Fp582pentraxin3 Expression in a Rat Model of Peritoneal Dialysis

Ishimatsu, Nana; Miyamoto, Tetsu; Morimoto, Hiroyuki; Nakamata, Junichi; Baba, Ryoko; Ueno, Hiroki; Fujimoto, Yoko; Bando, Kenichiro; Furuno, Yumi; Serino, Ryota; Tamura, Masahito

doi:10.1093/ndt/gfv180.34

Cited by 2 publications

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“…A PD rat model was established previously [ 16 ]. Briefly, 8-week-old male Wistar rats were instilled intraperitoneally twice a day for 8 weeks with 20 ml of lactate-buffered glucose contained PD fluid (Dianeal ® PD-4 4.25; Baxter Healthcare, Tokyo, Japan).…”

Section: Methodsmentioning

confidence: 99%

Glucose Induces ER Stress Response-Mediated Peritoneal Mesothelial Cell Death

Nakamata,

Morimoto,

Baba

et al. 2024

Acta Histochem. Cytochem

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Peritoneal dialysis (PD) fluid, which contains a high concentration of glucose, is involved in peritoneal damage after long-term use. The mechanisms through which glucose induces damage to the mesothelium have not been clearly elucidated. Although, endoplasmic reticulum (ER) stress response is associated with several diseases, the involvement of ER stress in peritoneal damage has not yet been demonstrated. Primary-cultured rat peritoneal mesothelial cells (RPMCs) and rat PD model were used to investigate the influence of glucose on the peritoneum. Cells treated with glucose were examined for cytotoxicity, induction of apoptosis, and activation of the ER stress pathway. Glucose treatment of RPMCs induced cell death at concentrations higher than 3%. Annexin V positive, that is a feature of apoptosis, occurred in dead cells. Treatment with glucose led to the activation of protein kinase R-like ER kinase (PERK) and eukaryotic translation initiation factor-2α (eIF-2α). Glucose also induced the expression and nuclear translocation of homologous protein C/EBP. Cell death was rescued by the integrated stress response inhibitor, ISRIB, which suppresses the integrated stress response pathway, including ER stress. Glucose in PD fluid induces PERK/eIF-2α-mediated ER stress in RPMCs, resulting in apoptosis. This cellular stress may cause peritoneal damage in patients receiving PD.

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Section: Methodsmentioning

confidence: 99%

Glucose Induces ER Stress Response-Mediated Peritoneal Mesothelial Cell Death

Nakamata,

Morimoto,

Baba

et al. 2024

Acta Histochem. Cytochem

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“…PTX3 was detected in peritoneal mesothelial cells, macrophages and fibroblasts in the thickened sub mesothelial area and glucose was found to induce PTX3 protein expression in cultured rat peritoneal mesothelial cells (RPMCs) as well as macrophage-like cells and fibroblasts. According to this, glucose may be a major driver for PDFinduced local micro-inflammation in the peritoneum [108].…”

Section: Ptx3 In Peritoneal Dialysis (Pd)mentioning

confidence: 99%

Pentraxin 3 in Kidney Disease and Renal Replacement Therapies

Losappio¹,

Infante²,

Maiorano³

et al. 2023

Preprint

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Chronic kidney disease (CKD) is actually considered a public health priority according to the increasing number of patients affected by this condition: this casuistry is not only related to specific glomerular, tubular or autoimmune diseases or a consequence of acute kidney injury (AKI) episodes leading to organ failure, but it is tied to the progression of life expectancy and the impact of comorbidities such as cardiovascular disease, diabetes and cancer. CKD and its comorbidities promote low grade inflammatory status with an impact on patients’ clinical conditions, reducing their possibility for kidney transplantation or graft survival and their survival when receiving renal replacement therapies such as hemodialysis (HD) or peritoneal dialysis (PD). CKD is often referred to as an ageing accelerator: innate immune system dysregulation, in the uraemic proinflammatory milieu, is involved in this accelerated senescence phenomena and pentraxins, particularly Pentraxin-3 (PTX-3), are of particular interest in the development of kidney disease. A complete understanding of the mechanism of CKD progression, innate immune system involvement and a proper definition of PTX-3 role in kidney disease, could redefine the approach for diagnosis and a more centered patients’ management to slow down CKD progression over time and reduce its clinical and social impact.

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Fp582pentraxin3 Expression in a Rat Model of Peritoneal Dialysis

Cited by 2 publications

References 0 publications

Glucose Induces ER Stress Response-Mediated Peritoneal Mesothelial Cell Death

Glucose Induces ER Stress Response-Mediated Peritoneal Mesothelial Cell Death

Pentraxin 3 in Kidney Disease and Renal Replacement Therapies

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