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MiRNA-21 promotes fibrosis in orbital fibroblasts from thyroid-associated ophthalmopathy.

Tong BD, Xiao MY, Zeng JX, Xiong W - Mol. Vis. (2015)

Bottom Line: Moreover, the effect of transforming growth factor-beta1 (TGF-β1) on miR-21 expression was also analyzed.Additional experiments demonstrated that miR-21 enhanced proliferation, decreased apoptosis, and promoted differentiation in TAO orbital fibroblasts.The present study shows that miR-21 regulates cell proliferation, apoptosis, and differentiation in orbital fibroblasts from TAO, and acts as a mediator in TGF-β1-induced collagen production.

View Article: PubMed Central - PubMed

Affiliation: Department of Ophthalmology and Eye Research Center, Hunan, China.

ABSTRACT

Purpose: This study aimed to determine the role of miR-21 in orbital fibroblasts obtained from donors with thyroid-associated ophthalmopathy (TAO) and to elucidate the regulation of fibrosis by miR-21 in the pathological process of TAO.

Methods: The expression of miR-21 was investigated in orbital tissues from 26 donors with TAO and 10 donors without TAO. Human orbital fibroblasts were cultivated from TAO donors, and the role of miR-21 in orbital fibroblast proliferation, apoptosis, and differentiation was analyzed. Moreover, the effect of transforming growth factor-beta1 (TGF-β1) on miR-21 expression was also analyzed. In addition, the regulation of miR-21 in TGF-β1-induced collagen production was determined.

Results: The expression of miR-21 in orbital fibroblasts from TAO was higher than in donors without TAO. Additional experiments demonstrated that miR-21 enhanced proliferation, decreased apoptosis, and promoted differentiation in TAO orbital fibroblasts. Moreover, this study also showed that TGF-β1 induced miR-21 expression in a time- and dose-dependent manner and miR-21 promoted collagen I mRNA expression and total collagen production induced by TGF-β1. Additionally, miR-21 activated the TGF-β1/Smad signaling pathway by enhancing Smad3 phosphorylation.

Conclusions: The present study shows that miR-21 regulates cell proliferation, apoptosis, and differentiation in orbital fibroblasts from TAO, and acts as a mediator in TGF-β1-induced collagen production. These data predict a close association between miR-21 and orbital muscle fibrosis, and provide a novel therapeutic target for TAO.

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Expression of miR-21 in orbital fibroblasts from the eye tissue of normal subjects (n=10) or TAO donors (n=26). Results are expressed as mean ± standard deviation (SD; *p<0.05 versus control).
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f1: Expression of miR-21 in orbital fibroblasts from the eye tissue of normal subjects (n=10) or TAO donors (n=26). Results are expressed as mean ± standard deviation (SD; *p<0.05 versus control).

Mentions: Expression of miR-21 is significantly upregulated in fibrotic-related disease and exerts a vital role in the progression of fibrosis. However, the related role of miR-21 in thyroid-related eye disease tissues remain poorly understood. We examined miR-21 expression in orbital fibroblasts from normal (n=10) or TAO (n=26) tissues. The results show that the expression levels of miR-21 were obviously higher in orbital fibroblasts from TAO tissues than those from the normal human eye tissues (p<0.05, Figure 1). Collectively, these results suggest dramatic upregulation of miR-21 in orbital fibroblasts from TAO donors.


MiRNA-21 promotes fibrosis in orbital fibroblasts from thyroid-associated ophthalmopathy.

Tong BD, Xiao MY, Zeng JX, Xiong W - Mol. Vis. (2015)

Expression of miR-21 in orbital fibroblasts from the eye tissue of normal subjects (n=10) or TAO donors (n=26). Results are expressed as mean ± standard deviation (SD; *p<0.05 versus control).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4384173&req=5

f1: Expression of miR-21 in orbital fibroblasts from the eye tissue of normal subjects (n=10) or TAO donors (n=26). Results are expressed as mean ± standard deviation (SD; *p<0.05 versus control).
Mentions: Expression of miR-21 is significantly upregulated in fibrotic-related disease and exerts a vital role in the progression of fibrosis. However, the related role of miR-21 in thyroid-related eye disease tissues remain poorly understood. We examined miR-21 expression in orbital fibroblasts from normal (n=10) or TAO (n=26) tissues. The results show that the expression levels of miR-21 were obviously higher in orbital fibroblasts from TAO tissues than those from the normal human eye tissues (p<0.05, Figure 1). Collectively, these results suggest dramatic upregulation of miR-21 in orbital fibroblasts from TAO donors.

Bottom Line: Moreover, the effect of transforming growth factor-beta1 (TGF-β1) on miR-21 expression was also analyzed.Additional experiments demonstrated that miR-21 enhanced proliferation, decreased apoptosis, and promoted differentiation in TAO orbital fibroblasts.The present study shows that miR-21 regulates cell proliferation, apoptosis, and differentiation in orbital fibroblasts from TAO, and acts as a mediator in TGF-β1-induced collagen production.

View Article: PubMed Central - PubMed

Affiliation: Department of Ophthalmology and Eye Research Center, Hunan, China.

ABSTRACT

Purpose: This study aimed to determine the role of miR-21 in orbital fibroblasts obtained from donors with thyroid-associated ophthalmopathy (TAO) and to elucidate the regulation of fibrosis by miR-21 in the pathological process of TAO.

Methods: The expression of miR-21 was investigated in orbital tissues from 26 donors with TAO and 10 donors without TAO. Human orbital fibroblasts were cultivated from TAO donors, and the role of miR-21 in orbital fibroblast proliferation, apoptosis, and differentiation was analyzed. Moreover, the effect of transforming growth factor-beta1 (TGF-β1) on miR-21 expression was also analyzed. In addition, the regulation of miR-21 in TGF-β1-induced collagen production was determined.

Results: The expression of miR-21 in orbital fibroblasts from TAO was higher than in donors without TAO. Additional experiments demonstrated that miR-21 enhanced proliferation, decreased apoptosis, and promoted differentiation in TAO orbital fibroblasts. Moreover, this study also showed that TGF-β1 induced miR-21 expression in a time- and dose-dependent manner and miR-21 promoted collagen I mRNA expression and total collagen production induced by TGF-β1. Additionally, miR-21 activated the TGF-β1/Smad signaling pathway by enhancing Smad3 phosphorylation.

Conclusions: The present study shows that miR-21 regulates cell proliferation, apoptosis, and differentiation in orbital fibroblasts from TAO, and acts as a mediator in TGF-β1-induced collagen production. These data predict a close association between miR-21 and orbital muscle fibrosis, and provide a novel therapeutic target for TAO.

Show MeSH
Related in: MedlinePlus