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Home / Equine Research Bank / Stem Cell Res Ther / TGF-β2 enhances expression of equine bone marrow-deriv...
Stem cell research & therapy2022; 13(1); 477; doi: 10.1186/s13287-022-03172-9

TGF-β2 enhances expression of equine bone marrow-derived mesenchymal stem cell paracrine factors with known associations to tendon healing.

Abstract: Mesenchymal stem cells (MSCs) secrete paracrine factors and extracellular matrix proteins that contribute to their ability to support tissue healing and regeneration. Both the transcriptome and the secretome of MSCs can be altered by treating the cells with cytokines, but neither have been thoroughly investigated following treatment with the specific cytokine transforming growth factor (TGF)-β2. RNA-sequencing and western blotting were used to compare gene and protein expression between untreated and TGF-β2-treated equine bone marrow-derived MSCs (BM-MSCs). A co-culture system was utilized to compare equine tenocyte migration during co-culture with untreated and TGF-β2-treated BM-MSCs. TGF-β2 treatment significantly upregulated gene expression of collagens, extracellular matrix molecules, and growth factors. Protein expression of collagen type I and tenascin-C was also confirmed to be upregulated in TGF-β2-treated BM-MSCs compared to untreated BM-MSCs. Both untreated and TGF-β2-treated BM-MSCs increased tenocyte migration in vitro. Treating equine BM-MSCs with TGF-β2 significantly increases production of paracrine factors and extracellular matrix molecules important for tendon healing and promotes the migration of tenocytes in vitro.
© 2022. The Author(s).
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Publication Date: 2022-09-16 PubMed ID: 36114555PubMed Central: PMC9482193DOI: 10.1186/s13287-022-03172-9Google Scholar: Lookup
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  • Journal Article
  • Research Support
  • N.I.H.
  • Extramural
  • Research Support
  • Non-U.S. Gov't

Summary

This research summary has been generated with artificial intelligence and may contain errors and omissions. Refer to the original study to confirm details provided. Submit correction.

The research assesses the impact of transforming growth factor (TGF)-β2 treatment on equine bone marrow-derived mesenchymal stem cells (BM-MSCs). The treatment increased gene expression of proteins and growth factors crucial for tendon healing and contributed to increased tenocyte movement in laboratory conditions.

Research Overview

The study investigated the effect of a specific cytokine, transforming growth factor (TGF)-β2, on equine BM-MSCs. The researchers were interested in understanding how the treatment influenced the stem cell’s genetic and protein expression and how this affected tissue healing capabilities.

  • The research used RNA-sequencing and western blotting to gauge differences in gene and protein expression between untreated and TGF-β2-treated equine bone marrow-derived MSCs.
  • The testing involved a comparison of equine tenocyte (tendon cells) migration during co-culture with untreated and TGF-β2-treated BM-MSCs.

Key Findings

The study found significant upregulation of gene expression of collagens, extracellular matrix molecules, and growth factors following the TGF-β2 treatment of the equine BM-MSCs.

  • There was a marked increase in the protein expression of collagen type I and tenascin-C in TGF-β2-treated BM-MSCs compared to untreated BM-MSCs.
  • Increased migration of tenocytes was observed both in untreated and TGF-β2-treated BM-MSCs. However, the impact was greater in TGF-β2-treated BM-MSCs.

Conclusions and Implications

The treatment of equine BM-MSCs with TGF-β2 significantly upregulates the production of certain paracrine factors and extracellular matrix molecules that are crucial for tendon healing.

  • This treatment strategy can potentially enhance the healing process by promoting the migration of tenocytes.
  • By comprehending the effect of TGF-β2 on MSCs, scientists can potentially develop more effective treatment options for a range of tendon injuries in animals and humans.

Cite This Article

APA
Koch DW, Schnabel LV, Ellis IM, Bates RE, Berglund AK. (2022). TGF-β2 enhances expression of equine bone marrow-derived mesenchymal stem cell paracrine factors with known associations to tendon healing. Stem Cell Res Ther, 13(1), 477. https://doi.org/10.1186/s13287-022-03172-9

Publication

Stem cell research & therapy
ISSN: 1757-6512
NlmUniqueID: 101527581
Country: England
Language: English
Volume: 13
Issue: 1
Pages: 477
PII: 477

Researcher Affiliations

Koch, Drew W
  • Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC, USA.
  • Comparative Medicine Institute, North Carolina State University, Raleigh, NC, USA.
Schnabel, Lauren V
  • Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC, USA. lvschnab@ncsu.edu.
  • Comparative Medicine Institute, North Carolina State University, Raleigh, NC, USA. lvschnab@ncsu.edu.
Ellis, Ilene M
  • Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC, USA.
Bates, Rowan E
  • Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC, USA.
Berglund, Alix K
  • Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC, USA. akberglu@nscu.edu.
  • Comparative Medicine Institute, North Carolina State University, Raleigh, NC, USA. akberglu@nscu.edu.

MeSH Terms

  • Animals
  • Bone Marrow / metabolism
  • Collagen Type I / metabolism
  • Cytokines / metabolism
  • Horses
  • Mesenchymal Stem Cells / metabolism
  • Paracrine Communication
  • RNA / metabolism
  • Tenascin / genetics
  • Tenascin / metabolism
  • Tendons / metabolism
  • Transforming Growth Factor beta2 / genetics
  • Transforming Growth Factors / metabolism

Grant Funding

  • T35OD11070 / NIH HHS
  • K01 OD027037 / NIH HHS
  • T32 OD011130 / NIH HHS
  • T35 OD011070 / NIH HHS
  • K01OD027037 / NIH HHS
  • T32OD011130 / NIH HHS

Conflict of Interest Statement

The authors declare that they have no competing interests.

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