# Glutamine Promotes Collagen Deposition via TGF-β/Smads Pathway in Swim Bladder of Chu’s Croaker (Nibea coibor)

## TL;DR

This study shows that glutamine increases collagen in fish swim bladders through the TGF-β/Smads pathway, offering new insights into amino acid nutrition in aquatic species.

## Contribution

The study identifies the TGF-β/Smads pathway as a novel mechanism by which glutamine promotes collagen deposition in fish.

## Key findings

- Transcriptomic analysis revealed upregulation of the TGF-β/Smads pathway with glutamine supplementation.
- Glutamine increased swim bladder cell proliferation and extracellular type I collagen content in vitro.
- Inhibition of the TGF-β/Smads pathway reduced glutamine-induced collagen deposition, confirming its role.

## Abstract

Our previous studies have confirmed that glutamine can promote collagen deposition in fish swim bladders of Chu’s croaker (Nibea coibor), and the purpose of this study is to further elucidate the potential mechanism of this effect. Transcriptomic results showed that the TGF-β/Smads pathway was significantly upregulated when glutamine was fed. In vitro experiments showed that glutamine promotes swim bladder cell proliferation and increases the extracellular type I collagen content, and this effect required the participation of the TGF-β/Smads pathway. Our research enriches the theory of amino acid nutrition and provides a theoretical basis for improving the quality of functional aquatic products.

Glutamine (Gln), one of the most abundant free conditionally essential amino acids in animals, plays a pivotal role in protein and energy metabolism. Beyond its nutritional importance, Gln also modulates key cellular processes through diverse signaling pathways. Our previous studies have shown that appropriate Gln (0.4%) can promote collagen deposition in the swim bladder of Nibea coibor; however, the mechanism has not been investigated. Therefore, this study used transcriptomic analysis on the control group (0.0% Gln) and the 0.4% Gln group to screen for possible pathways and validate the function of candidate pathways in vitro. The results showed that the TGF-β/Smads pathway was significantly upregulated in the 0.4% Gln group compared with 0.0% Gln. At the same time, Gln could also promote the swim bladder cells’ proliferation and increase the extracellular type I collagen content and gene expression (col1a1, col1a2) in vitro, accompanied by the activation of the TGF-β/Smads pathway (tgf-β, smad2, smad3, smad4 upregulated). Inhibition of the TGF-β/Smads pathway (tgf-β, smad2, smad3, smad4 downregulated) partially reversed the effect of Gln on collagen deposition (col1a1, col1a2 downregulated), thus proving that the TGF-β/Smads pathway is involved in the process of Gln on collagen deposition. In conclusion, the discovery not only expands our understanding of amino acid functions but establishes a foundational theory for further research on collagen regulation in fish.