# ARID3a, a repressor in aged kidney progenitors?

> **NIH NIH R21** · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · 2022 · $217,500

## Abstract

Abstract
 ARID3a, a DNA-binding protein, is a member of a large family of proteins associated with epigenetic
functions. ARID3a is expressed in hematopoietic progenitors where its expression and functions are altered
with age. Our recent studies indicate that ARID3a expression can be induced in multiple cell types from
healthy adults in association with inflammatory processes, and particularly with expression of Type I
interferons. Induction of ARID3a in adult cell types leads to differential gene expression patterns that are
cell type-specific. We linked ARID3a expression to kidney development in the mouse, where absence of
ARID3a in bulk-cultured mouse kidneys resulted in generation of developmentally plastic cells. Surprisingly,
these cells spontaneously developed into complex structures that express mature kidney markers when
plated in semi-solid cultures. This finding led us to determine if ARID3a is expressed in human adult
kidneys. Our preliminary data indicate that ARID3a expression in the human kidney appears to increase
with age and that it is co-expressed in three subsets of cells with progenitor surface markers. The same
subsets from younger individuals express little ARID3a. We hypothesize that increased ARID3a expression
in aged individuals impairs the functions of those ARID3a-expressing kidney progenitors compared to cells
from younger individuals that express lower levels of ARID3a. In Aim 1, we will test this hypothesis by
inhibiting ARID3a expression in these three cell subsets from aged individuals and comparing the ability of
those cells to proliferate and differentiate in vitro to cells from the same individuals with ARID3a. We will
also compare these cells to progenitors from younger adults. Further, we hypothesize that ARID3a alters
gene expression patterns in aged individuals resulting in changes in function. In Aim 2, we will identify
genes and pathways affected by ARID3a expression in older adult progenitor cells to determine the
pathway(s) associated with decreased responses in aged kidneys. Together, these experiments will provide
new information about the potential effects of ARID3a in aged kidneys and could ultimately result in new
therapeutics for kidney repair. In addition, results from these studies may identify markers relevant for aging
and inflammatory responses in other tissues.

## Key facts

- **NIH application ID:** 10390496
- **Project number:** 1R21AG076164-01
- **Recipient organization:** UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR
- **Principal Investigator:** Carol F Webb
- **Activity code:** R21 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $217,500
- **Award type:** 1
- **Project period:** 2022-09-01 → 2024-05-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10390496

## Citation

> US National Institutes of Health, RePORTER application 10390496, ARID3a, a repressor in aged kidney progenitors? (1R21AG076164-01). Retrieved via AI Analytics 2026-05-26 from https://api.ai-analytics.org/grant/nih/10390496. Licensed CC0.

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