scholarly journals Adipose-derived mesenchymal stem cells from the sand rat: transforming growth factor beta and 3D co-culture with human disc cells stimulate proteoglycan and collagen type I rich extracellular matrix

2008 ◽  
Vol 10 (4) ◽  
Author(s):  
Hazel Tapp ◽  
Ray Deepe ◽  
Jane A Ingram ◽  
Marshall Kuremsky ◽  
Edward N Hanley ◽  
...  
Keyword(s):  
Stem Cells ◽  
Extracellular Matrix ◽  
Transforming Growth Factor Beta ◽  
Collagen Type ◽  
Transforming Growth Factor ◽  
Collagen Type I ◽  
Type I ◽  
Sand Rat ◽  
Disc Cells ◽  
Growth Factor Beta

scholarly journals Calvaria Bone Transcriptome in Mouse Models of Osteogenesis Imperfecta

2021 ◽  
Vol 22 (10) ◽  
pp. 5290
Author(s):  
Pierre Moffatt ◽  
Iris Boraschi-Diaz ◽  
Juliana Marulanda ◽  
Ghalib Bardai ◽  
Frank Rauch
Keyword(s):  
Osteogenesis Imperfecta ◽  
Mouse Models ◽  
Transforming Growth Factor Beta ◽  
Collagen Type ◽  
Transforming Growth Factor ◽  
Collagen Type I ◽  
Bone Fragility ◽  
Type I ◽  
Growth Factor Beta ◽  
Upregulated Genes

Osteogenesis imperfecta (OI) is a bone fragility disorder that is usually caused by mutations affecting collagen type I. We compared the calvaria bone tissue transcriptome of male 10-week-old heterozygous Jrt (Col1a1 mutation) and homozygous oim mice (Col1a2 mutation) to their respective littermate results. We found that Jrt and oim mice shared 185 differentially expressed genes (upregulated: 106 genes; downregulated: 79 genes). A total of seven genes were upregulated by a factor of two or more in both mouse models (Cyp2e1, Slc13a5, Cgref1, Smpd3, Ifitm5, Cthrc1 and Rerg). One gene (Gypa, coding for a blood group antigen) was downregulated by a factor of two or more in both OI mouse models. Overrepresentation analyses revealed that genes involved in ‘ossification’ were significantly overrepresented among upregulated genes in both Jrt and oim mice, whereas hematopoietic genes were downregulated. Several genes involved in Wnt signaling and transforming growth factor beta signaling were upregulated in oim mice, but less so in Jrt mice. Thus, this study identified a set of genes that are dysregulated across various OI mouse models and are likely to play an important role in the pathophysiology of this disorder.

Paeoniflorin inhibits TGF-β1-mediated collagen production bySchistosoma japonicumsoluble egg antigenin vitro

Parasitology ◽  
2007 ◽  
Vol 134 (11) ◽  
pp. 1611-1621 ◽  
Author(s):  
D. CHU ◽  
Q. LUO ◽  
C. LI ◽  
Y. GAO ◽  
L. YU ◽  
...  
Keyword(s):  
Hepatic Fibrosis ◽  
Transforming Growth Factor Beta ◽  
Collagen Type ◽  
Transforming Growth Factor ◽  
Collagen Type I ◽  
Peritoneal Macrophages ◽  
Type I ◽  
Smad3 Expression ◽  
Egg Antigen ◽  
Tgf Β1

SUMMARYThe main pathological characteristics of hepatic fibrosis in schistosomiasis are the proliferation of hepatic stellate cells (HSCs) and the deposition of collagen type I (Col I) and collagen type III (Col III). Transforming growth factor beta-1 (TGF-β1) plays an important role in hepatic fibrosis. Paeoniflorin (PAE) has been reported to have immunoregulatory effects; however, the mechanism of its anti-hepatic fibrosis inS. japonicumhas not been elucidated. In the present study, we found that mouse peritoneal macrophages (PMφs) stimulated by soluble egg antigen (SEA) ofS. japonicumcould secrete TGF-β1, and the TGF-β1 in the peritoneal macrophage-conditioned medium (PMCM) could induce proliferation of HSCs and secretion of Col I and III. We selected PMCM at 1:2 dilution as the optimum PMCM (OPMCM). Then we treated HSCs pre-incubated with OPMCM with PAE, and found that the inhibition of HSC proliferation or Col I and III production were closely correlated with the concentration of PAE. Further investigation found that PAE significantly decreased the Smad3 transcription and phosphorylation in HSCs stimulated by OPMCM. In conclusion, SEA plays a key role in hepatic fibrosis by inducing TGF-β1 from PMφs. PAE can exert anti-fibrogenic effects by inhibiting HSCs proliferation and down-regulating Smad3 expression and phosphorylation through TGF-β1 signalling.

