Journal of Pathology and Translational Medicine

Original Articles

Expression of Transforming Growth Factor-beta and Morphologic Changes of Glomerulosclerosis in FGS/NgaKist Mouse.: Hoon Kyu Oh, Yong Jin Kim, Mi Ok Park, Chul Ho Lee, Byung Hwa Hyun, In Soo Shu; Korean J Pathol. 1998;32(1):35-42.

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Abstract PDF: Focal segmental glomerulosclerosis (FSGS) is presented as not only one of the primary glomerular diseases but also as a secondary phenomenon for chronic irreversible renal diseases. The main pathological feature of FSGS is the accumulation of extracellular matrix in the glomeruli, for which overexpression of transforming growth factor-beta (TGF-beta) may be responsible for the accumulation of pathological matrix. A new animal model (FGS/NgaKist mouse) of renal failure by spontaneously generating glomerulosclerosis was developed. To elucidate the role of TGF-beta for FSGS, authors observed glomeruli of FGS/NgaKist mouse periodically. FGS/NgaKist mouse strain showed progression of proteinuria and focal glomerular sclerosis with the aging. The glomeruli showed anti IgG, IgA, IgM and complement complex deposits and extracellular matrix accumulation in the mesangium. TGF-beta mRNA and beta2antibody expressions were increased with the advance of glomerular sclerosis. The results suggest the following; FSGS of FGS/NgaKist strain is immune mediated disease and this stimuli on mesangial or endothelial cells may activate TGF-beta gene in their nuclei. This activation, in turn, can cause sclerosis by increasing TGF-beta mRNA transcription followed by secretion of TGF-beta and its action as cytokine for making collagen fibrils.

A Study for IL-6, IL-13 and TIMP-3 Expressions of Placenta, Fetus and Endometrium in Pregnant Mice after Treatment with Lipopolysaccharide.: Sung Ran Hong, In Gul Moon, Ju Young Seoh, Yee Jeong Kim, Sung Sook Kim, Woon Sup Han; Korean J Pathol. 1998;32(5):352-361.

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Abstract: We examined C3H pregnant mice at 15 days (70% gestation) after treatment of lipopolysaccaride (LPS) to observe the changes of IL-6 concentration in maternal serum and amniotic fluid and expression of IL-6, IL-13 & TIMP-3 in placenta, fetus and endometrium, and to investigate the correlation among IL-6, IL-13 and TIMP-3. The results were as follows: 1) IL-6 in serum and amniotic fluid after treatment of LPS was significantly elevated; peaked at 1, 2, 4, 5 hours and decreased to control level at 8 hours (P<0.05). IL-6 in placental disc, chorioamnionic membrane, fetus, decidua and endometrial epithelium was overexpressed significantly at 1, 2, 4 hours after treatment of LPS (P<0.05). IL-6 overexpression was more significantly increased in maternal tissue than fetal tissue (P<0.05). 2) Increased concentration of amniotic fluid IL-6 was equally originated from transplacental crossage of maternal serum IL-6, and direct local production of IL-6 from placenta, fetus and endometrium (P<0.05). 3) IL-13 in placental disc, chorioamnionic membrane, fetus, decidua and endometrial epithelium was overexpressed after treatment of LPS, but not significant statistically. 4) TIMP-3 was overexpressed in placental disc, chorioamnionic membrane, fetus and decidua. TIMP-3 overexpression was more significant in placental disc than other tissues (P<0.05). 5) Overexpressions in IL-13 and IL-6 revealed direct proportional correlation coefficient (Spearman correlation coefficient, 0.5212 ; P<0.05). IL-6 expression was a head of overexpression of TIMP-3, but not significant. In conclusion, all of IL-6, IL-13 and TIMP-3 relate with inflammatory response, especially IL-6 in maternal serum, amniotic fluid and tissue of placenta, fetus and endometrium was so sensitive that it can be an indicator for antenatal diagnosis of chorioamnonitis, and amniotic fluid IL-6 is equally originated from maternal serum and from tissue of placenta, fetus and endometrium. IL-13 and TIMP-3 may have parallel correlation to the IL-6 in fetal and maternal tissue after treatment of LPS.

