The effect of transforming growth factor B on luteal angiogenesis and function in vitro

2016 ◽  
Author(s):  
Robert Thompson ◽  
Kathryn Woad ◽  
Robert Robinson
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Factor B ◽  
And Function

scholarly journals Fibronectin is a survival factor for differentiated osteoblasts

1998 ◽  
Vol 111 (10) ◽  
pp. 1385-1393 ◽  
Author(s):  
R.K. Globus ◽  
S.B. Doty ◽  
J.C. Lull ◽  
E. Holmuhamedov ◽  
M.J. Humphries ◽  
...  
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Nuclear Condensation ◽  
Transforming Growth Factor Beta1 ◽  
Amino Terminal ◽  
Characteristic Features ◽  
Induced Apoptosis ◽  
Carboxy Terminal ◽  
And Function

The skeletal extracellular matrix produced by osteoblasts contains the glycoprotein fibronectin, which regulates the adhesion, differentiation and function of various adherent cells. Interactions with fibronectin are required for osteoblast differentiation in vitro, since fibronectin antagonists added to cultures of immature fetal calvarial osteoblasts inhibit their progressive differentiation. To determine if fibronectin plays a unique role in fully differentiated osteoblasts, cultures that had already formed mineralized nodules in vitro were treated with fibronectin antagonists. Fibronectin antibodies caused >95% of the cells in the mature cultures to display characteristic features of apoptosis (nuclear condensation, apoptotic body formation, DNA laddering) within 24 hours. Cells appeared to acquire sensitivity to fibronectin antibody-induced apoptosis as a consequence of differentiation, since antibodies failed to kill immature cells and the first cells killed were those associated with mature nodules. Intact plasma fibronectin, as well as fragments corresponding to the amino-terminal, cell-binding, and carboxy-terminal domains of fibronectin, independently induced apoptosis of mature (day-13), but not immature (day-4), osteoblasts. Finally, transforming growth factor-beta1 partially protected cells from the apoptotic effects of fibronectin antagonists. Thus, in the course of maturation cultured osteoblasts switch from depending on fibronectin for differentiation to depending on fibronectin for survival. These data suggest that fibronectin, together with transforming growth factor-beta1, may affect bone formation, in part by regulating the survival of osteoblasts.

Expression and function of the Transforming Growth Factor-b system in the human and rat enteric nervous system

2013 ◽  
Vol 25 (7) ◽  
pp. 601-e464 ◽  
Author(s):  
C. Hagl ◽  
K.-H. Schäfer ◽  
I. Hellwig ◽  
M. Barrenschee ◽  
J. Harde ◽  
...  
Keyword(s):  
Nervous System ◽  
Growth Factor ◽  
Enteric Nervous System ◽  
Transforming Growth Factor ◽  
Factor B ◽  
And Function

Regulation and function of extracellular matrix intestinal epithelial restitution in vitro

1996 ◽  
Vol 271 (5) ◽  
pp. G729-G740 ◽  
Author(s):  
M. Goke ◽  
A. Zuk ◽  
D. K. Podolsky
Keyword(s):  
Extracellular Matrix ◽  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Attachment Site ◽  
Intestinal Epithelial ◽  
Epithelial Injury ◽  
Epithelial Restitution ◽  
And Function

Repair of epithelial injury in the gastrointestinal tract is initially accomplished by migration of epithelial cells from the wound edge (“restitution”). To assess expression and function of the extracellular matrix (ECM) in the restitution phase after epithelial injury, in vitro studies using wounded monolayers or a rat intestinal epithelium-derived cell line (IEC-6) were undertaken. IEC-6 cells expressed fibronectin (FN) mRNA and protein in large amounts and lesser quantities of laminin-beta 1 (LN beta 1) and LN gamma 1. Collagen IV (Col IV) was weakly expressed, and LN alpha 1 was not detected. After wounding a significant decrease in FN, LN beta 1, LN gamma 1, and Col IV alpha 1 mRNA steady-state levels was observed; mean content 24 h after wounding was reduced by 75–90%. FN, LN, and Col IV proteins were also reduced. The downregulation of these ECM transcripts and proteins could be substantially prevented by transforming growth factor-beta 1, a restitution-promoting growth factor. In addition to changes of expression, the distribution of FN and LN was also altered in migrating cells after wounding, as assessed by immunofluorescence. Arg-Gly-Asp peptides that recognize the major cell attachment site on FN and antibodies recognizing the main noncollagenous domain of Col IV inhibited cell migration, but immunoneutralizing anti-LN antisera did not affect restitution. In conclusion, although paradoxically downregulated after wounding, ECM proteins, in particular FN and Col IV molecules, are able to enhance intestinal epithelial restitution.

