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Expression of Bax/Bcl-2, TGF-β1, and Type III Collagen Fiber in Congenital Muscular Torticollis
BACKGROUND: This study investigated the expression of Bax/Bcl-2, TGF-β1 and type III collagen fiber in sternocleidomastoid of congenital muscular torticollis (CMT), and explored the possible mechanisms of fibrosis in sternocleidomastoid of CMT. MATERIAL/METHODS: The localization and expression of Ba...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
International Scientific Literature, Inc.
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6231324/ https://www.ncbi.nlm.nih.gov/pubmed/30390390 http://dx.doi.org/10.12659/MSM.909064 |
Sumario: | BACKGROUND: This study investigated the expression of Bax/Bcl-2, TGF-β1 and type III collagen fiber in sternocleidomastoid of congenital muscular torticollis (CMT), and explored the possible mechanisms of fibrosis in sternocleidomastoid of CMT. MATERIAL/METHODS: The localization and expression of Bax, Bcl-2, TGF-β1, and type III collagen were detected in the control group and experimental group by using immunohistochemical staining method. The RT-PCR assay was used to measure the expression of TGF-β1 in the control group and experimental group. RESULTS: HE staining results showed that the collagen fiber in the experimental group had more abundant hyperplasia compared to the control group (p<0.05). Immunohistochemical staining results showed that the expression of Bax, Bax/Bcl-2, TGF-β1, and type III collagen in the experimental group was significantly increased compared to the control group (p<0.01). There were positive correlations between expression of Bax/Bcl-2 and TGF-β1, and between expression of TGF-β1 and type III collagen fiber (p<0.05, r=0.32 and 0.83, respectively). The RT-PCR results showed that the expression of TGF-β1 mRNA was also significantly elevated in the experimental group compared to the control group (p<0.05). CONCLUSIONS: Increased muscular apoptosis may aggravate the formation of muscular fibrosis, which may be involved in the pathogenesis of sternocleidomastoid of CMT. |
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