• Title/Summary/Keyword: mouse kidney

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Differential Expression of $PKD2$-Associated Genes in Autosomal Dominant Polycystic Kidney Disease

  • Yook, Yeon-Joo;Woo, Yu-Mi;Yang, Moon-Hee;Ko, Je-Yeong;Kim, Bo-Hye;Lee, Eun-Ji;Chang, Eun-Sun;Lee, Min-Joo;Lee, Sun-Young;Park, Jong-Hoon
    • Genomics & Informatics
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    • v.10 no.1
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    • pp.16-22
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    • 2012
  • Autosomal dominant polycystic kidney disease (ADPKD) is characterized by formation of multiple fluid-filled cysts that expand over time and destroy renal architecture. The proteins encoded by the $PKD1$ and $PKD2$ genes, mutations in which account for nearly all cases of ADPKD, may help guard against cystogenesis. Previously developed mouse models of $PKD1$ and $PKD2$ demonstrated an embryonic lethal phenotype and massive cyst formation in the kidney, indicating that $PKD1$ and $PKD2$ probably play important roles during normal renal tubular development. However, their precise role in development and the cellular mechanisms of cyst formation induced by $PKD1$ and $PKD2$ mutations are not fully understood. To address this question, we presently created $Pkd2$ knockout and $PKD2$ transgenic mouse embryo fibroblasts. We used a mouse oligonucleotide microarray to identify messenger RNAs whose expression was altered by the overexpression of the $PKD2$ or knockout of the $Pkd2$. The majority of identified mutations was involved in critical biological processes, such as metabolism, transcription, cell adhesion, cell cycle, and signal transduction. Herein, we confirmed differential expressions of several genes including aquaporin-1, according to different $PKD2$ expression levels in ADPKD mouse models, through microarray analysis. These data may be helpful in $PKD2$-related mechanisms of ADPKD pathogenesis.

The Effect of Ginseng and Caffeine Products on the Antioxidative Activities of Mouse Kidney (인삼과 카페인 함유제품이 흰쥐 신장의 항산화활성에 미치는 영향)

  • Chang, Young-Sang;Chang, Yoon-Hyuk;Sung, Jong-Hwan
    • Journal of Ginseng Research
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    • v.30 no.1
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    • pp.15-21
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    • 2006
  • This study was carried out to determine the antioxidative activities of tissue cells of mouse kidney isolated from mice fed with different formulation of drinks. The swimming ability of experimental groups without caffeine showed the same pattern, but caffeine group decreased slightly. Superoxide dismutase(SOD) and catalase(CAT) activities of caffeine-containing groups were decreased significantly, but the control and ginseng-containing groups were increased. Hydroperoxide contents did not increase significantly all experimental groups. Hydroperoxlde contents of the control and ginseng-containing groups were similar, but caffeine-containing groups increased. Compared to the control and ginseng-containing groups, lipid peroxidation level and protein contents in caffeine-containing groups were decreased significantly. In conclusion, the antioxidative activities of mouse kidney isolated from mice fed with ginseng-containing products was increased slightly.

Mouse models of polycystic kidney disease induced by defects of ciliary proteins

  • Ko, Je Yeong;Park, Jong Hoon
    • BMB Reports
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    • v.46 no.2
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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.

Enhancing Venous Anastomosis Visualization in Murine Kidney Transplants: The Two Stay Suture Technique

  • Jong-Min Kim
    • Journal of Veterinary Clinics
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    • v.40 no.6
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    • pp.423-428
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    • 2023
  • The mouse kidney transplantation model serves as an invaluable tool for exploring various aspects of the transplant process, including acute rejection, cellular and humoral rejection, ischemia-reperfusion injury, and the evaluation of novel therapeutic strategies. However, conducting venous anastomosis in this model poses a significant challenge due to the thin and pliable characteristics of the renal vein, which often obstruct clear visualization of the resected vein's edge. This study proposes the adoption of a two stay suture technique to enhance the visualization of the renal vein's edge, thereby facilitating efficient and successful venous anastomosis. A total of 22 mice served as kidney donors in this study. The conventional anchoring suture technique was employed for venous anastomosis in 11 of these mice, while the remaining 11 underwent the two stay suture technique. The anastomosis duration and completion rates were then compared between these two groups. The conventional anchoring suture technique yielded an average anastomosis time of 29 minutes and a completion rate of 64%. In contrast, the two stay suture technique demonstrated a substantial improvement, with an average anastomosis time of 14 minutes and a completion rate of 100%. The two stay suture technique offers a promising solution to enhance visualization during venous anastomosis in murine kidney transplantation. This technique may particularly benefit novices by enabling them to perform venous anastomosis more easily, swiftly, and successfully.

