Mesangial proliferative glomerulonephritis in murine malaria parasite, Plasmodium chabaudi AS, infected NC mice

Yashima, Akihito; Mizuno, Masashi; Shimada, Kojiro; Suzuki, Norihiko; Tawada, Hideo; Sato, Waichi; Tsuboi, Naotake; Maruyama, Shoichi; Ito, Yasuhiko; Matsuo, Seiichi; Ohno, Tamio

doi:10.1007/s10157-016-1339-8

Cited by 8 publications

(10 citation statements)

References 14 publications

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“…Chylemia was observed in nephrotic NC/Jic mice (left side).) accompanied by severe edema, proteinuria, hypoalbuminemia, and hyperlipidemia. These results suggested that malarial nephrosis was a consequence of interactions between a specific genetic factor in NC/Jic mice and P. chabaudi chabaudi AS (Table 1) [97]. In these mice, diffuse mesangial proliferation was clearly seen at 8 days post-infection [97].…”

Section: Malaria Complications In the Kidneymentioning

confidence: 99%

“…These results suggested that malarial nephrosis was a consequence of interactions between a specific genetic factor in NC/Jic mice and P. chabaudi chabaudi AS (Table 1) [97]. In these mice, diffuse mesangial proliferation was clearly seen at 8 days post-infection [97]. Significant depositions of both IgG and C3 were also observed in the mesangial area [97].…”

Section: Malaria Complications In the Kidneymentioning

confidence: 99%

“…In these mice, diffuse mesangial proliferation was clearly seen at 8 days post-infection [97]. Significant depositions of both IgG and C3 were also observed in the mesangial area [97]. However, malaria parasites were almost eliminated from infected mice at 10 days post-infection; the degree of segmental sclerosis, adhesion/crescent, formation of thrombi in glomeruli, and degree of tubular injuries were markedly increased at that time [97].…”

Section: Malaria Complications In the Kidneymentioning

confidence: 99%

“…Significant depositions of both IgG and C3 were also observed in the mesangial area [97]. However, malaria parasites were almost eliminated from infected mice at 10 days post-infection; the degree of segmental sclerosis, adhesion/crescent, formation of thrombi in glomeruli, and degree of tubular injuries were markedly increased at that time [97]. In concert with this pathological progress, the levels of urine protein/urine, blood urea nitrogen, serum total cholesterol, and serum triglyceride were elevated [97].…”

Section: Malaria Complications In the Kidneymentioning

confidence: 99%

“…However, malaria parasites were almost eliminated from infected mice at 10 days post-infection; the degree of segmental sclerosis, adhesion/crescent, formation of thrombi in glomeruli, and degree of tubular injuries were markedly increased at that time [97]. In concert with this pathological progress, the levels of urine protein/urine, blood urea nitrogen, serum total cholesterol, and serum triglyceride were elevated [97]. The clinical and pathological features NC/Jic strain mice infected with P. chabaudi chabaudi AS have a number of similarities to quartan malarial nephropathy [3, 19, 31].…”

Section: Malaria Complications In the Kidneymentioning

confidence: 99%

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Mouse NC/Jic strain provides novel insights into host genetic factors for malaria research

et al. 2019

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Malaria is caused by Plasmodium parasites and is one of the most life-threatening infectious diseases in humans. Infection can result in severe complications such as cerebral malaria, acute lung injury/acute respiratory distress syndrome, and acute renal injury. These complications are mainly caused by P. falciparum infection and are major causes of death associated with malaria. There are a few species of rodent-infective malaria parasites, and mice infected with such parasites are now widely used for screening candidate drugs and vaccines and for studying host immune responses and pathogenesis associated with disease-related complications. We found that mice of the NC/Jic strain infected with rodent malarial parasites exhibit distinctive disease-related complications such as cerebral malaria and nephrotic syndrome, in addition to a rapid increase in parasitemia. Here, we focus on the analysis of host genetic factors that affect malarial pathogenesis and describe the characteristic features, utility, and future prospects for exploitation of the NC/Jic strain as a novel mouse model for malaria research.

