scholarly journals Huiyang Shengji Extract Improve Chronic Nonhealing Cutaneous through the TGF-β1/Smad3 Signaling Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Yan Lin ◽  
Xiujuan He ◽  
Xinran Xie ◽  
Qingwu Liu ◽  
Jia Chen ◽  
...  
Keyword(s):  
Gene Expression ◽  
Signaling Pathway ◽  
Type I Collagen ◽  
Chronic Wounds ◽  
Human Fibroblasts ◽  
Type Iii Collagen ◽  
Type I ◽  
Paracrine Factors ◽  
M1 Macrophages ◽  
Tgf Β1

Chronic nonhealing cutaneous wounds are a thorny problem in the field of surgery because of their prolonged and unhealed characteristics. Huiyang Shengji extract (HSE) is an extract of traditional Chinese medicine prescription for treating chronic wounds. This study aims to investigate the regulation of M1 macrophages on fibroblast proliferation and secretion and the intervention mechanism of Huiyang Shengji extract. We found that the effects of HSFs stimulated with paracrine factors from M1 macrophages were as follows: the proliferation of HSFs was reduced, the expression of MKI-67 was downregulated, and the content and gene expression of the inflammation factors and fibroblast MMPs were increased, while the content and gene expression of TIMP-1 are decreased, the content of human fibroblasts secreting type I collagen (COL1A1) and type III collagen (COL3A1) was decreased, and the TGF-β1/Smad3 signaling pathway was inhibited. Interestingly, HSE inhibited these effects of M1 macrophages on human fibroblasts after the intervention, and the inhibitory effect was related to the concentration. In conclusion, M1 macrophages caused changes in HSFs and secretion, while HSE has a specific regulatory effect on the proliferation and secretion of fibroblasts caused by M1 macrophages.

Stimulatory Auto-Antibodies to the PDGF Receptor in Patients with Chronic GVHD.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 454-454
Author(s):  
Attilio Olivieri ◽  
Silvia Svegliati ◽  
Nadia Campelli ◽  
Michele Maria Luchetti ◽  
Silvia Trappolini ◽  
...  
Keyword(s):  
Gene Expression ◽  
Reactive Oxygen Species ◽  
Type I Collagen ◽  
Human Fibroblasts ◽  
Reactive Oxygen ◽  
Type I ◽  
Collagen Gene ◽  
Pdgf Receptor ◽  
Oxygen Species ◽  
Normal Human

Abstract Background Experimental data are consistent with the hypothesis that activation of the PDGF receptor (PDGFR) is characteristic of scleroderma (SSc) fibroblasts and may contribute to their activation. We have recently demonstrated that fibroblasts from SSc patients contain high Ha Ras and ROS (Reactive Oxygen Species) levels and constitutive activation of ERK1/2 (Svegliati et al: JBC in press). Furthermore, SSc patients have circulating auto-antibodies against the PDGFR which induce type I collagen gene expression in normal human fibroblasts through the Ha Ras-ERK1/2- ROS pathway (Svegliati et al: Submitted). These findings suggest that anti PDGFR auto-antibodies play a pivotal role in the pathogenesis of scleroderma. Clinical chronic graft-versus-host disease (cGVHD) can show manifestations that are very similar to those of SSc. Although it is conceivable that the two diseases can share a similar pathophysiological mechanism there are no data supporting this assumption. In view of these considerations we tested the hypothesis that patients with cGVHD have serum auto-antibodies that stimulate PDGFR and activate collagen gene expression in fibroblasts. Methods Serum from 7 patients with extensive cGVHD showing scleroderma-like features either in the skin or in the lung was analyzed for the presence of stimulatory autoantibodies to PDGFR. Patients receiving allogeneic transplantation, but without any signs of cGVHD were used as controls. The median F-U after transplant was 23 months (range 16–36) in patients with cGVH and 42 (range 9–51) in the control group. The assay was carried by incubating purified IgG of the patients with mouse embryo fibroblasts carrying inactive copies of PDGFR α or β chains (PDGFR −/−) or the same cells expressing PDGFR α or β, respectively. Production of reactive oxygen species was assayed in the presence or absence of specific PDGFR inhibitors. The antibodies were characterized by immunoprecipitation, immunoblotting and absorption experiments in primary human fibroblasts and endothelial cells. Result Stimulatory antibodies to the PDGFR were selectively found in all patients with cGVHD and fibrotic lesions. The antibodies specifically recognized PDGFR, induced tyrosine phosphorylation and ROS accumulation. Their activity was completely and selectively abolished by pre-incubation with cells expressing PDGFR α or β chains or by PDGF receptor tyrosine kinase inhibitor. Anti-PDGFR antibodies induced selectively Ha-Ras-ERK1/2 and ROS cascade and stimulated the expression of type I collagen gene and myofibroblast phenotype conversion in normal human primary fibroblasts. Antibodies were absent in all controls. Conclusions Stimulatory auto-antibodies against PDGFR represent a specific hallmark of patients with cGVHD. Their biological activity on fibroblasts strongly argues for a causal role in the pathogenesis of the disease.

