A Homozygous Dab1<sup>−/−</sup> Is a Potential Novel Cause of Autosomal Recessive Congenital Anomalies of the Mice Kidney and Urinary Tract

A Homozygous Dab1<sup>−/−</sup> Is a Potential Novel Cause of Autosomal Recessive Congenital Anomalies of the Mice Kidney and Urinary Tract

This study aimed to explore morphology changes in the kidneys of <i>Dab1<sup>−/−</sup></i> (<i>yotari)</i> mice, as well as expression patterns of reelin, NOTCH2, LC3B, and cleaved caspase3 (CASP3) proteins, as potential determinants of normal kidney formation and...

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Main Authors: Anita Racetin, Natalija Filipović, Mirela Lozić, Masaki Ogata, Larissa Gudelj Ensor, Nela Kelam, Petra Kovačević, Koichiro Watanabe, Yu Katsuyama, Mirna Saraga-Babić, Merica Glavina Durdov, Katarina Vukojević
Format: Article
Language:English
Published: MDPI AG 2021-04-01
Series:Biomolecules
Subjects:
<i>yotari</i>
kidney function
postnatal kidney development
immunofluorescence staining
transmission electron microscopy
Online Access:https://www.mdpi.com/2218-273X/11/4/609
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spelling doaj-0a6f44a85a4b4d6d9383692aa5d520b02021-04-20T23:02:29ZengMDPI AGBiomolecules2218-273X2021-04-011160960910.3390/biom11040609A Homozygous Dab1<sup>−/−</sup> Is a Potential Novel Cause of Autosomal Recessive Congenital Anomalies of the Mice Kidney and Urinary TractAnita Racetin0Natalija Filipović1Mirela Lozić2Masaki Ogata3Larissa Gudelj Ensor4Nela Kelam5Petra Kovačević6Koichiro Watanabe7Yu Katsuyama8Mirna Saraga-Babić9Merica Glavina Durdov10Katarina Vukojević11Department of Anatomy, Histology and Embryology, University of Split School of Medicine, 21000 Split, CroatiaDepartment of Anatomy, Histology and Embryology, University of Split School of Medicine, 21000 Split, CroatiaDepartment of Anatomy, Histology and Embryology, University of Split School of Medicine, 21000 Split, CroatiaDivision of Anatomy, Faculty of Medicine, Tohoku Medical and Pharmaceutical University, Sendai, Miyagi 981-8558, JapanDepartment of Anatomy, Histology and Embryology, University of Split School of Medicine, 21000 Split, CroatiaDepartment of Anatomy, Histology and Embryology, University of Split School of Medicine, 21000 Split, CroatiaDepartment of Medical Genetics, School of Medicine, University of Mostar, 88000 Mostar, Bosnia and HerzegovinaDepartment of Anatomy, Shiga University of Medical Science, Ötsu 520-2192, JapanDepartment of Anatomy, Shiga University of Medical Science, Ötsu 520-2192, JapanDepartment of Anatomy, Histology and Embryology, University of Split School of Medicine, 21000 Split, CroatiaDepartment of Pathology, University Hospital of Split, 21000 Split, CroatiaDepartment of Anatomy, Histology and Embryology, University of Split School of Medicine, 21000 Split, CroatiaThis study aimed to explore morphology changes in the kidneys of <i>Dab1<sup>−/−</sup></i> (<i>yotari)</i> mice, as well as expression patterns of reelin, NOTCH2, LC3B, and cleaved caspase3 (CASP3) proteins, as potential determinants of normal kidney formation and function. We assumed that <i>Dab1</i> functional inactivation may cause disorder in a wide spectrum of congenital anomalies of the kidney and urinary tract (CAKUT). Animals were sacrificed at postnatal days P4, P11, and P14. Paraffin-embedded kidney tissues were sectioned and analyzed by immunohistochemistry using specific antibodies. Kidney specimens were examined by bright-field, fluorescence, and electron microscopy. Data were analyzed by two-way ANOVA and t-tests. We noticed that <i>yotari</i> kidneys were smaller in size with a reduced diameter of nephron segments and thinner cortex. TEM microphotographs revealed foot process effacement in the glomeruli (G) of <i>yotari</i> mice, whereas aberrations in the structure of proximal convoluted tubules (PCT) and distal convoluted tubules (DCT) were not observed. A significant increase in reelin expression, NOTCH2, LC3B and cleaved CASP3 proteins was observed in the glomeruli of <i>yotari</i> mice. Renal hypoplasia in conjunction with foot process effacement and elevation in the expression of examined proteins in the glomeruli revealed CAKUT phenotype and loss of functional kidney tissue of <i>yotari.</i>https://www.mdpi.com/2218-273X/11/4/609<i>yotari</i>kidney functionpostnatal kidney developmentimmunofluorescence stainingtransmission electron microscopy
