Atsuko Kamijo-Ikemori

St. Marianna University School of Medicine, Kawasaki Si, Kanagawa, Japan

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Publications (19)55.57 Total impact

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    ABSTRACT: To demonstrate the renoprotective function of human liver-type fatty acid binding protein (hL-FABP) expressed in proximal tubules in aldosterone (Aldo) induced renal injury, hL-FABP chromosomal transgenic (Tg) and wild-type (WT) mice received systemic aldosterone infusions and were given 1% NaCl water for 28 days (Tg-Aldo and WT-Aldo). In this model, elevation of systolic blood pressure, monocyte chemoattractant protein 1 expression, macrophage infiltration in the interstitium, tubulointerstitial damage, and depositions of type I and III collagens were observed. Elevation of systolic blood pressure did not differ in WT-Aldo versus Tg-Aldo, however renal injury was suppressed in Tg-Aldo compared with WT-Aldo mice. Dihydroethidium fluorescence was used to evaluate reactive oxidative stress, which was suppressed in Tg-Aldo compared with WT-Aldo mice. Gene expression of angiotensinogen in the kidney was up-regulated and excretion of urinary angiotensinogen was increased in WT-Aldo mice. This exacerbation was suppressed in Tg-Aldo mice. Expression of hL-FABP was up-regulated in proximal tubules of Tg-Aldo mice. Urinary excretion of hL-FABP was significantly greater in Tg-Aldo than in Tg-control mice. In conclusion, hL-FABP ameliorated the tubulointerstitial damage in Aldo induced renal injury via reducing oxidative stress and suppressing activation of the intrarenal renin-angiotensin system.
    American journal of physiology. Renal physiology 10/2014; 308(2):ajprenal.00469.2014. DOI:10.1152/ajprenal.00469.2014 · 3.30 Impact Factor
  • Atsuko Kamijo-Ikemori, Takeshi Sugaya, Kenjiro Kimura
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    ABSTRACT: In diabetic kidney disease, detection of urinary albumin is recommended to aid in diagnosis, evaluate disease severity, and determine effects of therapy. However, because typical histopathologic changes in diabetic kidney disease or early progressive renal decline may occur in patients with normoalbuminuria, urinary albumin may not be sufficient to identify patients with early-stage diabetic kidney disease or to predict its progression. Therefore, intensive efforts have been made to identify novel noninvasive urinary biomarkers to discriminate patients with a higher risk of end-stage renal failure. Because diabetic kidney disease progression is associated with the extent of histologic changes in the glomeruli and the degree of tubulointerstitial changes, urinary biomarkers that accurately reflect the degree of histopathologic damage may be excellent biomarkers. This review article summarizes the clinical significance of new urinary biomarkers in the early detection of diabetic kidney disease.
    Current Diabetes Reports 08/2014; 14(8):513. DOI:10.1007/s11892-014-0513-1 · 3.38 Impact Factor
  • Atsuko Kamijo-Ikemori, Kenjiro Kimura
  • Atsuko Kamijo-Ikemori, Takeshi Sugaya, Kenjiro Kimura
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    ABSTRACT: Liver-type fatty acid binding protein (L-FABP) is expressed in the cytoplasm of human renal proximal tubules. Renal L-FABP expression is up-regulated and urinary excretion of renal L-FABP is increased by various stressors, such as urinary protein, hyperglycemia, tubular ischemia, toxins, and salt-sensitive hypertension, which lead to the progression of kidney disease. Urinary L-FABP levels accurately reflect the degree of tubulointerstitial damage and are strongly correlated with the prognosis of chronic kidney disease (CKD) patients in clinical studies. In patients with type I or type II diabetes, urinary L-FABP levels were reported to be significantly higher in patients with normal levels of urinary albumin than in those with microalbuminuria. Urinary L-FABP may be useful for the early detection of diabetic nephropathy. Furthermore, in a longitudinal study, a higher level of urinary L-FABP was found to be a risk factor for the progression of diabetic nephropathy. With respect to acute kidney disease (AKI), urinary L-FABP facilitates the early detection of AKI before an increase in serum creatinine. Therefore, urinary L-FABP was approved as a new tubular biomarker by the Ministry of Health, Labour and Welfare of Japan.
    Rinsho byori. The Japanese journal of clinical pathology 02/2014; 62(2):163-70.
