Transforming Growth Factor-Beta (TGF-β) Signaling in Paravertebral Muscles in Juvenile and Adolescent Idiopathic Scoliosis

Author:

Nowak Roman1ORCID,Kwiecien Magdalena2,Tkacz Magdalena3ORCID,Mazurek Urszula2ORCID

Affiliation:

1. Department of Orthopedics, School of Medicine with the Division of Dentistry, Medical University of Silesia, Wojewódzki Szpital Specjalistyczny nr 5 Plac Medyków 1, 41-200 Sosnowiec, Poland

2. Department of Molecular Biology, Medical University of Silesia, Ulica Narcyzów 1, 41-100 Sosnowiec, Poland

3. Institute of Computer Science, Division of Information Systems, University of Silesia, Ulica Będzińska 39, 41-200 Sosnowiec, Poland

Abstract

Most researchers agree that idiopathic scoliosis (IS) is a multifactorial disease influenced by complex genetic and environmental factors. The onset of the spinal deformity that determines the natural course of the disease, usually occurs in the juvenile or adolescent period. Transforming growth factorsβ(TGF-βs) and their receptors, TGFBRs, may be considered as candidate genes related to IS susceptibility and natural history. This study explores the transcriptional profile of TGF-βs, TGFBRs, and TGF-βresponsive genes in the paravertebral muscles of patients with juvenile and adolescent idiopathic scoliosis (JIS and AIS, resp.). Muscle specimens were harvested intraoperatively and grouped according to the side of the curve and the age of scoliosis onset. The results of microarray and qRT-PCR analysis confirmed significantly higher transcript abundances of TGF-β2, TGF-β3, and TGFBR2 in samples from the curve concavity of AIS patients, suggesting a difference in TGF-βsignaling in the pathogenesis of juvenile and adolescent curves. Analysis of TGF-βresponsive genes in the transcriptomes of patients with AIS suggested overrepresentation of the genes localized in the extracellular region of curve concavity: LTBP3, LTBP4, ITGB4, and ITGB5. This finding suggests the extracellular region of paravertebral muscles as an interesting target for future molecular research into AIS pathogenesis.

Funder

Polish Ministry of Science and Higher Education

Publisher

Hindawi Limited

Subject

General Immunology and Microbiology,General Biochemistry, Genetics and Molecular Biology,General Medicine

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