scholarly journals Effects of paeonol on proliferation and collagen synthesis of rat cardiac fibroblasts induced by aldosterone

2021 ◽  
Vol 16 (2) ◽  
pp. 42-48
Author(s):  
Qian Xu ◽  
Li Na Wang ◽  
Jing Yi Zhao ◽  
Yan Hong Xiao ◽  
Chao Du
Keyword(s):  
Cell Viability ◽  
Molecular Mechanisms ◽  
Type I Collagen ◽  
Ventricular Remodeling ◽  
Cardiac Fibroblasts ◽  
Neonatal Rat ◽  
Type Iii Collagen ◽  
Type I ◽  
Rt Pcr ◽  
Tgf Β1

The aim of this study was to explore the possible molecular mechanisms of paeonol in preventing ventricular remodeling. The cell viability of neonatal rat cardiac fibroblasts was detected by the method of MTT. RT-PCR and Western blot were used to measure the expression of TGF-β1, type I collagen and type III collagen. After treating the cardiac fibroblasts with paeonol, the cell viability decreased (p<0.01), and the expression of TGF-β1, type I collagen and types III collagen was significantly reduced (p<0.01). Thus, paeonol can inhibit the proliferation of fibroblast cells induced by aldosterone. The molecular mechanism is related to the down-regulation of TGF-β1 and type I and III collagen gene expression.

Differential expression of type I and type III collagen genes during tooth development

Development ◽  
1991 ◽  
Vol 111 (3) ◽  
pp. 691-698
Author(s):  
M.B. Andujar ◽  
P. Couble ◽  
M.L. Couble ◽  
H. Magloire
Keyword(s):  
Gene Expression ◽  
Type I Collagen ◽  
Tooth Development ◽  
Expression Patterns ◽  
Type Iii Collagen ◽  
Type I ◽  
Collagen Gene ◽  
Type Iii ◽  
Collagen Gene Expression ◽  
Collagen Genes

Collagen gene expression during mouse molar tooth development was studied by quantitative in situ hybridization techniques. Different expression patterns of type I and type III collagen mRNAs were observed in the various mesenchymal tissues that constitute the tooth germ. High concentration for pro-alpha 1(I) and pro-alpha 2(I) collagen mRNAs were found within the osteoblasts. We found that the cellular content of type I collagen mRNAs in the odontoblasts varies throughout the tooth formation: whereas mRNA concentration for pro-alpha 1(I) collagen decreases and that of pro-alpha 2(I) increases, during postnatal development. Moreover, different amounts of pro-alpha 1(I) and pro-alpha 2(I) collagen mRNAs were observed in crown and root odontoblasts, respectively. Type III collagen mRNAs were detected in most of the mesenchymal cells, codistributed with type I collagen mRNAs, except in odontoblasts and osteoblasts. Finally, this study reports differential accumulation of collagen mRNAs during mouse tooth development and points out that type I collagen gene expression is regulated by distinct mechanisms during odontoblast differentiation process. These results support the independent expression of the collagen genes under developmental tissue-specific control.

scholarly journals Dioscin alleviates alcoholic liver fibrosis by attenuating hepatic stellate cell activation via the TLR4/MyD88/NF-κB signaling pathway

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Min Liu ◽  
Youwei Xu ◽  
Xu Han ◽  
Lianhong Yin ◽  
Lina Xu ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Signaling Pathway ◽  
Type I Collagen ◽  
Transforming Growth Factor ◽  
Stellate Cell ◽  
Pyrrolidine Dithiocarbamate ◽  
Type I ◽  
Tgf Β1