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    ABSTRACT: The aim of this study was to assess the renoprotective effect of renal human liver-type fatty acid binding protein (hL-FABP) and angiotensin II (Ang II) type 1a receptor (AT1a) loss in renal injury caused by renin-angiotensin system (RAS) activation. We established hL-FABP chromosomal transgenic mice (L-FABP(+/-)AT1a(+/+)), crossed the L-FABP(+/-)AT1a(+/+) with AT1a knock-down homo mice (L-FABP(-/-)AT1a(-/-)), generated L-FABP(+/-)AT1a hetero mice (L-FABP(+/-)AT1a(+/-)). After the back-cross of these cubs, L-FABP(+/-)AT1a(-/-) were obtained. In order to activate the renal RAS, wild type mice (L-FABP(-/-)AT1a(+/+)), L-FABP(+/-)AT1a(+/+), L-FABP(-/-)AT1a(+/-), L-FABP(+/-) AT1a(+/-), L-FABP(-/-)AT1a(-/-) , and L-FABP(+/-)AT1a(-/-) were administered high dose systemic Ang II infusion plus a high salt diet for 28 days. In the L-FABP(-/-)AT1a(+/+), RAS activation (L-FABP(-/-)AT1a(+/+)RAS) caused hypertension and tubulointerstitial damage. In the L-FABP(+/-)AT1a(+/+)RAS, tubulointerstitial damage was significantly attenuated compared with L-FABP(-/-)AT1a(+/+)RAS. In the AT1a partial knockout (AT1a(+/-)) or complete knockout (AT1a(-/-)) mice, reduction of AT1a expression led to a significantly lower degree of renal injury compared with L-FABP(-/-)AT1a(+/+)RAS or L-FABP(+/-)AT1a(+/+)RAS mice. Renal injury in L-FABP(+/-)AT1a(+/-)RAS mice was significantly attenuated compared with L-FABP(-/-)AT1a(+/-)RAS mice. In both L-FABP(-/-)AT1a(-/-)RAS and L-FABP(+/-)AT1a(-/-)RAS mice, renal damage was rarely found. The degrees of renal hL-FABP expression and urinary hL-FABP levels increased by RAS activation and gradually decreased along with reduction of AT1a expression levels. In conclusion, in this mouse model, renal hL-FABP expression and a decrease in AT1a expression attenuated tubulointerstitial damage due to RAS activation.
    AJP Renal Physiology 01/2014; 306(6). DOI:10.1152/ajprenal.00460.2013 · 4.42 Impact Factor
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    ABSTRACT: Deterioration of diabetic nephropathy (DN) is largely determined by the degree of tubulointerstitial changes rather than the extent of histological changes in the glomeruli. Therefore, a tubular marker that accurately reflects tubulointerstitial damage may be an excellent biomarker for early detection or prediction of DN. Liver-type fatty-acid binding protein (L-FABP) is a 14 kDa small molecule that is expressed in the cytoplasm of human proximal tubules. In vivo experimental studies revealed that renal L-FABP gene expression was up-regulated by various stresses that cause tubulointerstitial damage, such as massive proteinuria, hyperglycemia, hypertension, ischemia and toxins, and that urinary excretion of L-FABP was increased. Recent clinical studies of patients with type 1 or type 2 diabetes demonstrated that urinary excretion of L-FABP derived from proximal tubules is a suitable biomarker for predicting and monitoring deterioration of renal function in DN. Moreover, therapeutic interventions with renoprotective effects reduced urinary L-FABP concentrations. Therefore, urinary L-FABP measured using the Human L-FABP ELISA Kit developed by CMIC Co., Ltd. (Tokyo, Japan) was confirmed as a newly established tubular biomarker by the Ministry of Health, Labour and Welfare in Japan in 2010. This review article summarizes the clinical significance of urinary L-FABP in DN.
