ICR-derived glomerulonephritis (ICGN) mice are a novel inbred strain with hereditary nephrotic syndrome and are thus considered a good animal model of human idiopathic nephrotic syndrome. In the present study, we investigated the effect to erythrocyte production by human erythropoietin (hEPO) treatment in ICGN mice during the early nephrotic stage. Erythrocyte count, hemoglobin concentration and hematocrit value in hEPO-treated (5 U/body/day, for 5 days) ICGN mice were recovered to the levels found in normal ICR mice. In addition, there was no correlation between plasma creatinine level, a marker of renal function, and erythrocyte count after hEPO treatment. Therefore, anemia in ICGN mice may be caused by decreased production of EPO in the kidney following progressive parenchymal damage.
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http://dx.doi.org/10.1538/expanim.54.181 | DOI Listing |
Microcirculation
November 2024
Department of Nephrology and Hypertension, Kawasaki Medical School, Kurashiki, Okayama, Japan.
Objective: Endothelial dysfunction plays an important role in the pathogenesis of chronic kidney disease. Prostacyclin (PGI), an endothelial cell-produced endogenous prostaglandin, plays a crucial role in maintaining endothelial function. However, its effects on intestinal microcirculation and barrier function are not fully understood.
View Article and Find Full Text PDFJ Immunol Res
March 2022
Department of Medicine, University at Buffalo, Buffalo, NY 14203, USA.
Complement factor H (FH) is a key regulator of the alternative pathway of complement, in man and mouse. Earlier, our studies revealed that the absence of FH causes the C57BL6 mouse to become susceptible to chronic serum sickness (CSS) along with an increase in the renal infiltration of macrophages compared to controls. To understand if the increased recruitment of macrophages (Ms) to the kidney was driving inflammation and propagating injury, we examined the effect of M depletion with clodronate in FH knockout mice with CSS.
View Article and Find Full Text PDFFASEB J
November 2019
Department of Nephrology and Hypertension, Kawasaki Medical School, Kurashiki, Okayama, Japan.
Multiple clinical studies have shown that bardoxolone methyl, a potent activator of nuclear factor erythroid 2-related factor 2 (Nrf2), is effective in increasing glomerular filtration rate in patients with chronic kidney disease. However, whether an Nrf2 activator can protect tubules from proteinuria-induced tubular damage anti-inflammatory and antioxidative stress mechanisms is unknown. Using an Institute of Cancer Research-derived glomerulonephritis (ICGN) mouse model of nephrosis, we examined the effects of dihydro-CDDO-trifluoroethyl amide (dh404), a rodent-tolerable bardoxolone methyl analog, in protecting the tubulointerstitium; dh404 markedly suppressed tubular epithelial cell damage in the renal interstitium of ICGN mice.
View Article and Find Full Text PDFJ Diabetes Investig
March 2019
Laboratory of Laboratory Animal Science and Medicine, School of Veterinary Medicine, Kitasato University, Towada, Japan.
Aims/introduction: Diabetic animal models have made an enormous contribution to our understanding of the etiology of diabetes and the development of new medications. The aim of the present study was to develop and characterize a novel, non-obese murine strain with spontaneous diabetes - the insulin hyposecretion (ihs) mouse.
Materials And Methods: During the development of the ICGN.
BMC Genet
April 2018
Laboratory of Laboratory Animal Science and Medicine, School of Veterinary Medicine, Kitasato University, 35-1, Higashi-23, Towada, Aomori, 034-8628, Japan.
Background: Tensin2 is a focal adhesion-localized multidomain protein expressed in various tissues, and its dysfunction leads to alterations in podocytes. However, these podocyte-related manifestations are dependent on murine strain. Tensin2 dysfunction results in susceptible strains developing podocyte foot process effacement and massive albuminuria, whereas podocytes in resistant strains remain almost intact.
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