• Applied Microscopy
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• 제17권1호
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• pp.131-160
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• 1987

Anatomical features of the renal papilla and pelvis and ultrastructures of the epithelium covering these areas in four species of mammals were studied by means of light, scanning and transmission electron microscopy. In terms of the morphology of mammalian kidney types distinguished by Sperber(1944), Pfeiffer(1968) and Schmidt-Nielsen(1977), the kidneys of animal species used in this experiment were; 1) the mouse kidney with the fornix between a long conical papilla and the funnel-shaped pelvis, 2) the guinea pig kidney with the peripelvic column and pelvic pouch between a short conical papilla and the funnel-shaped pelvis, 3) the dog kidney with the peripelvic column and pelvic pouch between the crest-shaped papilla and the funnel-shaped pelvis, and 4) the cattle kidney which is divided into multiple renculi with minor and major calyces and pelvis. The renal papilla was lined with the simple or pseudostratified columnar epithelium which covered the inner zone of the renal medulla. The epithelial cells with numerous short microvilli on the surface contained a few organelles. In the mouse, the fornix was lined with one to two cell-layered cuboidal epithelium which covered the outer zone of the renal medulla and a part of the cortex. The epithelial cells of the fornix with numerous short microvilli or microridges on the surface had well-developed organelles. In the guinea pig, the peripelvic column was lined with the simple cuboidal or low columnar epithelium which covered the outer zone of the renal medulla. The epithelial cells with numerous short microvilli on the surface contained well-developed organelles. The pelvic pouch was lined with the pseudostratified columnar epithelium which was composed of four kinds of cells; the secretory cell with small electron-dense granules (310 nm), the secretory cell with large granules (720 nm) showing various electron densities, the mitochondria-rich cell with a single cilium, and the basal cell. Pelves of the mouse and guinea pig, peripelvic column, pelvic pouch and pelvis of the dog, and minor and major calyces and pelvis of the cattle were lined with the transitional epithelium. The fusiform vesicles in the superficial cells of the epithelium were highly developed in the dog, relatively well developed in the mouse and guinea pig, and poorly developed in the cattle. From the above findings, it is suggested that the transport of solutes and water of the urine in the pelvic cavity can take place through the epithelia covering the renal papilla and fornix of the mouse, papilla and peripelvic column of the guinea pig, and papillae of the dog and the cattle. And specialized cell types in the epithelium of the guinea pig pelvic pouch, two kinds of secretory cells and mitochondria-rich cell with a single cilium, could have peculiar functions in the renal pelvis, respectively.

• BMB Reports
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• 제46권2호
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• pp.73-79
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• 2013

Polycystic kidney disease (PKD) is a common hereditary disorder which is characterized by fluid-filled cysts in the kidney. Mutation in either PKD1, encoding polycystin-1 (PC1), or PKD2, encoding polycystin-2 (PC2), are causative genes of PKD. Recent studies indicate that renal cilia, known as mechanosensors, detecting flow stimulation through renal tubules, have a critical function in maintaining homeostasis of renal epithelial cells. Because most proteins related to PKD are localized to renal cilia or have a function in ciliogenesis. PC1/PC2 heterodimer is localized to the cilia, playing a role in calcium channels. Also, disruptions of ciliary proteins, except for PC1 and PC2, could be involved in the induction of polycystic kidney disease. Based on these findings, various PKD mice models were produced to understand the roles of primary cilia defects in renal cyst formation. In this review, we will describe the general role of cilia in renal epithelial cells, and the relationship between ciliary defects and PKD. We also discuss mouse models of PKD related to ciliary defects based on recent studies.

• 대한세포병리학회지
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• 제5권1호
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• pp.65-70
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• 1994

We describe a case of fine needle aspiration cytology of renal angiomyolipoma which was not associated with the clinical complex of tuberous sclerosis and was incidentally found. It was a solitary lesion and the clinical impression before needle aspiration was renal ceil carcinoma. The aspirated specimen showed mature fat cells, clusters of renal tubular epithelial cells and sheets of pleomorphic smooth muscle cells with fibrillary cytoplasm. The nuclei of smooth muscle celis varied in size and shape. Since the treatment of renal angiomyolipoma differs from that of renal ceil carcinoma, the preoperative cytological diagnosis is of great value.

• Childhood Kidney Diseases
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• 제19권2호
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• pp.79-88
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• 2015

Neutrophil gelatinase-associated lipocalin (NGAL) has emerged as one of the most promising biomarkers of renal epithelial injury. Numerous studies have presented the diagnostic and prognostic utility of urinary and plasma NGAL in patients with acute kidney injury, chronic kidney disease, renal injury after kidney transplantation, and other renal diseases. NGAL is a member of the lipocalin family that is abundantly expressed in neutrophils and monocytes/macrophages and is a mediator of the innate immune response. The biological significance of NGAL to hamper bacterial growth by sequestering iron-binding siderophores has been studied in a knock-out mouse model. Besides neutrophils, NGAL is detectable in most tissues normally encountered by microorganisms, and its expression is upregulated in epithelial cells during inflammation. A growing number of studies have supported the clinical utility of NAGL for detecting invasive bacterial infections. Several investigators including our group have reported that measuring NGAL can be used to help predict and manage urinary tract infections and acute pyelonephritis. This article summarizes the biology and pathophysiology of NGAL and reviews studies on the implications of NGAL in various renal diseases from acute kidney injury to acute pyelonephritis.

