• Genomics & Informatics
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• 제10권1호
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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.

• Journal of Ginseng Research
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• 제30권1호
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• pp.15-21
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• 2006

인삼성분과 카페인 함유제품을 마우스에 섭취시켜 4주간사육한 후, 마우스 신장 조직에서 Superoxide dismutase, Catalase, Hydroperoxide 등의 항산화 활성 및 조직학적 변화를 비교 검토하였다. 유영능력은 모든 실험군에서 유의적인 차이를 보이지 않았으나 무수카페인 실험군만은 다소 감소하는 경향을 보였다. Superoxide dismutase 및 Catalase 활성은 카페인함유 실험군에서 유의적으로 감소하였으나, 인삼성분함유 실험군에서는 활성도가 높게 나타났다. Hydroperoxide 함량은 모든 실험군에서 유의적인 증가를 보이지 않았으나 인삼성분함유 실험군은 대조군과 비슷한 함량을, 카페인함유 실험군은 대체로 증가하는 경향이었다. 과산화 지질 수준 및 단백질 함량 변화는 인삼성분 실험군은 대조군에 비하여 유의성 있게 증가하지 않았으나 카페인 함유제품 실험군은 유의성 있는 증가를 보였다. 신장 조직학적 변화는 인삼성분 및 카페인 함유 실험군에서 크나큰 조직적 차이를 보이지 않았다. 따라서 각 실험군과 실험방법에 따라 차이는 있겠으나 본 실험에 있어서는 인삼성분 함유제품이 카페인 함유제품보다 신장 조직의 항산화활성능력이 다소 증가하는 것으로 생각된다.

• 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.

• 한국임상수의학회지
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• 제40권6호
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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.

• Biomolecules & Therapeutics
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• 제10권2호
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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.

• 대한약리학회지
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• 제8권1호
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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.

• 한국발생생물학회지:발생과생식
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• 제22권4호
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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.

• BMB Reports
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• 제40권4호
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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 $Ca^{2+}$.

• Toxicological Research
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• 제15권1호
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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.

• Journal of Yeungnam Medical Science
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• 제18권1호
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• pp.85-93
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• 2001

신장 질환의 일부는 특히 초점성 분절 사구체 경화증, 사구체 수의 감소를 원인의 중요 요소로 생각하고 있지만 사구체수의 증감을 알 수 있는 신빙성 있는 계산법은 없다. 최근 신장을 일정 간격으로 절편을 만들어서 사구체 수를 헤아린 다음 전체 절편수를 곱하여 절대치를 구하는 방법이 인정을 받고 있지만 시간적으로 인력적으로 많은 노력이 필요하여 현실적 적용은 어렵다. 연구자들은 선천성으로 사구체 경화증이 생기면서 신기능 부전에 빠지는 FGS/Kist mouse와 모계나 병이 없는 RFM/Nga mouse의 신장을 이용하여 편리한 방법의 사구체 계산법을 개발하였다. 과거에 개발된 방법으로 사구체 수를 헤아려본 결과 절편을 이용한 계산법은 시간과 노력이 너무 많이 걸릴 뿐 아니라 개인차가 심하여 부정확하였다. 따라서 사구체의 수는 신장의 무게와 비례하고 이는 체중과 정비례한다는 이론을 적용하여 임의로 선택한 신장 절편 20개를 이용하여 사구체 수를 헤아린 다음 피질의 면적으로 나누고 이를 체중으로 나눈 신장무게로 곱해주는 비교치 계산 방법을 고안하였다(사구체 수/피질면적${\times}$신장무게/체중). 이 방법으로 FGS/Kist mouse의 사구체 수는 질환이 없는 mouse에 비하여 30%정도 감소되어 있음을 알 수 있었다.