cytokines are increased in patients with renal osteodystrophy 156,157 —a condition that is associated with erythropoietin resistance. A link between inflammation and decreased erythropoiesis was demonstrated by relatively decreased levels of serum erythropoietin in anaemic patients without renal failure who had inflammation caused by autoimmune disease 158 or malignancies 159 as opposed to levels in similarly anaemic patients without inflammation.…”

Section: Introductionmentioning

confidence: 99%

Anaemia in kidney disease: harnessing hypoxia responses for therapy

2015

View full text Add to dashboard Cite

Improved understanding of the oxygen-dependent regulation of erythropoiesis has provided new insights into the pathogenesis of anaemia associated with renal failure and has led to the development of novel therapeutic agents for its treatment. Hypoxia-inducible factor (HIF)-2 is a key regulator of erythropoiesis and iron metabolism. HIF-2 is activated by hypoxic conditions and controls the production of erythropoietin by renal peritubular interstitial fibroblast-like cells and hepatocytes. In anaemia associated with renal disease, erythropoiesis is suppressed due to inadequate erythropoietin production in the kidney, inflammation and iron deficiency; however, pharmacologic agents that activate the HIF axis could provide a physiologic approach to the treatment of renal anaemia by mimicking hypoxia responses that coordinate erythropoiesis with iron metabolism. This Review discusses the functional inter-relationships between erythropoietin, iron and inflammatory mediators under physiologic conditions and in relation to the pathogenesis of renal anaemia, as well as recent insights into the molecular and cellular basis of erythropoietin production in the kidney. It furthermore provides a detailed overview of current clinical experience with pharmacologic activators of HIF signalling as a novel comprehensive and physiologic approach to the treatment of anaemia.

show abstract

Section: Introductionmentioning

confidence: 99%

Anaemia in kidney disease: harnessing hypoxia responses for therapy

2015

View full text Add to dashboard Cite

show abstract

“…Parathyroid hyperplasia and vitamin D deficiency are the major factors that play a critical role in the pathogenesis and pathophysiology [1]. However, recent studies have showed that in addition to parathyroid hormone (PTH), a multitude of local factors such as interleukins, growth factors and cytokines, are involved in the process of renal osteodystrophy [2,3,4]. …”

Section: Introductionmentioning

confidence: 99%

Osteoprotegerin and RANKL Serum Levels and Their Relationship with Serum Ghrelin in Children with Chronic Renal Failure and on Dialysis

Özkaya

Buyan

Bıdecı³

et al. 2007

Nephron Clin Pract

View full text Add to dashboard Cite

Background: Osteoprotegerin (OPG) and receptor activator of the nuclear factor ĸB ligand (RANKL) constitute a complex system of mediators involved in the regulation of bone resorption process. Ghrelin, a growth hormone secretagogue, has been shown to modulate proliferation and differentiation of osteoblasts. The present study was carried out to evaluate the serum concentrations of OPG and sRANKL in children with chronic renal impairment (CRI) and on dialysis, and to establish a possible relationship between their serum levels and that of ghrelin. Methods: 33 patients including 10 patients with CRI, 12 peritoneal dialysis (PD) and 11 hemodialysis (HD) patients and 22 healthy controls were enrolled into the study. OPG, sRANKL and ghrelin levels were studied with radioimmunoassay. Results: Serum OPG levels in CRI, PD and HD groups were significantly higher than the healthy controls (p = 0.002, p < 0.001, p < 0.001, respectively) whereas sRANKL levels were significantly lower than the healthy controls (p = 0.03, p = 0.01, p = 0.001, respectively). Ghrelin levels were significantly higher in CRI, PD and HD groups compared to healthy controls (p = 0.001, p < 0.001, p < 0.001, respectively). We observed a negative correlation between the sRANKL and OPG levels (r = –0.27, p = 0.04) as well as between sRANKL and ghrelin levels (r = –0.31, p = 0.02). OPG levels showed a positive correlation with ghrelin levels (r = 0.63, p < 0.001). Conclusion: We found a lower RANKL bioactivity index in children with CRI and on dialysis. The mechanism and the role of elevated OPG and low sRANKL in uremia are unclear, but they might partly represent a compensatory mechanism to the negative balance of bone remodeling in renal bone disease in children. Additionally, we demonstrated for the first time that ghrelin and the RANKL/OPG system have a close relationship in CRF. Therefore, ghrelin may be of importance in mediating the effects of the RANKL/OPG system in renal bone disease.

show abstract

“…Using immunohistochemistry, Duarte et al [81] also demonstrated intense TGF-β expression in bone samples with osteitis fibrosa from patients with ROD, which is accompanied by extremely high bone turnover. A study conducted by Santos et al [82] indicated that TGF-β expression in bone changes before and after parathyroidectomy. Because TGF-β modulates the functions of both osteoblasts and osteoclasts, these results are rational.…”

Section: Possible Role Of Tgf-β In Chronic Kidney Disease-mineral mentioning

confidence: 99%

“…They also presented that activation of Runx2 or TCF-4 coenhances TCF and Runx2 activity and increases TGF-β receptor I expression [86]. As described above, high TGF-β protein expression has been observed in high-turnover bones from patients with end-stage renal disease [81,82]. Existence of a positive regulatory loop between TGF-β and Wnt signaling may lead to the pathogenesis of high-turnover bone disease in CKD.…”

Section: Possible Role Of Tgf-β In Chronic Kidney Disease-mineral mentioning

confidence: 99%

TGF-Beta Signaling in Bone with Chronic Kidney Disease

Iwasaki

Yamato

Fukagawa

2018

IJMS

View full text Add to dashboard Cite

Transforming growth factor (TGF)-β signaling is not only important in skeletal development, but also essential in bone remodeling in adult bone. The bone remodeling process involves integrated cell activities induced by multiple stimuli to balance bone resorption and bone formation. TGF-β plays a role in bone remodeling by coordinating cell activities to maintain bone homeostasis. However, mineral metabolism disturbance in chronic kidney disease (CKD) results in abnormal bone remodeling, which leads to ectopic calcification in CKD. High circulating levels of humoral factors such as parathyroid hormone, fibroblast growth factor 23, and Wnt inhibitors modulate bone remodeling in CKD. Several reports have revealed that TGF-β is involved in the production and functions of these factors in bone. TGF-β may act as a factor that mediates abnormal bone remodeling in CKD.

show abstract

IL-1β, TNF-α, TGF-β, and bFGF expression in bone biopsies before and after parathyroidectomy

Abstract: Based on these results, we suggest that IL-1beta, TNF-alpha, TGF-beta, and bFGF are involved in bone remodeling regulation, acting as local effectors, possibly under the control of PTH.

Cited by 44 publications

References 40 publications

Anaemia in kidney disease: harnessing hypoxia responses for therapy

Anaemia in kidney disease: harnessing hypoxia responses for therapy

Osteoprotegerin and RANKL Serum Levels and Their Relationship with Serum Ghrelin in Children with Chronic Renal Failure and on Dialysis

TGF-Beta Signaling in Bone with Chronic Kidney Disease

Contact Info

Product

Resources

About