# Aging increases UT‐B urea transporter protein abundance in brains of male mice

**Authors:** Farhana Pinki, Lauren McKeever, Derek A. Costello, Gavin Stewart

PMC · DOI: 10.14814/phy2.70175 · Physiological Reports · 2025-02-18

## TL;DR

Aging increases the amount of UT-B urea transporter protein in the brains of male mice, particularly in multiple brain regions.

## Contribution

This study shows that aging increases UT-B1 protein abundance in multiple brain regions of male mice.

## Key findings

- UT-B RNA expression increased in the aged cortex and hippocampus of male mice.
- UT-B1 protein abundance was significantly higher in aged brain tissues compared to young ones.
- Increased UT-B1 protein was observed in the hippocampus, cerebellum, and multiple cortical regions.

## Abstract

Facilitative UT‐B urea transporters in the brain play an important role in regulating levels of urea in various cell types, including astrocytes. Numerous studies have reported increased UT‐B RNA expression with aging and in neurological disorders, such as Alzheimer's Disease. However, much less is known about the effects of these conditions on UT‐B transporter protein abundance. This current study compared the levels of UT‐B RNA and protein in young and aged male C57BL/6 mice. Endpoint RT‐PCR experiments showed UT‐B RNA expression increased in both aged cortex and aged hippocampus. Importantly, these changes were coupled with an increase in protein abundance, as western blotting revealed that 30–35 kDa UT‐B1 protein was significantly increased in aged mouse brain tissues compared with tissue from young animals. An increased UT‐B1 protein abundance was observed in the hippocampus, cerebellum, frontal cortex, and occipital cortex. In contrast, no such changes were observed in the abundance of MCT1 short‐chain fatty acid transporters in these aged tissues. These data therefore confirmed that specific increases in UT‐B1 protein abundance occur in multiple regions of the aged male mouse brain. Further studies are now needed to determine cell‐specific changes and the functional consequence of increased UT‐B1 protein in aged brain tissues.

## Linked entities

- **Proteins:** Slc14a1 (solute carrier family 14 member 1 (Kidd blood group)), SLC14A1 (solute carrier family 14 member 1 (Kidd blood group)), CMA1 (chymase 1)
- **Diseases:** Alzheimer's Disease (MONDO:0004975)

## Full-text entities

- **Genes:** mct1 (modifier of curly tail 1) [NCBI Gene 17236], Slc14a1 (solute carrier family 14 (urea transporter), member 1) [NCBI Gene 108052] {aka 2610507K20Rik, 3021401A05Rik, UT-B, Utb1}
- **Diseases:** neurological disorders (MESH:D009461), Alzheimer's Disease (MESH:D000544)
- **Chemicals:** urea (MESH:D014508)
- **Species:** Mus musculus (house mouse, species) [taxon 10090]
- **Cell lines:** C57BL/6 — Mus musculus (Mouse), Transformed cell line (CVCL_C0MU)

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC11835958/full.md

## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC11835958/full.md

## References

30 references — full list in the complete paper: https://tomesphere.com/paper/PMC11835958/full.md

---
Source: https://tomesphere.com/paper/PMC11835958