scholarly journals Platelet-Released Growth Factors and Platelet-Rich Fibrin Induce Expression of Factors Involved in Extracellular Matrix Organization in Human Keratinocytes

2020 ◽  
Vol 21 (12) ◽  
pp. 4404
Author(s):  
Andreas Bayer ◽  
Bernard Wijaya ◽  
Lena Möbus ◽  
Franziska Rademacher ◽  
Meno Rodewald ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Wound Healing ◽  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Collagen Type ◽  
Transforming Growth Factor ◽  
Enzyme Linked Immunosorbent Assay ◽  
Type I ◽  
Related Factors ◽  
Platelet Rich Fibrin

Platelet-released growth factor (PRGF) is a thrombocyte concentrate lysate which, like its clinically equivalent variations (e.g., Vivostat PRF® (platelet-rich fibrin)), is known to support the healing of chronic and hard-to-heal wounds. However, studies on the effect of PRGF on keratinocytes remain scarce. This study aims to identify genes in keratinocytes that are significantly influenced by PRGF. Therefore, we performed a whole transcriptome and gene ontology (GO) enrichment analysis of PRGF-stimulated human primary keratinocytes. This revealed an increased expression of genes involved in extracellular matrix (ECM) organization. Real-time polymerase chain reaction (PCR) and enzyme-linked immunosorbent assay (ELISA) analysis confirmed the PRGF-mediated induction of selected ECM-related factors such as transforming growth factor beta-induced protein, fibronectin 1, matrix metalloproteinase-9, transglutaminase 2, fermitin family member 1, collagen type I alpha 1 and collagen type XXII alpha 1. PRGF-induced expression of the above factors was influenced by blockade of the epidermal growth factor receptor (EGFR), a receptor playing a crucial role in wound healing. A differential induction of the investigated factors was also detected in skin explants exposed to PRGF and in experimentally generated in vivo wounds treated with Vivostat PRF®. Together, our study indicates that the induction of ECM-related factors may contribute to the beneficial wound-healing effects of PRGF-based formulations.

scholarly journals Epithelium-dependent extracellular matrix synthesis in transforming growth factor-beta 1-growth-inhibited mouse mammary gland.

1990 ◽  
Vol 110 (6) ◽  
pp. 2209-2219 ◽  
Author(s):  
G B Silberstein ◽  
P Strickland ◽  
S Coleman ◽  
C W Daniel
Keyword(s):  
Extracellular Matrix ◽  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Messenger Rna ◽  
Transforming Growth Factor ◽  
Type I ◽  
Tgf Beta ◽  
Matrix Synthesis ◽  
The Matrix ◽  
Growth Factor Beta

Exogenous transforming growth factor beta (TGF-beta 1) was shown in earlier studies to reversibly inhibit mouse mammary ductal growth. Using small plastic implants to treat regions of developing mammary glands in situ, we now report that TGF-beta 1 growth inhibition is associated with an ectopic accumulation of type I collagen messenger RNA and protein, as well as the glycosaminoglycan, chondroitin sulfate. Both macromolecules are normal components of the ductal extracellular matrix, which, under the influence of exogenous TGF-beta 1, became unusually concentrated immediately adjacent to the epithelial cells at the tip of the ductal growth points, the end buds. Stimulation of extracellular matrix was confined to aggregations of connective tissue cells around affected end buds and was not present around the TGF-beta 1 implants themselves, indicating that the matrix effect was epithelium dependent. Ectopic matrix synthesis was specific for TGF-beta 1 insofar as it was absent at ducts treated with other growth inhibitors, or at ducts undergoing normal involution in response to endogenous regulatory processes. These findings are consistent with the matrix-stimulating properties of TGF-beta 1 reported for other systems, but differ in their strict dependence upon epithelium. A possible role for endogenous TGF-beta 1 in modulating a mammary epithelium-stroma interaction is suggested.