• 대한의생명과학회지
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• 제8권4호
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• pp.251-256
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• 2002

This study was undertaken to determine the underlying mechanisms of reactive oxygen species-induced cell injury in renal epithelial cells and whether there is a difference in the role of lipid peroxidation between freshly isolated renal cells and cultured renal cells. Rabbit renal cortical slices were used as a model of freshly isolated cells and opossum kidney (OK) cells as a model of cultured cells. Cell injury was estimated by measuring lactate dehydrogenase (LDH) release in renal cortical slices and frypan blue exclusion in OK cells. $H_2O$$_2$ was used as a drug model of reactive oxygen species. $H_2O$$_2$ induced cell injury in a dose-dependent manner in both cell types. However, renal cortical slices were resistant to $H_2O$$_2$ approximately 50-fold than OK cells. $H_2O$$_2$-induced cell injury was prevented by thiols (glutathione and dithiothreitol) and iron chelators (deferoxamine and phenanthroline) in both cell types. $H_2O$$_2$-induced cell injury in renal cortical slices was completely prevented by antioxidants N,N-diphenyl-p -phenylenediamine and Trolox, but the cell injury was not affected by these antioxidants in OK cells. $H_2O$$_2$ increased lipid peroxidation in both cell types, which was completely inhibited by the antioxidants. These results suggest that $H_2O$$_2$ induces cell injury through a lipid peroxidation-dependent mechanism in freshly isolated renal cells, but via a mechanism independent of lipid peronidation in cultured cells.

• 대한임상검사과학회지
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• 제41권2호
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• pp.83-92
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• 2009

This study was undertaken to examine the effect of oxidants on membrane transport function in renal epithelial cells. Hydrogen peroxide ($H_2O_2$) was used as a model oxidant and the membrane transport function was evaluated by measuring $Na^+$-dependent phosphate ($Na^+$-Pi) uptake in opossum kidney (OK) cells. $H_2O_2$ inhibited $Na^+$-Pi uptake in a dose-dependent manner. The oxidant also caused loss of cell viability in a dose-dependent fashion. However, the extent of inhibition of the uptake was larger than that in cell viability. $H_2O_2$ inhibited $Na^+$-dependent uptake without any effect on $Na^+$-independent uptake. $H_2O_2$-induced inhibition of $Na^+$-Pi uptake was prevented completely by catalase, dimethylthiourea, and deferoxamine, suggesting involvement of hydroxyl radical generated by an iron-dependent mechanism. In contrast, antioxidants Trolox, N,N'-diphenyl-p-phenylenediamine, and butylated hydroxyanisole did not affect the $H_2O_2$ inhibition. Kinetic analysis indicated that $H_2O_2$ decreased Vmax of $Na^+$-Pi uptake with no change in the Km value. Phosphonoformic acid binding assay did not show any difference between control and $H_2O_2$-treated cells. $H_2O_2$ also did not cause degradation of $Na^+$-Pi transporter protein. Reduction in $Na^+$-Pi uptake by $H_2O_2$ was associated with ATP depletion and direct inhibition of $Na^+$-$K^+$-ATPase activity. These results indicate that the effect of $H_2O_2$ on membrane transport function in OK cells is associated with reduction in functional $Na^+$-pump activity. In addition, the inhibitory effect of $H_2O_2$ was not associated with lipid peroxidation.

• BMB Reports
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• 제45권3호
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• pp.189-193
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• 2012

Cyst formation is a major characteristic of ADPKD and is caused by the abnormal proliferation of epithelial cells. Renal cyst formation disrupts renal function and induces diverse complications. The mechanism of cyst formation is unclear. mIMCD-3 cells were established to develop simple epithelial cell cysts in 3-D culture. We confirmed previously that Mxi1 plays a role in cyst formation in Mxi1-deficient mice. Cysts in Mxi1 transfectanted cells were showed by collagen or mebiol gels in 3-D cell culture system. Causative genes of ADPKD were measured by q RT-PCR. Herein, Mxi1 transfectants rarely formed a simple epithelial cyst and induced cell death. Overexpression of Mxi1 resulted in a decrease in the PKD1, PKD2 and c-myc mRNA relating to the pathway of cyst formation. These data indicate that Mxi1 influences cyst formation of mIMCD-3 cells in 3-D culture and that Mxi1 may control the mechanism of renal cyst formation.