collection DOAJ
language English
format Article
sources DOAJ
author Anita Racetin
Natalija Filipović
Mirela Lozić
Masaki Ogata
Larissa Gudelj Ensor
Nela Kelam
Petra Kovačević
Koichiro Watanabe
Yu Katsuyama
Mirna Saraga-Babić
Merica Glavina Durdov
Katarina Vukojević
spellingShingle Anita Racetin
Natalija Filipović
Mirela Lozić
Masaki Ogata
Larissa Gudelj Ensor
Nela Kelam
Petra Kovačević
Koichiro Watanabe
Yu Katsuyama
Mirna Saraga-Babić
Merica Glavina Durdov
Katarina Vukojević
A Homozygous Dab1<sup>−/−</sup> Is a Potential Novel Cause of Autosomal Recessive Congenital Anomalies of the Mice Kidney and Urinary Tract
Biomolecules
<i>yotari</i>
kidney function
postnatal kidney development
immunofluorescence staining
transmission electron microscopy
author_facet Anita Racetin
Natalija Filipović
Mirela Lozić
Masaki Ogata
Larissa Gudelj Ensor
Nela Kelam
Petra Kovačević
Koichiro Watanabe
Yu Katsuyama
Mirna Saraga-Babić
Merica Glavina Durdov
Katarina Vukojević
author_sort Anita Racetin
title A Homozygous Dab1<sup>−/−</sup> Is a Potential Novel Cause of Autosomal Recessive Congenital Anomalies of the Mice Kidney and Urinary Tract
title_short A Homozygous Dab1<sup>−/−</sup> Is a Potential Novel Cause of Autosomal Recessive Congenital Anomalies of the Mice Kidney and Urinary Tract
title_full A Homozygous Dab1<sup>−/−</sup> Is a Potential Novel Cause of Autosomal Recessive Congenital Anomalies of the Mice Kidney and Urinary Tract
title_fullStr A Homozygous Dab1<sup>−/−</sup> Is a Potential Novel Cause of Autosomal Recessive Congenital Anomalies of the Mice Kidney and Urinary Tract
title_full_unstemmed A Homozygous Dab1<sup>−/−</sup> Is a Potential Novel Cause of Autosomal Recessive Congenital Anomalies of the Mice Kidney and Urinary Tract
title_sort homozygous dab1<sup>−/−</sup> is a potential novel cause of autosomal recessive congenital anomalies of the mice kidney and urinary tract
publisher MDPI AG
series Biomolecules
issn 2218-273X
publishDate 2021-04-01
description This study aimed to explore morphology changes in the kidneys of <i>Dab1<sup>−/−</sup></i> (<i>yotari)</i> mice, as well as expression patterns of reelin, NOTCH2, LC3B, and cleaved caspase3 (CASP3) proteins, as potential determinants of normal kidney formation and function. We assumed that <i>Dab1</i> functional inactivation may cause disorder in a wide spectrum of congenital anomalies of the kidney and urinary tract (CAKUT). Animals were sacrificed at postnatal days P4, P11, and P14. Paraffin-embedded kidney tissues were sectioned and analyzed by immunohistochemistry using specific antibodies. Kidney specimens were examined by bright-field, fluorescence, and electron microscopy. Data were analyzed by two-way ANOVA and t-tests. We noticed that <i>yotari</i> kidneys were smaller in size with a reduced diameter of nephron segments and thinner cortex. TEM microphotographs revealed foot process effacement in the glomeruli (G) of <i>yotari</i> mice, whereas aberrations in the structure of proximal convoluted tubules (PCT) and distal convoluted tubules (DCT) were not observed. A significant increase in reelin expression, NOTCH2, LC3B and cleaved CASP3 proteins was observed in the glomeruli of <i>yotari</i> mice. Renal hypoplasia in conjunction with foot process effacement and elevation in the expression of examined proteins in the glomeruli revealed CAKUT phenotype and loss of functional kidney tissue of <i>yotari.</i>
topic <i>yotari</i>
kidney function
postnatal kidney development
immunofluorescence staining
transmission electron microscopy
url https://www.mdpi.com/2218-273X/11/4/609
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