    Clinica Chimica Acta 09/2013; 424:104–108. DOI:10.1016/j.cca.2013.05.020 · 2.76 Impact Factor
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    ABSTRACT: Liver-type fatty acid binding protein (L-FABP) is a 14kDa protein found in the cytoplasm of human renal proximal tubules. Fatty acids are bound with L-FABP and transported to the mitochondria or peroxisomes, where fatty acids are beta-oxidized, and this may play a role in fatty acid homeostasis. Moreover, L-FABP has high affinity and capacity to bind long-chain fatty acid oxidation products, and may be an effective endogenous antioxidant. Renal L-FABP is rarely expressed in the kidneys of rodents. In order to evaluate the pathological dynamics of renal L-FABP in kidney disease, human L-FABP chromosomal transgenic mice were generated. Various stress, such as massive proteinuria, hyperglycemia, hypertension, and toxins overloaded in the proximal tubules were revealed to up-regulate the gene expression of renal L-FABP and increase the excretion of L-FABP derived from the proximal tubules into urine. In clinical studies of chronic kidney disease (CKD), urinary L-FABP accurately reflected the degree of tubulointerstitial damage and correlated with the rate of CKD progression. Furthermore, a multicenter trial has shown that urinary L-FABP is more sensitive than urinary protein in predicting the progression of CKD. With respect to diabetic nephropathy and acute kidney disease (AKI), urinary L-FABP is an early diagnostic of kidney disease or a predictive marker for renal prognosis. After many clinical studies, urinary L-FABP was approved as a new tubular biomarker promulgated by the Ministry of Health, Labour and Welfare in Japan.
    Rinsho byori. The Japanese journal of clinical pathology 07/2013; 61(7):635-40.
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    ABSTRACT: Background The aim of this study was to determine whether a single moderate-intensity exercise session induces renal injury based on various parameters that reflect kidney dysfunction, including urinary L-type fatty acid-binding protein (L-FABP). Methods Adult outpatients (n = 31) with chronic kidney disease (CKD) not receiving renal replacement therapy participated in this study. Urine was collected before and after a single 20-min moderate-intensity exercise session. Urinary levels of L-FABP, albumin, N-acetyl--d-glucosaminidase (NAG), and 1-microglobrin (1MG) were measured. In addition, 12 patients with estimated glomerular filtration fraction less than 30 ml/min/1.73 ml(2) were selected from all patients and evaluated using the same analysis. ResultsUrinary values of L-FABP, albumin, NAG, and 1MG did not increase significantly after exercise compared with before exercise (urinary L-FABP, from 8.3 to 9.4 g/g of creatinine; urinary albumin, from 293.1 to 333.7 mg/g of creatinine; urinary NAG, from 9.2 to 8.2 U/g of creatinine; urinary 1MG, from 11.4 to 9.8 mg/g of creatinine, not significant). Similar findings were seen in all patients, regardless of degree of renal dysfunction. ConclusionsA single session of moderate-intensity exercise was not associated with an increase in renal parameters used to assess renal damage. (C) 2013 Wiley Periodicals, Inc.
    Journal of Clinical Laboratory Analysis 05/2013; 27(3):177-180. DOI:10.1002/jcla.21579 · 1.14 Impact Factor
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    ABSTRACT: To investigate the role of human liver-type fatty acid binding protein (hL-FABP) in angiotensin (Ang) II-induced renal injury, Ang II was infused systemically into hL-FABP chromosomal transgenic (Tg) and wild-type (WT) mice (Tg-Ang II and WT-Ang II) for 28 days. Control mice were injected with saline only (Tg-control and WT-control). hL-FABP was expressed in proximal tubules of Tg mice. After a high-dose injection of Ang II, renal gene and protein expressions of hL-FABP in Tg-Ang II mice increased significantly compared with Tg-control mice. Urinary excretion of L-FABP was significantly greater in Tg-Ang II than in Tg-control mice. Blood pressure levels in both groups increased to a similar extent. Upregulation of monocyte chemoattractant protein 1 expression, macrophage infiltration in the interstitium, tubulointerstitial damage, and depositions of type I and III collagens were observed in both Tg-Ang II and WT-Ang II mice. However, these effects were less pronounced in Tg-Ang II compared with WT-Ang II mice. The level of renal N-(hexanoyl)lysine, an oxidative stress marker, was significantly higher in WT-Ang II than in Tg-Ang II mice. In conclusion, renal hL-FABP reduced oxidative stress in Ang II-induced renal injury and attenuated tubulointerstitial damage.
