# Impact of Serum Amyloid A Protein in the Human Breast: An In Vitro Study

**Authors:** Carolina Dumke de Siqueira, Fátima Regina Mena Barreto Silva, Leandro Borges, Ana Carolina Rabello de Moraes, Elaine Hatanaka, Fabíola Branco Filippin-Monteiro

PMC · DOI: 10.3390/nu16142283 · 2024-07-16

## TL;DR

This study explores the role of serum amyloid A protein in human breast cells and its potential impact on milk production and breastfeeding.

## Contribution

The study identifies new functions of serum amyloid A protein in mammary epithelial cells, linking it to inflammation and reduced glucose uptake.

## Key findings

- SAA expression was observed in mammary epithelial cells.
- SAA stimulates IL-6 expression and inhibits glucose uptake.
- SAA induces morphological changes indicative of cellular stress.

## Abstract

The mammary gland is an exocrine gland whose main function is to produce milk. Breast morphogenesis begins in the embryonic period; however, its greatest development takes place during the lactation period. Studies have found the expression of serum amyloid A protein (SAA) in both breast cells and breast milk, yet the function of this protein in these contexts remains unknown. Insufficient milk production is one of the most frequent reasons for early weaning, a problem that can be related to the mother, the newborn, or both. This study aims to investigate the relationship between lactogenesis II (the onset of milk secretion) and the role of SAA in the human breast. To this end, mammary epithelial cell cultures were evaluated for the expression of SAA and the influence of various cytokines. Additionally, we sought to assess the activation pathway through which SAA acts in the breast, its glucose uptake capacity, and the morphological changes induced by SAA treatment. SAA expression was observed in mammary epithelial cells; however, it was not possible to establish its activation pathway, as treatments with inhibitors of the ERK1/2, p38MAPK, and PI3K pathways did not alter its expression. This study demonstrated that SAA can stimulate IL-6 expression, inhibit glucose uptake, and cause morphological changes in the cells, indicative of cellular stress. These mechanisms could potentially contribute to early breastfeeding cessation due to reduced milk production and breast involution.

## Linked entities

- **Proteins:** SAA1 (serum amyloid A1), IL6 (interleukin 6), erk1/2 (mitogen-activated protein kinase), P38mapk (p38 map kinase)
- **Species:** Homo sapiens (taxon 9606)

## Full-text entities

- **Genes:** IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, SAA1 (serum amyloid A1) [NCBI Gene 6288] {aka PIG4, SAA, TP53I4}
- **Diseases:** Insufficient milk production (MESH:D000309)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

8 figures with captions in the complete paper: https://tomesphere.com/paper/PMC11280015/full.md

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Source: https://tomesphere.com/paper/PMC11280015