• Journal of Acupuncture Research
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• 제20권6호
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• pp.128-139
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• 2003

Juglans sinensis Dode has been reported to have antioxidant activity. However, the effect of Juglans sinensis Dode aquacupuncture(JS) on reactive oxygen species(ROS)-induced alterations in membrane transport function in renal tubular cells. This study was performed to evaluate the effect of JS on the organic hydroperoxide t-butylhydroperoxide(tBHP)-induced inhibition of $Na^+$-dependent phosphate($Na^+$-Pi) uptake in opossum kidney (OK) cells, an established renal proximal epithelial cell line. tBHP inhibited $Na^+$-Pi uptake in a time-dependent manner. The inhibitory effect of tBHP was prevented by JS over concentration range of 0.05-1mg/100ml in a dose-dependent manner. Kinetic studies showed that tBHP caused an decrease in Vmax for $Na^+$-Pi uptake without any a significant change in Km. $Na^+$-dependent phosphonoformic acid binding, a irreversible inhibitor of renal $Na^+$-Pi uptake, was decreased by tBHP treatment. The reduction in Vmax and phosphonoformic acid binding by tBHP was prevented by JS. tBHP induced lipid peroxidation and its effect was completely inhibited by JS and antioxidant N,N'-diphenyl-p-phenylenediamine. These data suggest that the oxidant inhibits phosphate uptake by a reduction in the number of active carrier across the membrane. JS may prevent oxidant-induced inhibition of membrane transport function by a mechanism similar to antioxidants in renal epithelial cells. Although the precise constituents remain to be explored, JS may be employed as a useful candidate herb for drug development to prevent and treat oxidant-mediated renal failure.

• 동의생리병리학회지
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• 제34권2호
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• pp.61-66
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• 2020

Epithelial-mesenchymal transition (EMT) is the process by which epithelial cells lose their characters and acquire the properties of mesenchymal cells. EMT has been reported to exert an essential role in embryonic development. Recently, EMT has emerged as a pivotal mechanism in the metastasis of cancer and the fibrosis of chronic diseases. In particular, EMT is drawing attention as a mechanism of renal fibrosis in chronic kidney diseases such as diabetic nephropathy. In this study, we developed an EMT model by treating TGF-β1 on the podocytes, which play a key role in the renal glomerular filtration. This study explored the effects of Hwanggeum-tang (HGT) recorded in Dongeuibogam as being able to be used for the treatment of Sogal whose concept had been applied to Diabetes Mellitus (DM), on the TGF-β1-induced podocyte EMT. HGT suppressed the expression of vimentin and α-SMA, the EMT marker, in the human podocytes stimulated by TGF-β1. However, HGT increased the expression of ZO-1 and nephrin. Interestingly, HGT selectively inhibited the mTOR pathway rather than the classical Smad pathway. HGT also activated the AMPK signaling. HGT's inhibitory effect on the podocyte EMT through regulation of the mTOR pathway was achieved through the activation of AMPK, which was confirmed by comparison with cells treated with compound C (CC), an inhibitor of AMPK signaling. In conclusion, HGT can be applied to the renal fibrosis by preventing TGF-β1-induced EMT of podocytes through AMPK activation and mTOR inhibition.

• The Korean Journal of Physiology and Pharmacology
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• 제22권2호
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• pp.135-143
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• 2018

Tumor necrosis $factor-{\alpha}$ ($TNF{\alpha}$) and the angiotensin system are involved in inflammatory diseases and may contribute to acute kidney injury. We investigated the mechanisms by which $TNF{\alpha}$-converting enzyme (TACE) contributes to lipopolysaccharide (LPS)-induced renal inflammation and the effect of TACE inhibitor treatment on LPS-induced cellular injury in human renal proximal tubule epithelial (HK-2) cells. Mice were treated with LPS (10 mg/kg, i.p.) and HK-2 cells were cultured with or without LPS ($10{\mu}g/ml$) in the presence or absence of a type 1 TACE inhibitor ($1{\mu}M$) or type 2 TACE inhibitor ($10{\mu}M$). LPS treatment induced increased serum creatinine, $TNF{\alpha}$, and urinary neutrophil gelatinase-associated lipocalin. Angiotensin II type 1 receptor, mitogen activated protein kinase (MAPK), and TACE increased, while angiotensin-converting enzyme-2 (ACE2) expression decreased in LPS-induced acute kidney injury and LPS-treated HK-2 cells. LPS induced reactive oxygen species and the down-regulation of ACE2, and these responses were prevented by TACE inhibitors in HK-2 cells. TACE inhibitors increased cell viability in LPS-treated HK-2 cells and attenuated oxidative stress and inflammatory cytokines. Our findings indicate that LPS activates renin angiotensin system components via the activation of TACE. Furthermore, inhibitors of TACE are potential therapeutic agents for kidney injury.