Morphologic Characterization of Polycystic Kidney in inv Transgenic Mouse.: Yeon Lim Suh, Mi Kyung Kim, Joungho Han; Korean J Pathol. 1998;32(7):479-487.

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Abstract: The aim of this study was to characterize the morphology of a polycystic kidney which was found in 100% of the transgenic mice homozygous for inv mutation and to gain insight into the pathogenesis of inherited polycystic kidney disease during the pre- and postnatal periods. The fetal and postnatal kidneys from the homozygous and heterozygous transgenic mice were examined by the light, transmission and scanning electron microscopes, image analyzer, and an immunohistochemistry utilizing the antibodies specific for each segment of the renal tubules (Tetragonolobus purpureas, Arachis hypogaea, Tamm-Horsfall protein, AE1/AE3, EMA, vimentin, Phaseolus vulgaris) was performed to determine the site of origin of renal cysts. Two developmental phases of a cystic disease were identified. The first phase, seen in fetal kidneys, was characterized by dilatation mainly of the proximal tubules and a few distal tubules. The later phase, in postnatal period, was characterized by progressive enlargement of the kidneys due to mainly cystic change of the collecting ducts, which distorted the normal architecture of both cortex and medulla and almost completely replaced the renal parenchyma. The cystic dilatation involved all segments of the nephron and the collecting duct as well as the Bowman's spaces of glomeruli. The epithelial cell hyperplasia was found as a micropolyp formation within the renal cysts and an increase in PCNA positive cells. These findings suggest that a cyst is not simply a ballooning of a renal tubule and the stretching of cells, formerly thought to be due to an altered compliance of an abnormal basement membrane, but indeed the result of increased numbers of tubular epithelial cells.

Abnormal Development and Apoptosis Observed in Brains of the Trisomy 16 Mouse.: Eun youn Cho, Yeon Lim Suh, Je Geun Chi; Korean J Pathol. 1999;33(8):570-580.

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Abstract PDF: We have studied morphologic characteristics and apoptosis on the fetal brain of the trisomy 16 mouse, a model for human trisomy 21 syndrome. This study was based on serial sections of the whole brain from a sample of sixteen trisomy 16 mice and forty-six age-matched control littermates from embryonic day (ED) 12 to ED 18. Trisomy 16 brains showed a reduction of telencephalic size and abnormal cortical development. At ED 13 trisomy 16 and control brains appeared similar. By ED 14 difference in the cortical thickness and telencephalic growth became evident, and by ED 16 a marked size difference had developed between the trisomy 16 and control brains. By ED 18, however, the thickness of the trisomy 16 cortex had increased considerably and was not significantly different with respect to the thickness and cross-sectional areas of the pallium and its constituent cortical layers. The cell density of the trisomy 16 cortex had persistently decreased before ED 17, when the cell density of control and trisomy 16 corteces was similar within each layer. At ED 18 cell density of trisomy 16 cortex in each layer increased. There was inverse relationship between a number of TUNEL positive apoptotic cells and cell density in the trisomy 16 brains. Our results suggest that developmental abnormalities of the trisomy 16 brain indicated developmental delay of the telencephalon growth, which may be caused by apoptosis rather than by a proliferation defect.

Expression of Laminin Chains in the Neuronal Cells of Mouse Brain.: Gi Jin Kim, Yong Jin Choi, Suk Keun Lee, Je Geun Chi; Korean J Pathol. 1999;33(12):1163-1174.

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Abstract PDF: Laminin-1 is biologically active and can effect cellular proliferation, differentiation, migration, and apoptosis. In the central nervous system, neuronal cells are rarely reported to give positive reaction by laminin antibody staining. However, the original cell type which can produce the laminin molecule has not been well established. Since the neuronal cells of brain are derived from neuroectoderm, we thought that the neuronal cells should be able to produce the laminin molecules as other epithelial cells. In this study we aimed to explore whether the neuronal cells express the laminin chain mRNAs, and further to identify which types of laminin isoform are expressed at the specific sites of the brain structure. We found that neuronal cell was the important cell type in mouse brain, which could produce laminin isoforms. Although immunostainings disclosed reactivity of laminins in the basement membrane of capillaries as well as neuronal cells, mRNA expressions of laminins were intense only in the neuronal cells. It was relatively weak in the endothelial cells. Among neuronal cells the cortical cells of cerebrum, pyramidal cells of hippocampus, and Purkinje cells of cerebellum showed pronounced expression of laminin chain mRNA. Glial cells, especially astrocytes, were negative for laminin subtypes both in immunohistochemistry and in situ hybridization. Taken together, our data indicate that the neuronal cells of mouse brain actively produce laminin isoforms, and the resultant polymerized laminins are accumulated mainly in the basement membrane of capillaries. In conclusion, the results indicate that neuronal cells produce and utilize the different laminin chains to maintain the neurovascular environment of brain.