Apigenin Alleviates Renal Fibroblast Activation through AMPK and ERK Signaling Pathways In Vitro

2020 ◽  
Vol 21 (11) ◽  
pp. 1107-1118
Author(s):  
Ningning Li ◽  
Zhan Wang ◽  
Tao Sun ◽  
Yanfei Lei ◽  
Xianghua Liu ◽  
...  
Keyword(s):  
Renal Fibrosis ◽  
Transforming Growth Factor ◽  
Therapeutic Potential ◽  
Protective Role ◽  
Fibroblast Proliferation ◽  
Fibroblast Activation ◽  
And Function ◽  
Activated Fibroblasts ◽  
Tgf Β1

Objective: Renal fibrosis is a common pathway leading to the progression of chronic kidney disease. Activated fibroblasts contribute remarkably to the development of renal fibrosis. Although apigenin has been demonstrated to play a protective role from fibrotic diseases, its pharmacological effect on renal fibroblast activation remains largely unknown. Materials and Methods: Here, we examined the functional role of apigenin in the activation of renal fibroblasts response to transforming growth factor (TGF)-β1 and its potential mechanisms. Cultured renal fibroblasts (NRK-49F) were exposed to apigenin (1, 5, 10 and 20 μM), followed by the stimulation of TGF-β1 (2 ng/mL) for 24 h. The markers of fibroblast activation were determined. In order to confirm the anti-fibrosis effect of apigenin, the expression of fibrosis-associated genes in renal fibroblasts was assessed. As a consequence, apigenin alleviated fibroblast proliferation and fibroblastmyofibroblast differentiation induced by TGF-β1. Result: Notably, apigenin significantly inhibited the fibrosis-associated genes expression in renal fibroblasts. Moreover, apigenin treatment significantly increased the phosphorylation of AMP-activated protein kinase (AMPK). Apigenin treatment also obviously reduced TGF-β1 induced phosphorylation of ERK1/2 but not Smad2/3, p38 and JNK MAPK in renal fibroblasts. Conclusion: In a summary, these results indicate that apigenin inhibits renal fibroblast proliferation, differentiation and function by AMPK activation and reduced ERK1/2 phosphorylation, suggesting it could be an attractive therapeutic potential for the treatment of renal fibrosis.

Met -/- kidneys express epithelial cells that chemotax and form tubules in response to EGF receptor ligands

1997 ◽  
Vol 272 (2) ◽  
pp. F222-F228
Author(s):  
C. Kjelsberg ◽  
H. Sakurai ◽  
K. Spokes ◽  
C. Birchmeier ◽  
I. Drummond ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epithelial Cell ◽  
Egf Receptor ◽  
Transforming Growth Factor ◽  
Growth Factor Receptor ◽  
Receptor Ligands ◽  
Tubule Formation ◽  
Human Papillomavirus 16 ◽  
Immortalized Cells

The growth factor/receptor combination of hepatocyte growth factor (HGF)/c-met has been postulated to be critical for mesenchymal-to-epithelial conversion and tubule formation in the developing kidney. We therefore isolated and immortalized cells from embryonic kidneys of met -/- transgenic mice to determine whether these cells were epithelial and able to chemotax and form tubules in vitro. The cells were immortalized with retrovirus expressing human papillomavirus 16 (HPV 16) E6/E7 genes. Two rapidly dividing clones were isolated and found to express the epithelial cell markers cytokeratin, zonula occludens-1, and E-cadherin but not to express the fibroblast marker vimentin. The met -/- cells were able to chemotax in response to epidermal growth factor and transforming growth factor-alpha (TGF-alpha) and form tubules in vitro in response to TGF-alpha but not HGF. These experiments suggest that the HGF/c-met axis is not essential for epithelial cell development in the embryonic kidney and demonstrate that other growth factors are capable of supporting early tubulogenesis.

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