Expression Profiles of ITGA8 and VANGL2 Are Altered in Congenital Anomalies of the Kidney and Urinary Tract (CAKUT)

Author:

Pavlović Nikola1,Kelam Nela1ORCID,Racetin Anita1,Filipović Natalija1ORCID,Pogorelić Zenon23ORCID,Prusac Ivana Kuzmić4,Vukojević Katarina156ORCID

Affiliation:

1. Department of Anatomy, Histology and Embryology, School of Medicine, University of Split, 21000 Split, Croatia

2. Department of Pediatric Surgery, University Hospital of Split, 21000 Split, Croatia

3. Department of Surgery, School of Medicine, University of Split, 21000 Split, Croatia

4. Department of Pathology, University Hospital Centre Split, Spinciceva 1, 21000 Split, Croatia

5. Department of Anatomy, School of Medicine, University of Mostar, 88000 Mostar, Bosnia and Herzegovina

6. Center for Translational Research in Biomedicine, School of Medicine, University of Split, 21000 Split, Croatia

Abstract

Kidney failures in infants are mostly caused by congenital anomalies of the kidney and urinary tract (CAKUT), which are among the most common congenital birth disorders worldwide when paired with cardiac abnormalities. People with CAKUT often have severe kidney failure as a result of a wide range of abnormalities that can occur alone or in conjunction with other syndromic disorders. In this study, we aimed to investigate the expression pattern of CAKUT candidate genes alpha-8 integrin (ITGA8) and Van Gogh-like 2 (VANGL2) in fetal tissues of healthy and CAKUT-affected kidneys using immunohistochemistry and immunofluorescence. We found that under CAKUT circumstances, the expressions of ITGA8 and VANGL2 are changed. Additionally, we showed that VANGL2 expression is constant during fetal aging, but ITGA8 expression varies. Moreover, compared to normal healthy kidneys (CTRL), ITGA8 is poorly expressed in duplex kidneys (DKs) and dysplastic kidneys (DYS), whereas VANGL2 is substantially expressed in dysplastic kidneys (DYS) and poorly expressed in hypoplastic kidneys (HYP). These results point to VANGL2 and ITGA8 as potential prognostic indicators for CAKUT malformations. Further research is necessary to explore the molecular mechanisms underlying this differential expression of ITGA8 and VANGL2.

Funder

Croatian Science Foundation

Publisher

MDPI AG

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