Messenger RNA expression of monocyte chemoattractant protein‐1 and interleukin‐6 in stone‐containing kidneys

Boonla, Chanchai; Hunapathed, Chanutra; Bovornpadungkitti, Sombat; Poonpirome, Kanitta; Tungsanga, Kriang; Sampatanukul, Pichet; Tosukhowong, Piyaratana

doi:10.1111/j.1464-410x.2008.07461.x

Cited by 44 publications

(33 citation statements)

References 28 publications

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“…We also show an increased expression of 8-OHdG lesion in stone-containing renal tissues [182]. MCP-1 and IL-6 mRNA expression in stone-containing kidney tissues are increased, and their increment is related to declined creatinine clearance [183]. Our findings indicate that patients with nephrolithiasis persistently have increased oxidative stress and intrarenal inflammation, and these pathological changes contribute to renal impairment.…”

Section: Oxidative Stress In Urolithiasissupporting

confidence: 53%

Oxidative Stress in Urolithiasis

Boonla¹

2018

Reactive Oxygen Species (ROS) in Living Cells

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Oxygen is absolutely essential for the survival of our life. However, metabolic consumption of oxygen inevitably yields reactive oxygen species (ROS). Imbalance of ROS production and antioxidant capacity causes oxidative stress that potentially damages biomolecules leading to cell injury and death. In fact, ROS have two-faceted functions. Under physiologic condition, ROS function as signaling molecules and participate in maintaining redox balance. In pathology, ROS induce oxidative stress that critically involves in the development of several diseases including urolithiasis (UL). UL or urinary stone disease is a common urologic condition in all countries with progressively increasing prevalence. Most of UL are multifactorial with polygenic susceptibility and highly recurrent nature. Formation of urinary stones is driven by supersaturation of urinary lithogenic ions, and calcium oxalate (CaOx) is the most prevalent stone type. Oxidative stress clearly plays an active role in UL development. In vitro, lithogenic crystals induce ROS generation in renal tubular cells leading to oxidative stress, cell injury and release of inflammatory mediators. In nephrolithic rats, oxidative stress and CaOx deposit are gradually increased in the rats' kidneys. Intervention with antioxidants efficiently reduces oxidative damage and crystal deposits. Human studies show that patients with UL have increased oxidative stress and renal tubular injury relative to the non-stone-forming individuals. Increased oxidative lesions and inflammation are observed in the stone-containing kidneys of the patients. Furthermore, renal fibrosis mediated through tubular epithelial-mesenchymal transition is observed in kidneys of stone patients. Increased renal fibrosis is significantly associated with decreased kidney function. From therapeutic point of view, nutraceutical regimens that are able to reduce oxidative stress may be clinically useful alternatives for preventing stone formation and recurrence. This chapter has an intention to provide a basic knowledge of ROS generation and oxidative stress and up-to-date research findings of oxidative stress in UL based on the published articles as well as the author's studies.

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Section: Oxidative Stress In Urolithiasissupporting

confidence: 53%

Oxidative Stress in Urolithiasis

Boonla¹

2018

Reactive Oxygen Species (ROS) in Living Cells

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“…Previous studies have hypothesized that renal cell injury and inflammation are related to the development of renal stones and demonstrated an increase in IL-6 in patients with urolithiasis [25][26][27]. Boonla et al, also showed increased mRNA expression of IL-6 and monocyte chemoattractant protein -1 in tissue from renal biopsy from kidneys containing calculi [28].…”

Section: Discussionmentioning

confidence: 81%

Is Urolithiasis Associated with Increased Levels of High Sensitivity C-Reactive Protein and Interleukin-6 in Diabetic Patients?

Hasna

Meiyappan

Periyasam

et al. 2015

JCDR

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“…IL-6 has been previously demonstrated to enhance osteoclastogenesis by the induction of the NF-κB ligand in osteoblastic cells (66) and has also shown to be the central pathogenic player in arthritis. Given the multifacted role of IL-6, our findings therefore suggest that the increased production of IL-6 under basal conditions in the kidney may explain the development of both hypercalciuria and nephrolithiasis in Clcn5 KO mice, although a direct correlation has not been established (67, 68). Moreover, elevated IL-6 is involved in defective bone mineralization, which may also explain the sporadic presentation of rickets/osteomalacia in patients with Dent disease (27, 51, 69–71).…”

Section: Discussionmentioning

confidence: 83%

Clcn5 Knockout Mice Exhibit Novel Immunomodulatory Effects and Are More Susceptible to Dextran Sulfate Sodium-Induced Colitis

Alex

Zachos

et al. 2010

The Journal of Immunology

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Although the intracellular Cl−/H+ exchanger Clc-5 is expressed in apical intestinal endocytic compartments, its pathophysiological role in the gastrointestinal tract is unknown. In light of recent findings that CLC-5 is downregulated in active ulcerative colitis (UC), we tested the hypothesis that loss of CLC-5 modulates the immune response, thereby inducing susceptibility to UC. Acute dextran sulfate sodium (DSS) colitis was induced in Clcn5 knockout (KO) and wild-type (WT) mice. Colitis, monitored by disease activity index, histological activity index, and myeloperoxidase activity were significantly elevated in DSS-induced Clcn5 KO mice compared with those in WT mice. Comprehensive serum multiplex cytokine profiling demonstrated a heightened Th1–Th17 profile (increased TNF-α, IL-6, and IL-17) in DSS-induced Clcn5 KO mice compared with that in WT DSS colitis mice. Interestingly, Clcn5 KO mice maintained on a high vitamin D diet attenuated DSS-induced colitis. Immunofluorescence and Western blot analyses of colonic mucosa validated the systemic cytokine patterns and further revealed enhanced activation of the NF-κB pathway in DSS-induced Clcn5 KO mice compared with those in WT mice. Intriguingly, high baseline levels of IL-6 and phospho-IκB were observed in Clcn5 KO mice, suggesting a novel immunopathogenic role for the functional defects that result from the loss of Clc-5. Our studies demonstrate that the loss of Clc-5 1) exhibits IL-6–mediated immunopathogenesis, 2) significantly exacerbated DSS-induced colitis, which is influenced by dietary factors, including vitamin D, and 3) portrays distinct NF-κB–modulated Th1–Th17 immune dysregulation, implying a role for CLC-5 in the immunopathogenesis of UC.

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Messenger RNA expression of monocyte chemoattractant protein‐1 and interleukin‐6 in stone‐containing kidneys

Cited by 44 publications

References 28 publications

Oxidative Stress in Urolithiasis

Oxidative Stress in Urolithiasis

Is Urolithiasis Associated with Increased Levels of High Sensitivity C-Reactive Protein and Interleukin-6 in Diabetic Patients?

Clcn5 Knockout Mice Exhibit Novel Immunomodulatory Effects and Are More Susceptible to Dextran Sulfate Sodium-Induced Colitis

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