BICELLULAR LOCALIZATION OF THE TRICELLULAR JUNCTION PROTEIN ANGULIN-3 AS A MARKER OF PODOCYTE INJURY

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Abstract Title *

BICELLULAR LOCALIZATION OF THE TRICELLULAR JUNCTION PROTEIN ANGULIN-3 AS A MARKER OF PODOCYTE INJURY

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Co-author 1

Atsuko Higashi ahigashi@fmu.ac.jp Fukushima Medical University Department of Nephrology and Hypertension Fukushima Japan *

Co-author 2

Tomohito Higashi tohigash@fmu.ac.jp Fukushima Medical University Department of Basic Pathology Fukushima Japan -

Co-author 3

Junichiro Kazama jjkaz@fmu.ac.jp Fukushima Medical University Department of Nephrology and Hypertension Fukushima Japan -

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Introduction

Podocytes play a central role in maintaining the glomerular filtration barrier. Angulin-3(also known as ILDR2), a member of the tricellular junction protein angulin family, may serve as a novel marker of podocyte injury. In this study, we aimed to (1) delineate the spatiotemporal localization of angulin-3 in healthy, developing, and injured podocytes, and (2) evaluate its potential as an indicator of podocyte injury.

Methods

We generated a monoclonal antibody against angulin-3. Using rodent models of podocyte injury and human renal biopsy specimens from patients with nephrotic syndrome, we analyzed the localization of angulin-3 by immunostaining. In rodent glomeruli, localization was assessed during development and in response to podocyte injury. In human biopsy specimens, we quantified the linear accumulation of angulin-3 between foot processes and correlated the measured line length with subsequent relapse under glucocorticoid therapy.

Results

In developing rodent glomeruli, angulin-3 was initially confined to the tricellular junctions of primordial podocytes, then transiently redistributed to bicellular contacts as foot process interdigitation progressed, and finally appeared as a sparse punctate pattern in adult glomeruli. Upon induction of podocyte injury, angulin-3 immunostaining shifted from a punctate to a linear pattern at bicellular junctions between effaced foot processes. In human nephrotic syndrome biopsies, angulin-3 also exhibited linear accumulation between foot processes. Furthermore, the measured line length of angulin-3 staining significantly correlated with relapse risk in patients with minimal change nephrotic syndrome (MCNS) undergoing steroid therapy. These findings suggest that redistribution of angulin-3 to bicellular junctions is a marker of foot process derangement.

Conclusion

Our findings demonstrate that angulin-3 localizes to bicellular contacts in response to podocyte injury, and that the extent of its linear accumulation correlates with clinical relapse risk in MCNS. Thus, angulin-3 immunostaining may serve as a sensitive morphological biomarker for assessing podocyte injury severity and as a predictive tool to guide therapeutic decisions regarding relapse in MCNS.

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