Expression of Taurine Transporter in Cell Lines and Murine Organs (세포주와 마우스 조직에서 타우린수송체의 발현분석)

  • 김하원;안희창;안혜숙;현진원;이은방
    • Biomolecules & Therapeutics
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    • v.10 no.2
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    • pp.78-84
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    • 2002
  • Taurine (2-ethaneaminosulfonic acid, $^+{NH}_3{CH_2}{CH_2}{SO_3^{-}}$) is endogenous amino acid with functions as modulator of osmoregulation, antioxidation, detoxification, transmembrane calcium transport, and a free radical scavenger in mammalian tissues. Taurine transporter(TAUT) contains 12 transmembrane helices, which are typical of the $Na^+$- and $Cl^-$-dependent transporter gene family, and has been cloned recently from several species and tissues. To analyze the expression of TAUT mRNA, one step RT-PCR was performed from human and mouse cultured cell lines and from various mouse tissues. The primers were designed to encode highly conserved amino acid sequences at the second transmembrane domain and at the fourth and fifth intracellular domains. RT-PCR analysis showed both of the human intestine HT-29 and mouse macrophage RAW264.7 cell lines expressed mRNA of TAUT. To define the expression patterns of the TAUT mRNA in the murine organs, RT-PCR was performed to detect cDNA representing TAUT mRNA from seven different mouse tissues. The TAUT was detected in all of the mouse tissues analyzed such as heart, lung, thymus, kidney, liver, spleen and brain. A large amount of transcript was fecund from heart, liver, spleen, kidney, and brain, while lung contained a very small amount of transcript.

Effect of Xanthine Derivatives on the Carbonic Anhydrase Activity in the Mouse (마우스 Carbonic anhydrase 활성에 미치는 Xanthine 유도체의 영향)

  • Yu, Myung-Yul;Park, Hyung-Kyung;Lee, Chung-Ik
    • The Korean Journal of Pharmacology
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    • v.8 no.1
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    • pp.59-62
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    • 1972
  • This study was undertaken to observe the effect of xanthine such as caffeine and aminophylline on the activity of carbonic anhydrase in the kidney and stomach of the mouse. Carbonic anhydrase activities were measured by Philpot & Philpot method (1936). The results of this experiment were as follows: 1. The activity of carbonic anhydrase in the kidney of the mouse was silightly inhibited by the administration of caffeine (0.1 mg/gm, B.W.) or aminophylline (0.08 mg/gm, B.W.). The inhibition was more pronounced by the administration of aminophylline than that of caffeine. 2. In the stomach, there was no significant change in the activity of the carbonic anhydrase after the administration of either caffeine or aminophylline.

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Tissue-Specific Localization NUCB2/nesfatin-1 in the Liver and Heart of Mouse Fetus

  • Sun, Sojung;Yang, Hyunwon
    • Development and Reproduction
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    • v.22 no.4
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    • pp.331-339
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    • 2018
  • NUCB2/nesfatin-1 is first known to be expressed in the hypothalamus while controlling appetite and energy metabolism. However, recent studies have shown that NUCB2/nesfatin-1 was expressed in the various organs as well as the hypothalamus. Our previous reports also demonstrated that NUCB2/nesfatin-1 was expressed in the ovary, testis, pituitary gland, lung, kidney, and stomach of fetal and adult mice. However, the role of NUCB2/nesfatin-1 in mouse fetus remains unknown. Thus, the aim of this study was to investigate whether NUCB2/nestatin-1 is expressed in mouse fetus at the developmental stage in which organogenesis begins. To do this, we performed in situ hybridization (ISH) and immunohistochemistry (IHC) staining to examine the distribution of NUCB2 mRNA and nesfatin-1 protein in the mouse fetal organs during early developmental stages, especially at embryonic day (E) 10.5. As a result of ISH, NUCB2 mRNA positive signals were more frequent in the liver, but there were relatively few positive signals in heart. On the other hand, no positive signals were detected in other organs. These ISH results were validated by IHC staining and qRT-PCR analysis. Expression of nesfatin-1 protein detected by IHC staining was similar to that of NUCB2 mRNA detected by ISH in the liver and heart. In addition, the levels of NUCB2 mRNA expression analyzed by qRT-PCR were significantly increased in the liver and heart compared to other organs of the mouse fetus at E13.5, whereas its level was extensively decreased in the liver, but increased in the lung, stomach, and kidney of the mouse fetus at E17.5. These results suggest that NUCB2/nesfatin-1 may play an important role in liver and heart development and physiological functions in the developmental process of mouse fetus. Further studies are needed on the function of NUCB2/nesfatin-1, which is highly expressed in the various organs, including liver and heart during mouse development.