Gene Expressions of Mouse Submandibular Gland during the Developmental Stage and Their Antisense Inhibition in Organ Culture.: Yeon Sook Kim, Suk Keun Lee, Je G Chi; Korean J Pathol. 2000;34(6):395-412.

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Abstract PDF: This study is aimed to observe the expressions of different genes, including the extracellular matrix proteins, growth factors, and transcription factors during different developmental stages of mouse submandibular gland. Reverse transcription-polymerase chain reaction (RT-PCR) and the antisense inhibition in organ culture system were performed using mouse embryos and newborns. Total 140 mouse embryos (E14(80), E15(20), E16(20), E18(20)) and 30 newborn mice (D2(10), D3(10), D6(10)) obtained from 60 pregnant mice and 3 adult mice (3 weeks old) were used for the cDNA production and the salivary gland organ culture. Syndecan, perlecan, laminin alpha1 chain, TGF beta1, beta 3, and sonic hedgehog mRNAs were expressed in the early stage (E14~E16) of the submandibular gland development, whereas transglutaminase C (TGase C), E-cadherin, epimorphin, laminin beta2 and gamma1 chains, and HGF mRNAs were expressed in the middle and late stages (E16~E18, D2~D6). Antisense inhibition of different genes in the organ culture of E14 mouse embryos of submandibular gland showed specific growth retardation in the development of ductal and acinar cells. Especially, the antisense inhibition of perlecan, E-cadherin, laminin alpha1 chain, laminin beta2 chain, and syndecan mRNA arrested the growth of ductal and acinar cells. While the antisense inhibition of integrin beta5 greatly affected the acinar cell differentiation and also produced cystic dilatation of salivary ducts, the antisense inhibition of fibronectin showed aberrant growth of ectomesenchymal tissues of the mouse submandibular gland.

Craniofacial Morphogenesis of Mouse with Trisomy 16.: Jung Sun Kim, Jeong Wook Seo, Suk Wha Kim, Je G Chi; Korean J Pathol. 1994;28(6):596-604.

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Abstract PDF: Based on the genetic homology between mouse chromosome 16 and human chromosome 21, experimentally induced trisomy 16 mouse has been considered to serve as a suitable model for human Down syndrome. Mice with trisomy 16 express several phenotypic characteristics of human trisomy 21 syndrome; i.e., intrauterine growth retardation, anarsarca, congenital heart disease, brain abnormality, etc. To elucidate morphogenesis of characteristic craniofacial malformation in human Down syndrome, we studied trisomy 16 mouse fetuses that were produced by crossing karyotypically normal C57BL/6 female ice with males carrying the two Robertsonian translocation chromosome Rb(16.17)/Rb(11.16). We examined a series of trisomy 16 conecptuses and their normal littermate controls from day 14 to day 18 of gestation by gross observation and serial microscopic sections. In addition to smaller size and generalized edema, we observed variable, but definite delay in brain and craniofacial development in trisomy 16 mice. The brain revealed less stratified telencephalon, underdeveloped thalamus and hypothalmus with relatively wide third ventricle, and small rhombencephalon. Craniofacial underdevelopment was characterized by persistent open eye, cochlea with fewer turns, delayed closure of the palate, more simple nasal cavity, etc. The tongue was shorter and convex upward, that were especially prominent at 14 days of gestation. The convex tongue and underdeveloped brain made the cranial base convex upward, and the angle between the cranial base an vertebral axis more obtuse. Small head with increase cephalic index and midfacial hypoplasia appeared to account for brain underdevelopment.

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