    Hypertension 08/2012; 60(4):973-80. DOI:10.1161/HYPERTENSIONAHA.112.199828 · 7.63 Impact Factor
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    ABSTRACT: Acute kidney injury (AKI) is a common complication after cardiac surgery. Urinary liver-type fatty acid-binding protein (L-FABP) reflects the presence of renal tubular injury. The aim of the present study was to evaluate the utility of urinary L-FABP compared with other urinary biomarkers for the early detection of postoperative AKI among adult patients undergoing cardiac surgery. Patients were divided into the AKI (n=48) and non-AKI groups (n=37) according to whether they developed postoperative AKI within 48h after surgery. Changes in various biomarkers were evaluated. Urine and serum samples were obtained from each patient at the following time points: before the operation, immediately after the operation, and 3, 6, 18, 24, and 48h postoperatively. The urinary L-FABP level was significantly higher in the AKI group than in the non-AKI group at every time point, while other biomarkers did not show such a tendency. The biomarker with the largest area under the curve at every time point for predicting the onset of AKI was urinary L-FABP. On multiple logistic regression analysis, the urinary L-FABP level before operation and within the first 6h after cardiac surgery was significantly associated with the onset of AKI. Urinary L-FABP is a useful biomarker for early detection of AKI and is a good early predictor of the onset of AKI.
    Circulation Journal 11/2011; 76(1):213-20. DOI:10.1253/circj.CJ-11-0342 · 3.69 Impact Factor
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    ABSTRACT: Kidney disease develops to renal failure over a period of days, months or years, hence, clinical markers that indicate the real-time renal pathophysiological conditions is important. Liver type fatty acid binding protein (L-FABP) is a 14 kDa molecule predominantly expressed in human proximal tubules. Clinical studies demonstrate that urinary excretion of L-FABP derived from the proximal tubules is an excellent biomarker for predicting and monitoring deterioration of renal function or for early detection of kidney disease. However, in order to clarify the pathophysiological roles or dynamics of renal L-FABP in diseased settings, in vivo experimental studies of kidney diseases are indispensable. Since L-FABP is not endogenously expressed in murine kidneys, a transgenic (Tg) mouse model with expression of the human L-FABP gene was established. This review article summarizes the findings on the pathophysiological roles and dynamics of renal human L-FABP in the recent experimental studies performed using this Tg mouse model.
    Nephrology 04/2011; 16(6):539-44. DOI:10.1111/j.1440-1797.2011.01469.x · 1.86 Impact Factor
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    ABSTRACT: Urinary liver-type fatty acid-binding protein (L-FABP) is a promising indicator of tubular but not glomerular damage. The aim of this study was to evaluate the clinical usefulness of urinary L-FABP as a prognostic biomarker in impaired diabetic nephropathy in type 2 diabetes. This investigation involved a cross-sectional and longitudinal analysis of the relationship between urinary L-FABP levels and progressive nephropathy. Urinary L-FABP was measured with enzyme-linked immunosorbent assay. In the cross-sectional analysis, the association of urinary L-FABP, with the severity of diabetic nephropathy, was investigated in 140 patients with type 2 diabetes and in 412 healthy control subjects. Of the patients in the former study, 104 have been followed for 4 years. The progression of diabetic nephropathy was defined as progressive albuminuria, end-stage renal disease, or induction of hemodialysis. Urinary L-FABP levels were progressively increased in subjects with normo-, micro-, or macroalbuminuria and further increased in patients with end-stage renal disease. In the longitudinal analysis, high urinary L-FABP levels were associated with the increase in albuminuria, progression to end-stage renal disease, or induction of hemodialysis. This was particularly demonstrated in the subgroup of patients without renal dysfunction (n = 59), where high urinary L-FABP levels were associated with the progression of diabetic nephropathy. Urinary L-FABP accurately reflected the severity of diabetic nephropathy in type 2 diabetes, and its level was high in the patients with normoalbuminuria. Moreover, higher urinary L-FABP was a risk factor for progression of diabetic nephropathy.
