# TGF-βl Suppresses Inflammation in Cell Therapy for Intervertebral Disc Degeneration

**Authors:** Huilin Yang, Cheng Cao, Chunshen Wu, Chenxi Yuan, Qiaoli Gu, Qing Shi, Jun Zou

PMC · DOI: 10.1038/srep13254 · 2015-08-20

## TL;DR

This study shows that TGF-β1 in cell therapy reduces inflammation and improves disc repair in degenerative intervertebral discs.

## Contribution

The study reveals that TGF-β1 enhances cell therapy outcomes by suppressing inflammation and promoting disc tissue regeneration.

## Key findings

- Co-culturing cells increased TGF-β1 secretion, which inhibited NF-κB activation.
- Cell therapy with TGF-β1 improved disc recovery in rabbits compared to controls.
- TGF-β1 increased collagen II and aggrecan expression, reducing disc degradation.

## Abstract

Recent studies suggest that cell therapy may be an effective way to repair intervertebral disc degeneration. As a strong immune suppressor, TGF-β1 has been shown to inhibit inflammation respond effectively. The objective of this study was to explore the effects of TGF-β1 during bone marrow mesenchymal stem cells-based therapy for disc degeneration. In vitro assays demonstrated that co-culturing of nucleus pulposus cells with bone marrow mesenchymal stem cells resulted in significantly higher levels of TGF-βl secretion. This increase inhibited IκB phosphorylation and NF-κB activation, detected by western blot analysis. Meanwhile, in a rabbit model, MRI analysis revealed significant recovery of signal intensity in the degenerative discs of rabbits receiving cells transplantation, than receiving cells treated with a TGF-β1 inhibitor or saline. These findings indicated that enhanced TGF-β1 production recovered the degeneration of intervertebral disc. And also immunohistochemical staining detected enhanced collagen II expression in the rabbits treated with cell transplantation. However, the NF-κB positive cells were significantly less than other two control groups. Thus, cell therapy promoted TGF-β1 expression in nucleus pulposus, leading to anti-inflammatory effects via the inhibition of NF-κB, and the amelioration of disc degradation due to increased expression of collagen II and aggrecan in degenerative intervertebral disc.

## Linked entities

- **Proteins:** TGFB1 (transforming growth factor beta 1), Nfkbib (nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, beta), NFKB1 (nuclear factor kappa B subunit 1), acan.L (aggrecan L homeolog)
- **Diseases:** intervertebral disc degeneration (MONDO:0011385)

## Full-text entities

- **Genes:** TGF-beta1 [NCBI Gene 100008645], beta-actin [NCBI Gene 100350495], TGFB1 (transforming growth factor beta 1) [NCBI Gene 7040] {aka CAEND1, CED, DPD1, IBDIMDE, LAP, TGF-beta1}, GAPDH [NCBI Gene 100009074], transforming growth factor-beta1 [NCBI Gene 100353067], osteocalcin [NCBI Gene 100340503], Aggrecan [NCBI Gene 100009079], osteopontin [NCBI Gene 100008982], NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790] {aka CVID12, EBP-1, KBF1, NF-kB, NF-kB1, NF-kappa-B1}, NFKBIA (NFKB inhibitor alpha) [NCBI Gene 4792] {aka EDAID2, IKBA, MAD-3, NFKBI}
- **Diseases:** nucleus pulposus (MESH:C537927), Inflammation (MESH:D007249), low back pain (MESH:D017116), pain (MESH:D010146), Degeneration of intervertebral discs (MESH:D055959), pathologic disc (MESH:D005598), and degeneration (MESH:D009410), inflammatory cytokine (MESH:D000080424),  (MESH:D004195)
- **Species:** Homo sapiens (human, species) [taxon 9606], Canis lupus familiaris (dog, subspecies) [taxon 9615], Oryctolagus cuniculus (domestic rabbit, species) [taxon 9986]

## Figures

8 figures with captions in the complete paper: https://tomesphere.com/paper/PMC4542522/full.md

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Source: https://tomesphere.com/paper/PMC4542522