PKHD1 Gene Silencing May Cause Cell Abnormal Proliferation through Modulation of Intracellular Calcium in Autosomal Recessive Polycystic Kidney Disease

  • Yang, Ji-Yun;Zhang, Sizhong;Zhou, Qin;Guo, Hong;Zhang, Ke;Zheng, Rong;Xiao, Cuiying
    • BMB Reports
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    • v.40 no.4
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    • pp.467-474
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    • 2007
  • Autosomal recessive polycystic kidney disease (ARPKD) is one of the important genetic disorders in pediatric practice. Mutation of the polycystic kidney and hepatic disease gene 1 (PKHD1) was identified as the cause of ARPKD. The gene encodes a 67-exon transcript for a large protein of 4074 amino acids termed fibrocystin, but its function remains unknown. The neoplastic-like in cystic epithelial proliferation and the epidermal growth factor/epidermal growth factor receptor (EGF/EGFR) axis overactivity are known as the most important characteristics of ARPKD. Since the misregulation of $Ca^{2+}$ signaling may lead to aberrant structure and function of the collecting ducts in kidney of rat with ARPKD, present study aimed to investigate the further mechanisms of abnormal proliferation of cystic cells by inhibition of PKHD1 expression. For this, a stable PKHD1-silenced HEK-293T cell line was established. Then cell proliferation rates, intracellular $Ca^{2+}$ concentration and extracellular signal-regulated kinase 1/2 (ERK1/2) activity were assessed after treatment with EGF, a calcium channel blocker and agonist, verapamil and Bay K8644. It was found that PKHD1-silenced HEK-293T cell lines were hyperproliferative to EGF stimulation. Also PKHD1-silencing lowered the intracellular $Ca^{2+}$ and caused EGF-induced ERK1/2 overactivation in the cells. An increase of intracellular $Ca^{2+}$ in PKHD1-silenced cells repressed the EGF-dependent ERK1/2 activation and the hyperproliferative response to EGF stimulation. Thus, inhibition of PKHD1 can cause EGF-induced excessive proliferation through decreasing intracellular $Ca^{2+}$ resulting in EGF-induced ERK1/2 activation. Our results suggest that the loss of fibrocystin may lead to abnormal proliferation in kidney epithelial cells and cyst formation in ARPKD by modulation of intracellular $Ca^{2+}$.

Effects of Oenanthe javanica Extracts on Mercury Accumulation in Organs of the Mouse (미나리 추출물이 마우스의 장기내 수은 축적에 미치는 영향)

  • 조현욱;김명훈;황규영;민병운;박종철;김종홍
    • Toxicological Research
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    • v.15 no.1
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    • pp.1-8
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    • 1999
  • This study was performed to investigate the antitoxic effect of Oenanthe javanica extracts on orally administered mercury compound. Adult male ICR mice were exposed to methylmercuric chloride (CH3HgCl)through drinking water. The control, mercury treated and Oenanthe javanica treated groups not showed significant differences in mean body and organ weights of mice. The distribution of mercury in the cerebellum, kidney, liver and spleen of the mouse were examined according to a histochemical mathod. Grains of mercury traces were located in the purkinje cell and granular layers of the cerebellum and cortex of kidney respectively. Lesser staining of the grains was seen in the collecting tubules of medulla. in the liver, mercury accumulations were present primarily in the hepatocytes around portal area containing interlobular bile duct, artery and portal vein. Also grains of mercury traces were accumulated in the white pulp of the spleen. In the group of Oenanthe javanica extracts, staining intensity of mercury was decreased in the Purkinje cell layer of cerebellum and in the portal area of liver respectively. Staining patterns in kidney and spleen of extracts group were similar to that of only mercury treated group.

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Standard Index Development for Comparing the Glomerular Number (사구체 수의 증감을 비교할 수 잇는 기준 개발)

  • Kim, Yong-Jin;Lee, Chi-Eun;Lee, Kook-Joo;Choi, Young-Ho;Hong, Jung-Suk
    • Journal of Yeungnam Medical Science
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    • v.18 no.1
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    • pp.85-93
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    • 2001
  • Background: The number of glomerulus has been considered one of the etiologic factors especially for focal segmental glomerulosclerosis. However, glomeruli are too many to calculate them correctly. Although the fractionator method has became convinced, in which they used selected sections, not whole kidney sections, with same intervals, it is also very hard to get good results. Because it is still very time-consuming and laborous work which leads to make big observers' biases. Methods and Materials: We designed the index for glomerular number to estimate the tendency of increase or decrease of the number of it in different kidneys and which was evaluated by other conventional methods including fractionator method. Index was based upon the theory by Nyengaard; "the number of glomerulus correlates with the weight of kidney, which is positively correlated with body weight". Calculating formula is the number of glomeruli/surface areas of cortices, which contain calculated glomeruli multiplies by kidney weight/body weight. Results: We applied this index to kidneys of FGS/Kist mouse and those of RFM/Nga mouse. The former is spontaneous glomerulosclerosis model with heavy protein uria and renal failure and the latter is the mother side of FGS/Kist mouse but has no glomerular disease or protein uria. The number of glomerulus of FGS/Kist mouse was decreased by 30% to those of RFM/Nga mouse. Conclusion: This index was useful and reliable for estimating the relative glomerular number between two groups.

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