    Diabetes care 02/2011; 34(3):691-6. DOI:10.2337/dc10-1392 · 8.57 Impact Factor
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    ABSTRACT: Acute kidney injury (AKI) is a common complication in critically ill patients. Urinary excretion of liver-type fatty acid-binding protein (L-FABP), which is expressed in the proximal tubules, reflects the presence of tubular injury. Urinary excretion of podocalyxin (PCX), a glycoprotein prominently expressed on podocytes, is associated with podocyte injury. Our aims were to evaluate the utility of urinary L-FABP for the early detection of AKI and to examine whether podocyte injury is present in AKI patients using the biomarker of urinary PCX. Patients admitted to the intensive care unit (ICU) were divided into the AKI group (n = 14) and non-AKI group (n = 11), according to the occurrence of AKI during hospitalization in the ICU. Changes in various biomarkers were evaluated. In the AKI group, elevation of urinary L-FABP level [maximum value of L-FABP, 199.0 (92.5-433.6) μg/g creatinine, median (25-75% interquartile range)], which reflects tubular injury (area under the curve 0.95, cut-off value 44.1 μg/g Cr), occurred between -30 and 0 h before the occurrence of AKI (i.e., the time at which serum creatinine peaked), and elevation of urinary PCX level [maximum value of PCX, 389.5 (267.0-501.0) μg/g creatinine; upper limit of reference value, 160 μg/g creatinine] occurred during the time of recovery from AKI when serum creatinine levels were decreasing between 34.0 and 72.0 h after the occurrence of AKI. Furthermore, a parameter with the primary large AUC for predicting the onset of AKI was urinary L-FABP. Our study suggests that L-FABP is a useful biomarker for early detection of AKI and that podocyte injury was induced during the recovery phase of AKI.
    Clinical and Experimental Nephrology 12/2010; 15(2):220-5. DOI:10.1007/s10157-010-0384-y · 1.71 Impact Factor
  • Atsuko Kamijo-Ikemori, Takeshi Sugaya
    Nippon rinsho. Japanese journal of clinical medicine 11/2010; 68 Suppl 9:406-9.
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    ABSTRACT: To investigate the relationship between liver-type fatty acid-binding protein (L-FABP), a biomarker of chronic kidney disease, in the kidney and the degree of tubulointerstitial damage, folic acid (FA)-induced nephropathy was studied in a mouse model system. As renal L-FABP is not expressed in wild-type mice, human L-FABP (hL-FABP) transgenic mice were used in this study. hL-FABP is expressed in the renal proximal tubules of the transgenic mice that were injected intraperitoneally with FA in NaHCO3 (the FA group) or only NaHCO3 (the control group) and oral saline solution daily during the experimental period. The FA group developed severe tubulointerstitial damage with the infiltration of macrophages and the deposition of type I collagen on days 3 and 7 and recovered to the control level on day 14. The gene and protein expression levels of hL-FABP in the kidney were significantly enhanced on days 3 and 7. Urinary hL-FABP in the FA group was elevated on days 3 and 7 and decreased to the control level on day 14. The protein expression levels of hL-FABP in both the kidney and urine significantly correlated with the degree of tubulointerstitial damage, the infiltration of macrophages, and the deposition of type I collagen. In conclusion, renal expression and urinary excretion of hL-FABP significantly reflected the severity of tubulointerstitial damage in FA-induced nephropathy.
    American Journal Of Pathology 06/2009; 174(6):2096-106. DOI:10.2353/ajpath.2009.080780 · 4.60 Impact Factor
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    ABSTRACT: The aims of this clinical study were to investigate the associations of urinary free fatty acid (FFA) levels with tubulointerstitial damage, and to determine the clinical significance of urinary liver-type fatty acid binding protein (L-FABP) in diabetic nephropathy. Fifteen patients with nephrotic syndrome due to diabetic nephropathy and 12 patients with minimal-change nephrotic syndrome (MCNS) were studied. Urinary and serum FFA concentrations (palmitic, oleic, linoleic, and arachidonic acids) were measured by gas chromatography, and urinary L-FABP levels were quantified using an ELISA technique. Tubulointerstitial damage was assessed using renal biopsy specimens. The levels of urinary linoleic and arachidonic acids were significantly elevated in diabetic nephropathy compared to MCNS patients, though serum FFA levels were lower in diabetic nephropathy than MCNS patients. The degree of tubulointerstitial damage was significantly severer in the patients with diabetic nephropathy than MCNS. Urinary L-FABP and 8-OHdG (8-hydroxydeoxyguanosine) concentrations were significantly higher in the diabetic nephropathy subjects. Elevated urinary excretion of FFA may be a reflection of FFA overload in the proximal tubules, and FFA may be an important promoter of tubulointerstitial damage in diabetic nephropathy patients. Urinary L-FABP levels may reflect the stress induced by FFA to the proximal tubules, leading to severe tubulointerstitial damage.