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Section: Malaria Complications In the Kidneymentioning

confidence: 99%

Section: Malaria Complications In the Kidneymentioning

confidence: 99%

Section: Malaria Complications In the Kidneymentioning

confidence: 99%

Section: Malaria Complications In the Kidneymentioning

confidence: 99%

Section: Malaria Complications In the Kidneymentioning

confidence: 99%

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Mouse NC/Jic strain provides novel insights into host genetic factors for malaria research

et al. 2019

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Complement regulation and kidney diseases: recent knowledge of the double-edged roles of complement activation in nephrology

2017

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The complement activation system plays important roles to maintain homeostasis in the host and to fight foreign invaders to protect the host. Therefore, the complement system is considered a core part of innate immunity which also cross-talks to acquired immunity. In the history of nephrology, the complement system is familiar to us, because complement protein or fragment deposition, including C3, C4, C1q, and/or C4d, is routinely estimated by immunohistochemistry to diagnose renal pathologies. The relationships between pathological mechanisms and complement activation have been investigated for renal diseases such as post-infectious glomerulonephritis, lupus nephritis, and primary membranoproliferative glomerulonephritis, which are usually accompanied by hypocomplementemia. However, unregulated complement activation in local areas might be associated with progression of various renal injuries even in the normocomplementemic patient. Recently, attention has focused on dysfunction of complement regulation in various diseases including renal diseases such as atypical hemolytic uremic syndrome and C3 glomerulopathy. Some mechanisms associated with complement activation in these diseases were clarified. In addition, lots of anti-complement agents were developed and some of the agents have become clinically available. Now, anti-complement therapies represent a realistic choice of therapeutic approaches for complement-related diseases. Research on roles of complement activation is proceeding into new stages in the field of nephrology and in other fields involving both basic and clinical research. We herein summarize relationships between the complement activation and regulation systems, their physiological effects and roles in maintenance of homeostasis in the host, and how dysregulation of the complement system triggers disease, especially renal disease.

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Phosphoproteomic profile of peripheral blood mononuclear cells in mesangial proliferative glomerulonephritis patients

Zhang¹,

Sun²,

Li³

et al. 2020

Integr Mol Med

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To insight the pathogenesis of Mesangial proliferative glomerulonephritis (MsPGN), we investigated the phosphoproteomic profile of PBMCs from MsPGN patients and normal subjects by integrating TiO 2 enrichment technology, 2D nano-liter liquid chromatography and linear ion trap quadrupole mass spectrometry. We identified totally 693 differential phosphorylation sites and corresponded to 439 genes. Gene ontology (GO) analysis showed that protein or nucleic acid binding took up the largest proportion of molecular function, followed by nucleobase, nucleoside, nucleotide and nucleic acid metabolic process in the nucleus. KEGG Pathway analysis showed that most of differential gene enrich in mitogen-activated protein kinase (MAPK) signaling pathway and focal adhesion pathway. Gene network analysis showed that serine/arginine repetitive matrix (SRRM) 1, histone deacetylase (HDAC) 1 and protein kinase C delta (PRKED) were significantly regulators in the network. These results suggested that abnormal changes of protein phosphorylation modification may contribute to MsPGN, and may be derived from the dysregulation of MAPK signaling pathway and focal adhesion pathway. In these pathways, the differential genes SRRM1, HDAC1 and PRKCD with higher connection may be the promising biomarker for MsPGN.

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Mesangial proliferative glomerulonephritis in murine malaria parasite, Plasmodium chabaudi AS, infected NC mice

Cited by 8 publications

References 14 publications

Mouse NC/Jic strain provides novel insights into host genetic factors for malaria research

Mouse NC/Jic strain provides novel insights into host genetic factors for malaria research

Complement regulation and kidney diseases: recent knowledge of the double-edged roles of complement activation in nephrology

Phosphoproteomic profile of peripheral blood mononuclear cells in mesangial proliferative glomerulonephritis patients

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