Abstract The present work aimed to investigate the activities and underlying mechanisms of dioscin against alcoholic liver fibrosis (ALF). In vivo liver fibrosis in mice was induced by an alcoholic liquid diet and in vitro studies were performed on activated HSC-T6 and LX2 cells treated with lipopolysaccharide. Our results showed that dioscin significantly attenuated hepatic stellate cells (HSCs) activation, improved collagen accumulation and attenuated inflammation through down-regulating the levels of myeloid differentiation factor 88 (MyD88), nuclear factor κB (NF-κB), interleukin (IL)-1, IL-6 and tumour necrosis factor-α by decreasing Toll-like receptor (TLR)4 expression both in vivo and in vitro. TLR4 overexpression was also decreased by dioscin, leading to the markedly down-regulated levels of MyD88, NF-κB, transforming growth factor-β1 (TGF-β1), α-smooth muscle actin (α-SMA) and type I collagen (COL1A1) in cultured HSCs. Suppression of cellular MyD88 by ST2825 or abrogation of NF-κB by pyrrolidine dithiocarbamate eliminated the inhibitory effects of dioscin on the levels of TGF-β1, α-SMA and COL1A1. In a word, dioscin exhibited potent effects against ALF via altering TLR4/MyD88/NF-κB signaling pathway, which provided novel insights into the mechanisms of this compound as an antifibrogenic candidate for the treatment of ALF in the future.

The p38 signaling pathway mediates the TGF‐β1‐induced increase in type I collagen deposition in human granulosa cells

2020 ◽  
Vol 34 (11) ◽  
pp. 15591-15604
Author(s):  
Hui Li ◽  
Hsun‐Ming Chang ◽  
Zhendan Shi ◽  
Peter C. K. Leung
Keyword(s):  
Signaling Pathway ◽  
Granulosa Cells ◽  
Type I Collagen ◽  
Type I ◽  
Collagen Deposition ◽  
Human Granulosa Cells ◽  
Tgf Β1

scholarly journals C-myb, but not B-myb, Upregulates Type I Collagen Gene Expression in Human Fibroblasts

1999 ◽  
Vol 112 (2) ◽  
pp. 191-196 ◽  
Author(s):  
Gina Piccinini ◽  
Josée Golay ◽  
Adriano Flora ◽  
Simona Songia ◽  
Michele Luchetti ◽  
...  
Keyword(s):  
Gene Expression ◽  
Type I Collagen ◽  
Human Fibroblasts ◽  
Type I ◽  
Collagen Gene ◽  
Collagen Gene Expression

scholarly journals Bioflavonoid Galangin Suppresses Hypertrophic Scar Formation by the TGF-β/Smad Signaling Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Zha Ru ◽  
Ying Hu ◽  
Shenghua Huang ◽  
Li Bai ◽  
Kun Zhang ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Hypertrophic Scar ◽  
Healing Process ◽  
Scar Formation ◽  
Type Iii Collagen ◽  
Type I ◽  
Smad Signaling ◽  
Type Iii ◽  
Smad Signaling Pathway ◽  
Tgf Β1

Background. Hypertrophic scar (HS) is a benign fibroproliferative skin disease resulting from an aberrant wound healing process and can cause aesthetic and functional damage to patients. Currently, there is no ideal treatment to treat this disease. Galangin, a natural active bioflavonoid compound, is suggested to inhibit fibrosis and proliferation in certain cells. Methods. In this study, we found Galangin could attenuate abnormal scar formation in an HS rabbit ear model. Additionally, the HE staining shows Galangin reduced scar elevation index (SEI) and Masson’s trichrome staining changed collagen deposition. Results. The expressions of type I collagen, type III collagen, and TGF-β1 were much lower under a proper dose of Galangin treatment, and Smad7 expression was also enhanced, which are examined by real-time PCR, immunohistochemistry, and western blot. Conclusion. Our data indicated that Galangin can alleviate dermal scarring via the TGF-β/Smad signaling pathway probably by upregulating Smad 7 expression and, thus, suppressing the expression of type I and type III collagens and TGF-β1.

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