    Nephron Clinical Practice 05/2009; 112(3):c148-56. DOI:10.1159/000214210 · 1.65 Impact Factor
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    ABSTRACT: Renoprotection of liver-type fatty acid binding protein (L-FABP) was demonstrated in a streptozotocin (STZ)-induced diabetic mouse model. Established human L-FABP (hL-FABP) transgenic (Tg) mice and wild-type (WT) mice were divided into two groups: diabetic mice were uninephrectomized and injected with STZ; control mice were uninephrectomized and injected with a citrate buffer alone. Although mouse L-FABP was not expressed in WT mice, hL-FABP was expressed in the proximal tubules of the diabetic Tg mice and in the control Tg mice at 8 and 14 weeks after these injections. The expression of renal hL-FABP increased significantly in diabetic Tg mice compared to control Tg mice. A number of macrophages (F4/80) infiltrating the interstitium, the gene expressions of MCP-1, MCP-3, TGF-beta, Fas, Bax and RAGE were significantly lower in diabetic Tg kidneys compared with diabetic WT kidneys. In the diabetic Tg kidneys, the degree of the tubulointerstitial injury and the deposition of type IV collagen were significantly lower than that of diabetic WT kidneys. The expressions of catalase and glutathione peroxidase-1 were significantly lower in diabetic Tg kidneys compared with diabetic WT kidneys. Renal L-FABP ameliorated the tubulointerstitial damage of type 1 diabetic mice.
    Nephrology Dialysis Transplantation 11/2008; 24(3):788-800. DOI:10.1093/ndt/gfn573 · 3.49 Impact Factor
  • Atsuko Kamijo-Ikemori, Takeshi Sugaya, Kenjiro Kimura
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    ABSTRACT: The number of patients with end stage renal failure has been increasing throughout the world. The importance of measuring clinical parameters in renal injury has been emphasized for administering appropriate treatment and preventing a worsening of the disease. However, there are no clinically useful markers in predicting and monitoring the progression of renal disease. Liver type fatty acid binding protein (L-FABP) of 14.4 kDa is expressed in human proximal tubules. In order to evaluate the clinical significance of urinary L-FABP as a biomarker in renal disease, a monoclonal antibody against human L-FABP was developed and a two step sandwich enzyme linked immunosorbent assay (ELISA) method was established for determining human L-FABP in urine. In some clinical studies, urinary excretion of L-FABP was shown to be an excellent clinical marker that can help predict and monitor the progression of renal disease. The dynamics of renal L-FABP in pathophysiological settings has been revealed in experimental studies using transgenic mice with the human L-FABP gene. This review presents recent findings on the function and pathophysiological role of L-FABP, and summarizes the clinical importance of measuring urinary L-FABP in renal disease.
    Clinica Chimica Acta 01/2007; 374(1-2):1-7. DOI:10.1016/j.cca.2006.05.038 · 2.76 Impact Factor
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    ABSTRACT: Liver-type fatty-acid-binding protein (L-FABP), which has high affinity for long-chain fatty acid oxidation products, may be an effective endogenous antioxidant. To examine the role of L-FABP in tubulointerstitial damage, we used a unilateral ureteral obstruction (UUO) model. We established human L-FABP (hL-FABP) gene transgenic (Tg) mice and compared the tubulointerstitial pathology of the Tg mice (n = 23) with that of the wild-type (WT) mice (n = 23). Mice were sacrificed on days 2, 4, 5, or 7 after UUO. Although mouse L-FABP was not expressed in WT mice, hL-FABP was expressed in the proximal tubules of the Tg mice with UUO (UUO-Tg) and in sham-operated Tg mice. The expression of renal hL-FABP was significantly increased in UUO-Tg compared with sham-operated Tg mice. The number of macrophages (F4/80) infiltrating the interstitium and the level of expression of MCP-1 and MCP-3 were significantly lower in UUO-Tg kidneys compared with UUO-WT kidneys. In UUO-Tg kidneys, the degree of the tubulointerstitial injury and the deposition of type I collagen were significantly lower than that of UUO-WT kidneys. On day 7, lipid peroxidation product accumulated in the UUO-WT kidneys but not in that of UUO-Tg kidneys. In conclusion, renal L-FABP may reduce the oxidative stress in the UUO model, ameliorating tubulointerstitial damage.
    American Journal Of Pathology 11/2006; 169(4):1107-17. DOI:10.2353/ajpath.2006.060131 · 4.60 Impact Factor