Stretching-Induced Collagen Type I Synthesis in Human Tendon Fibroblasts Is Mediated by TGF-β1

2003 ◽  
Author(s):  
Guoguang Yang ◽  
Richard C. Crawford ◽  
James H.-C. Wang
Keyword(s):  
Protein Synthesis ◽  
Transforming Growth Factor Beta ◽  
Collagen Type ◽  
Transforming Growth Factor ◽  
Collagen Type I ◽  
Type I ◽  
Dependent Manner ◽  
Gene And Protein Expression ◽  
Mechanical Stretching ◽  
Tgf Β1

This study investigated the effect of cyclic mechanical stretching on the collagen gene expression and protein synthesis of human patellar tendon fibroblasts (HPTFs). We hypothesized that cyclic mechanical stretching of HPTFs would increase collagen synthesis via transforming growth factor-beta 1 (TGF-β1). To test the hypothesis, the tendon fibroblasts were cultured on microgrooved surfaces of silicone dishes under serum-free conditions. The cells were subjected to cyclic uniaxial stretching with a constant frequency and duration (0.5Hz, 4hr), and one of three stretching magnitudes (no stretch, 4%, and 8%) followed by 4 hours of rest. It was found that the gene and protein expression of both collagen type I and TGF-β1 were significantly increased in a stretching-magnitude dependent manner, whereas collagen type III gene and protein levels were not significantly changed. The exogenous addition of antibody to TGF-β1 eliminated the stretching-induced increase in collagen type I protein synthesis. The results therefore confirmed our working hypothesis and suggest that mechanical stretching of tendon fibroblasts can lead to matrix remodeling by modulating the collagen production of tendon fibroblasts, a process at least particially mediated by TGF-β1.

scholarly journals Effect of adipose tissue-derived stem cell injection in a rat model of urethral fibrosis

2016 ◽  
Vol 10 (5-6) ◽  
pp. 175 ◽  
Author(s):  
Premsant Sangkum ◽  
Faysal A. Yafi ◽  
Hogyoung Kim ◽  
Mostafa Bouljihad ◽  
Manish Ranjan ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Rat Model ◽  
Transforming Growth Factor Beta ◽  
Collagen Type ◽  
Transforming Growth Factor ◽  
Collagen Type I ◽  
Type I ◽  
Sprague Dawley ◽  
Group 10 ◽  
Tgf Β1

Introduction: We sought to evaluate the therapeutic effect of adipose tissue-derived stem cells (ADSCs) in a rat model of urethral fibrosis.Methods: Eighteen (18) male Sprague-Dawley rats (300‒350 g) were divided into three groups: (1) sham (saline injection); (2) urethral fibrosis group (10 μg transforming growth factor beta 1 (TGF-β1) injection); and (3) ADSCs group (10 μg TGF-β1 injection plus 2 x 105 ADSCs). Rat ADSCs were harvested from rat inguinal fat pads. All study animals were euthanized at two weeks afterurethral injection. Following euthanasia, rat urethral tissue was were quantitated by Western blot analysis. Results: TGF-β1 injection induced significant urethral fibrosis and increased collagen type I and III expression (p<0.05). Significant decrease in submucosal fibrosis and collagen type I and III expression were noted in the ADSCs group compared with the urethral fibrosis group (p<0.05). TGF-β1 induced fibrotic changes were ameliorated by injection of ADSCs.Conclusions: Local injection of ADSCs in a rat model of urethral fibrosis significantly decreased collagen type I and III. These findings suggest that ADSC injection may prevent scar formation and potentially serve as an adjunct treatment to increase the success rate of primary treatment for urethral stricture disease. Further animal and clinical studies are needed to confirm these results.

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