A Selenium-Enriched Ziyang Green Tea Polysaccharide Induces Bax-Dependent Mitochondrial Apoptosis and Inhibits TGF-β1-Stimulated Collagen Expression in Human Keloid Fibroblasts via NG2 Inactivation

Background: Metabolic syndrome is a significant risk factor for cardiovascular diseases. Green tea and green coffee extracts, antioxidant and anti-inflammatory agents may participate in metabolic syndrome-induced cardiac fibrosis alleviation. However, the effect of combination of those extracts still needs exploration. Therefore, this study investigated the effect of green tea and decaffeinated light roasted green coffee extracts and their combination in metabolic syndrome-induced cardiac fibrosis rats. Methods: Metabolic syndrome rat model was i1nduced through high-fat high sucrose diets feeding for 8 weeks and injection of low dose streptozotocin at the 2nd week. The metabolic syndrome rats were divided into 4 experimental groups metabolic syndrome rats (MS); metabolic syndrome rats treated with 300 mg/ kg b.w green tea extract (GT); metabolic syndrome rats treated with 200 mg/ kg b.w decaffeinated light roasted green coffee extract (GC); metabolic syndrome rats treated with the combination of the two extracts (CE); and a normal control (NC) group was added. Angiotensin 2 level was analyzed by ELISA method. Gene expression of NF-κB, TNF-α, IL-6, Tgf-β1, Rac-1, and α-sma were analyzed by touchdown polymerase chain reaction methods. Results: Metabolic syndrome rats treated with green tea and decaffeinated light roasted green coffee significantly decreased angiotensin-2 serum level and cardiac inflammation and fibrosis gene expression level (NF-κB, TNF-α, IL-6, Tgf-β1, Rac-1, and α-sma). More significant alleviation was observed in the combination group. Conclusion: This study suggested that combination of green tea and decaffeinated light roasted green coffee extracts showed better improvement in metabolic syndrome-induced cardiac fibrosis rat model compared to that of single extract administration through inflammation inhibition

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The effect of inhibiting exosomes derived from adipose-derived stem cells via the TGF-β1/Smad pathway on the fibrosis of keloid fibroblasts

Gland Surgery ◽

10.21037/gs-21-4 ◽

2021 ◽

Vol 10 (3) ◽

pp. 1046-1056

Author(s):

Zhi-Yuan Wu ◽

Hui-Jun Zhang ◽

Zhi-Hong Zhou ◽

Zhan-Peng Li ◽

Si-Mu Liao ◽

...

Keyword(s):

Stem Cells ◽

Adipose Derived Stem Cells ◽

Smad Pathway ◽

Tgf Β1 ◽

Keloid Fibroblasts

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Growth Differentiation Factor-9 Promotes Fibroblast Proliferation and Migration in Keloids through the Smad2/3 Pathway

Cellular Physiology and Biochemistry ◽

10.1159/000452538 ◽

2016 ◽

Vol 40 (1-2) ◽

pp. 207-218 ◽

Cited By ~ 8

Author(s):

Zhaohua Jiang ◽

Qingxiong Yu ◽

Lingling Xia ◽

Yi Zhang ◽

Xiuxia Wang ◽

...

Keyword(s):

Cell Cycle ◽

Wound Healing ◽

Growth Factor ◽

Fibroblast Proliferation ◽

Differentiation Factor ◽

Cox 2 ◽

And Migration ◽

Tgf Β1 ◽

Keloid Fibroblasts ◽

Proliferation And Migration

Background: Keloids are fibroproliferative scars that develop as a result of a dysregulated wound healing process; however, the molecular mechanisms of keloid pathogenesis remain unclear. Keloids are characterized by the ability to spread beyond the original boundary of the wound, and they represent a significant clinical challenge. Previous work from our group suggested that growth differentiation factor (GDF)-9 plays a role in the invasive behavior of keloids. Here, we examined the involvement of GDF-9 in keloid formation and spread and elucidated a potential underlying mechanism. Methods: The expression of GDF-9, cyclooxygenase (COX)-2, vascular epidermal growth factor (VEGF)-C, matrix metalloprotease (MMP)-2, MMP-9, transforming growth factor (TGF)-β1, and the related signaling pathway components in human keloid tissues or keloid fibroblasts (kFBs) was monitored by qRT-PCR and western blot. A series of overexpression and silencing experiments in normal and keloid fibroblasts were used to modify the expression of GDF-9. The effects of GDF-9 on kFB proliferation and migration were assessed using the CCK-8, cell cycle and scratch wound healing assays. Results: GDF-9 promotes fibroblast proliferation and migration. GDF-9 silencing in kFBs decreased cell proliferation, blocked cell cycle progression, downregulated the angiogenic markers COX-2 and VEGF-C, and downregulated MMP-2 and MMP-9 expression, whereas it had no effect on the levels of TGF-β1. GDF-9 silencing significantly inhibited Smad2 and Smad3 phosphorylation in kFBs. Conclusions: GDF-9 promotes the proliferation and migration of kFBs via a mechanism involving the Smad2/3 pathway.

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Mechanical stretch modulates TGF-β1 and α1(I) collagen expression in fetal human intestinal smooth muscle cells

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1999.277.5.g1074 ◽

1999 ◽

Vol 277 (5) ◽

pp. G1074-G1080 ◽

Cited By ~ 14

Author(s):

Jorge A. Gutierrez ◽

Hilary A. Perr

Keyword(s):

Smooth Muscle ◽

Smooth Muscle Cells ◽

Type I Collagen ◽

Intestinal Smooth Muscle ◽

Type I ◽

Collagen Mrna ◽

Collagen Expression ◽

Collagen Protein ◽

Mrna Content ◽

Tgf Β1

Intestinal muscle undergoes stretch intermittently during peristalsis and persistently proximal to obstruction. The influence of this pervasive biomechanical force on developing smooth muscle cell function remains unknown. We adapted a novel in vitro system to study whether stretch modulates transforming growth factor-β1 (TGF-β1) and type I collagen protein and component α1 chain [α1(I) collagen] expression in fetal human intestinal smooth muscle cells. Primary confluent cells at 20-wk gestation, cultured on flexible silicone membranes, were subjected to two brief stretches or to 18 h tonic stretch. Nonstretched cultures served as controls. TGF-β1 protein was measured by ELISA and type I collagen protein was assayed by Western blot. TGF-β1 and α1(I) collagen mRNA abundance was determined by Northern blot analysis, quantitated by phosphorimaging, and normalized to 18S rRNA. Transcription was examined by nuclear run-on assay. Tonic stretch increased TGF-β1 protein 40%, type I collagen protein 100%, TGF-β1 mRNA content 2.16-fold, and α1(I) collagen mRNA 3.80-fold and enhanced transcription of TGF-β1 and α1(I) collagen by 3.1- and 4.25-fold, respectively. Brief stretch stimulated a 50% increase in TGF-β1 mRNA content but no change in α1(I) collagen. Neutralizing anti-TGF-β1 ablated stretch-mediated effects on α1(I) collagen. Therefore, stretch upregulates transcription for TGF-β1, which stimulates α1(I) collagen gene expression in smooth muscle from developing gut.

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