Amelioration of Anemia in the ICGN Mouse, a Renal Anemia Model, with a Subcutaneous Bolus Injection of Erythropoietin Adsorbed to Hydroxyapatite Matrix

Nagasaki, Ken‐ichi; Ikoma, Toshiyuki; Katsuda, Shin-ichi; Tonegawa, Toru; Tanaka, Junzo; Ohyama, Minami; Hayashida, Kosuke; Nakamura, Teppei; Sato, Hidetaka; S, Itó; Sasaki, Nobuya; Agui, Takashi

doi:10.1292/jvms.001365

Cited by 3 publications

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References 38 publications

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“…3). Furthermore, a significant decrease in the number of red blood cells (RBC), hemoglobin concentration (HGB) and hematocrit (HCT) value have been reported in ICGN mice exhibiting severe anemia with aging [13]; however, these values remained normal in the B6-Tns2 nep mice, and no signs of anemia were observed (Fig 3). Figure 4 shows representative sections, taken at the indicated time points from each group of female mice, that demonstrate the pathological changes in the kidney in each strain.…”

Section: Resultsmentioning

confidence: 94%

Genetic Background Strongly Influences the Severity of Glomerulosclerosis in Mice

Nishino

Sasaki

Nagasaki

et al. 2010

The Journal of Veterinary Medical Science

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ABSTRACT. The ICGN mouse strain is a glomerulosclerosis (GS) model that shows characteristic proteinuria, podocyte morphological abnormalities and increased extracellular matrix accumulation in the glomeruli, which are the final common pathology associated with a variety of kidney diseases leading to end-stage renal failure. Previously, we performed a quantitative trait locus (QTL) analysis to identify the causative genes for GS in ICGN mice and found the deletion mutation of the tensin2 (Tns2) gene that creates both a premature stop codon and dramatically decreases mRNA expression levels within the region of the major QTL (this mutation was designated Tns2 nep ). The severity of GS varies considerably in humans and other animals, indicating the influence of several genes controlling the disease phenotype. In this study, to identify the modifier/resistant gene(s) for GS, we produced congenic strains carrying the Tns2 nep mutation on the C57BL/6J (B6) genetic background and analyzed GS severity. Interestingly, the B6 congenic mice exhibited milder phenotypes than the ICGN strain mice. The results suggest that B6 mice have a modifier(s) of GS resistance. Therefore, identification of the modifier loci in B6 mice will provide important new information regarding gene interactions controlling GS.KEY WORDS: genetic background, glomerulosclerosis, ICGN mice, tensin2.J. Vet. Med. Sci. 72(10): 1313-1318, 2010 Glomerulosclerosis (GS) is characterized by capillary obsolescence and increased extracellular matrix (ECM) accumulation, which is the final common pathology in a variety of kidney diseases leading to end-stage renal disease. ICR-derived glomerulonephritis (ICGN) mice are an inbred strain that exhibit the pathological hallmarks of GS: diffuse/global glomerular lesions characterized by marked glomerular hypertrophy, mesangial expansion, foot process effacement of podocytes and thickening of the glomerular basement membrane (GBM). ICGN mice also develop the typical symptoms of nephrotic disease: proteinuria, hypoproteinemia, hyperlipidemia, anemia and systemic edema [14,15]. Previously, we performed a quantitative trait locus (QTL) analysis to isolate the causative genes for these phenotypes and identified a major QTL on Chr 15 that is identical to a single recessive locus causing GS. This result was consistent with earlier report that designated this locus as the nep in ICGN mice [16]. In addition, we found an 8-base deletion in the coding region of tensin2 (Tns2), leading to a frameshift and giving rise to a premature termination codon. Analyses of in situ hybridization and immunohistochemistry revealed that Tns2 was expressed in podocytes in the glomeruli [2]. Tensin has been shown to contribute both to the formation of actin cytoskeletal structures and to signal transduction through integrin [8]. To maintain an intact glomerular filter barrier, podocyte-podocyte, podocytemesangial cell and podocyte-GBM interactions are essential. Multiple lines of evidences have clarified the importance of the role of the podocyte ...

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Section: Resultsmentioning

confidence: 94%

Genetic Background Strongly Influences the Severity of Glomerulosclerosis in Mice

Nishino

Sasaki

Nagasaki

et al. 2010

The Journal of Veterinary Medical Science

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“…Urine samples were collected from the bladder and urinary albumin was measured using Albuwell M (Exocell Inc.). Blood tests were performed as described previously (7). Sections (2-μm thick) were prepared from paraffin-embedded kidney tissues and stained with periodic acid-Schiff (PAS) reaction.…”

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confidence: 99%

The 129 genetic background affects susceptibility to glomerulosclerosis in tensin2-deficient mice

et al. 2012

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The ICGN mouse strain is a glomerulosclerosis (GS) model that shows significant proteinuria, podocyte morphological abnormalities and increased extracellular matrix accumulation in the glomeruli, which represent the final common pathology associated with a variety of kidney diseases leading to end-stage renal failure. Previously, we demonstrated that GS in ICGN mice can be attributed to the deletion mutation of the tensin2 (Tns2) gene (Tns2 nep ). Further, the C57BL/6J (B6) mouse is resistant to GS caused by this mutation. 129/Sv is also a popular strain; however, its susceptibility to GS has not been defined. Thus, to determine whether 129/Sv is resistant or susceptible to GS, we produced a congenic strain carrying Tns2 nep on the 129 +Ter /Sv (129T) background. 129T congenic mice (129T-Tns2

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Protein release parameters estimated with a flow system on zinc-containing apatite

Inaba

Kanno

Tada

et al. 2011

IOP Conf. Ser.: Mater. Sci. Eng.

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Amelioration of Anemia in the ICGN Mouse, a Renal Anemia Model, with a Subcutaneous Bolus Injection of Erythropoietin Adsorbed to Hydroxyapatite Matrix

Cited by 3 publications

References 38 publications

Genetic Background Strongly Influences the Severity of Glomerulosclerosis in Mice

Genetic Background Strongly Influences the Severity of Glomerulosclerosis in Mice

The 129 genetic background affects susceptibility to glomerulosclerosis in tensin2-deficient mice

Protein release parameters estimated with a flow system on zinc-containing apatite

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