Hemoperfusion Treatment in a Septic Shock Patient with Autosomal Dominant Polycystic Kidney Disease and Increased HMGB1 Protein Levels

Nakamura, Tsukasa; Kawagoe, Yasuhiro; Ueda, Yoshihiko; Yamada, Shingo; Koide, Hikaru

doi:10.1159/000325731

Cited by 10 publications

(8 citation statements)

References 32 publications

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“…Recently, increasing numbers of studies have reported that the RAGE ligands and their stimulatory signals are highly increased in ADPKD. These include the HMGB1, for which high secretion was noted in the serum of ADPKD patients with septic shock or hypertension (19, 20). In addition, S100A8 and S100A9 were previously found to be highly expressed in cyst‐lining epithelial cells, as observed in Pkd2 transgenic mice, one of the ADPKD rodent models with polycystic kidneys.…”

Section: Discussionmentioning

confidence: 99%

Soluble receptor for advanced glycation end products inhibits disease progression in autosomal dominant polycystic kidney disease by down-regulating cell proliferation

et al. 2015

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Autosomal polycystic kidney disease (ADPKD) is a highly prevalent genetic renal disorder in which epithelial-lining fluid-filled cysts appear in kidneys. It is accompanied by hyperactivation of cell proliferation, interstitial inflammation, and fibrosis around the cyst lining cells, finally reaching end-stage renal disease. Previously, we found high expression of ligands stimulating the receptor for advanced glycation end products (RAGE) in ADPKD mice. Furthermore, gene silencing of RAGE was revealed to cause reduction of cystogenesis via down-regulation of cell proliferation in vitro, and intravenous administration of anti-RAGE adenovirus in vivo also displayed alleviation of the disease. Here, we attempted to identify the role of soluble RAGE (sRAGE) in inhibiting the progression of ADPKD using 2 different ADPKD mouse models. sRAGE is an endogenously expressed form of RAGE that has no membrane-anchoring domain, thereby giving it the ability to neutralize the ligands that stimulate RAGE signals. Both overexpression of sRAGE and sRAGE treatment blocked RAGE-mediated cell proliferation in vitro. In addition, sRAGE-injected ADPKD mice showed reduced cysts accompanied by enhanced renal function, inhibition of cell proliferation, inflammation, and fibrosis. These positive therapeutic effects of sRAGE displayed little liver toxicity, suggesting it as a new potential therapeutic target of ADPKD with low side effects.

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Section: Discussionmentioning

confidence: 99%

Soluble receptor for advanced glycation end products inhibits disease progression in autosomal dominant polycystic kidney disease by down-regulating cell proliferation

et al. 2015

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“…Serum HMGB1 level is increased and correlates with oxidative stress status in autosomal dominant polycystic kidney disease (Nakamura et al, 2011a; Nakamura et al, 2012a). …”

Section: Hmgb1 and Diseasementioning

confidence: 99%

HMGB1 in health and disease

Kang

Chen

Zhang

et al. 2014

Molecular Aspects of Medicine

823

828

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Complex genetic and physiological variations as well as environmental factors that drive emergence of chromosomal instability, development of unscheduled cell death, skewed differentiation, and altered metabolism are central to the pathogenesis of human diseases and disorders. Understanding the molecular bases for these processes is important for the development of new diagnostic biomarkers, and for identifying new therapeutic targets. In 1973, a group of non-histone nuclear proteins with high electrophoretic mobility was discovered and termed High-Mobility Group (HMG) proteins. The HMG proteins include three superfamilies termed HMGB, HMGN, and HMGA. High-mobility group box 1 (HMGB1), the most abundant and well-studied HMG protein, senses and coordinates the cellular stress response and plays a critical role not only inside of the cell as a DNA chaperone, chromosome guardian, autophagy sustainer, and protector from apoptotic cell death, but also outside the cell as the prototypic damage associated molecular pattern molecule (DAMP). This DAMP, in conjunction with other factors, thus has cytokine, chemokine, and growth factor activity, orchestrating the inflammatory and immune response. All of these characteristics make HMGB1 a critical molecular target in multiple human diseases including infectious diseases, ischemia, immune disorders, neurodegenerative diseases, metabolic disorders, and cancer. Indeed, a number of emergent strategies have been used to inhibit HMGB1 expression, release, and activity in vitro and in vivo. These include antibodies, peptide inhbitiors, RNAi, anti-coagulants, endogenous hormones, various chemical compounds, HMGB1-receptor and signaling pathway inhibition, artificial DNAs, physical strategies including vagus nerve stimulation and other surgical approaches. Future work further investigating the details of HMGB1 localizationtion, structure, post-translational modification, and identifccation of additional partners will undoubtedly uncover additional secrets regarding HMGB1’s multiple functions.

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“…Autosomal dominant polycystic kidney disease (ADPKD) is the most common monogenic kidney disease and the fourth leading cause of end-stage kidney disease in adults worldwide (42). Recently, two research groups reported that the serum level of HMGB1 was increased in ADPKD patients (43,44) which suggests that HMGB1 may play a role in ADPKD.…”

Section: Hmgb1 and Autosomal Dominant Polycystic Kidney Diseasementioning

confidence: 99%

High mobility group box 1 and kidney diseases (Review)

Zhu

Xie

Ding

et al. 2013

International Journal of Molecular Medicine

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High mobility group box 1 (HMGB1), a non-histone DNA-binding protein, regulates nucleosome function and transcription in the nuclei of all metazoans and plants. However, extracellular HMGB1, which is actively or passively released under different conditions, can act as a key inflammatory mediator through MyD88/mitogen-activated protein kinase signaling by binding to its receptors including the receptor for advanced glycation end products or Toll-like receptors. A growing body of evidence indicates that HMGB1 plays an important role in kidney diseases, such as glomerulonephritis, lupus nephritis, antineutrophilic cytoplasmatic antibody-associated vaculitis, diabetic nephropathy, renal allograft rejection and acute kidney injury. In this review, we focus on the biology of HMGB1 and the association of HMGB1 with kidney diseases.

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Hemoperfusion Treatment in a Septic Shock Patient with Autosomal Dominant Polycystic Kidney Disease and Increased HMGB1 Protein Levels

Cited by 10 publications

References 32 publications

Soluble receptor for advanced glycation end products inhibits disease progression in autosomal dominant polycystic kidney disease by down-regulating cell proliferation

Soluble receptor for advanced glycation end products inhibits disease progression in autosomal dominant polycystic kidney disease by down-regulating cell proliferation

HMGB1 in health and disease

High mobility group box 1 and kidney diseases (Review)

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