scholarly journals Silencing of Long Non-Coding RNA X Inactive Specific Transcript (Xist) Contributes to Suppression of Bronchopulmonary Dysplasia Induced by Hyperoxia in Newborn Mice via microRNA-101-3p and the transforming growth factor-beta 1 (TGF-β1)/Smad3 Axis

2020 ◽  
Vol 26 ◽  
Author(s):  
Wenhao Yuan ◽  
Xiaoyan Liu ◽  
Lingkong Zeng ◽  
Hanchu Liu ◽  
Baohuan Cai ◽  
...  
Keyword(s):  
Growth Factor ◽  
Bronchopulmonary Dysplasia ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Newborn Mice ◽  
Specific Transcript ◽  
Non Coding Rna ◽  
Growth Factor Beta ◽  
Long Non Coding Rna ◽  
Tgf Β1

Transforming Growth Factor Beta 1 Serum Levels in Patients with Preinvasive and Invasive Lesions of the Breast

2004 ◽  
Vol 19 (3) ◽  
pp. 236-239 ◽  
Author(s):  
A. Lebrecht ◽  
C. Grimm ◽  
G. Euller ◽  
E. Ludwig ◽  
E. Ulbrich ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Serum Levels ◽  
Breast Carcinogenesis ◽  
Receptor Status ◽  
Healthy Women ◽  
Growth Factor Beta ◽  
Tgf Β1

Transforming growth factor beta (TGF-β)1 is thought to be involved in breast carcinogenesis. TGF-β1 acts in an antiproliferative manner in the early stages of breast carcinogenesis, but promotes tumor progression and metastases in the advanced stages of the disease. No data have been published on serum TGF-β1 in breast cancer. We investigated TGF-β1 serum levels in patients with breast cancer (n=135), ductal carcinoma in situ (DCIS) I to III (n=67) or fibroadenoma (n=35), and in healthy women (n=40) to determine its value as a differentiation marker between malignant, pre-invasive and benign diseases and as a predictive marker for metastatic spread. Median (range) TGF-β1 serum levels in patients with breast cancer, DCIS I-III or benign breast lesions and in healthy women were 48.8 (18–82.4) pg/mL, 45.3 (26.9–58.3) pg/mL, 47.2 (17.2–80.5) pg/mL and 51.6 (30.9–65.1) pg/mL, respectively (p=0.2). In breast cancer patients TGF-β1 serum levels showed no statistically significant correlation with tumor stage, lymph node involvement, histological grade, estrogen receptor status and progesterone receptor status. Our data fail to indicate any correlation between serum TGF-β1 levels and clinicopathological parameters of breast diseases. Serum TGF-β1 levels do not provide clinical information in addition to established tumor markers.

scholarly journals Featured Article: TGF-β1 dominates extracellular matrix rigidity for inducing differentiation of human cardiac fibroblasts to myofibroblasts

2018 ◽  
Vol 243 (7) ◽  
pp. 601-612 ◽  
Author(s):  
Nathan Cho ◽  
Shadi E Razipour ◽  
Megan L McCain
Keyword(s):  
Extracellular Matrix ◽  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Cardiac Fibroblasts ◽  
Myofibroblast Differentiation ◽  
Matrix Rigidity ◽  
Growth Factor Beta ◽  
Human Cardiac Fibroblasts ◽  
Tgf Β1

Cardiac fibroblasts and their activated derivatives, myofibroblasts, play a critical role in wound healing after myocardial injury and often contribute to long-term pathological outcomes, such as excessive fibrosis. Thus, defining the microenvironmental factors that regulate the phenotype of cardiac fibroblasts and myofibroblasts could lead to new therapeutic strategies. Both chemical and biomechanical cues have previously been shown to induce myofibroblast differentiation in many organs and species. For example, transforming growth factor beta 1, a cytokine secreted by neutrophils, and rigid extracellular matrix environments have both been shown to promote differentiation. However, the relative contributions of transforming growth factor beta 1 and extracellular matrix rigidity, two hallmark cues in many pathological myocardial microenvironments, to the phenotype of human cardiac fibroblasts are unclear. We hypothesized that transforming growth factor beta 1 and rigid extracellular matrix environments would potentially have a synergistic effect on the differentiation of human cardiac fibroblasts to myofibroblasts. To test this, we seeded primary human adult cardiac fibroblasts onto coverslips coated with polydimethylsiloxane of various elastic moduli, introduced transforming growth factor beta 1, and longitudinally quantified cell phenotype by measuring expression of α-smooth muscle actin, the most robust indicator of myofibroblasts. Our data indicate that, although extracellular matrix rigidity influenced differentiation after one day of transforming growth factor beta 1 treatment, ultimately transforming growth factor beta 1 superseded extracellular matrix rigidity as the primary regulator of myofibroblast differentiation. We also measured expression of POSTN, FAP, and FSP1, proposed secondary indicators of fibroblast/myofibroblast phenotypes. Although these genes partially trended with α-smooth muscle actin expression, they were relatively inconsistent. Finally, we demonstrated that activated myofibroblasts incompletely revert to a fibroblast phenotype after they are re-plated onto new surfaces without transforming growth factor beta 1, suggesting differentiation is partially reversible. Our results provide new insights into how microenvironmental cues affect human cardiac fibroblast differentiation in the context of myocardial pathology, which is important for identifying effective therapeutic targets and dictating supporting cell phenotypes for engineered human cardiac disease models. Impact statement Heart disease is the leading cause of death worldwide. Many forms of heart disease are associated with fibrosis, which increases extracellular matrix (ECM) rigidity and compromises cardiac output. Fibrotic tissue is synthesized primarily by myofibroblasts differentiated from fibroblasts. Thus, defining the cues that regulate myofibroblast differentiation is important for understanding the mechanisms of fibrosis. However, previous studies have focused on non-human cardiac fibroblasts and have not tested combinations of chemical and mechanical cues. We tested the effects of TGF-β1, a cytokine secreted by immune cells after injury, and ECM rigidity on the differentiation of human cardiac fibroblasts to myofibroblasts. Our results indicate that differentiation is initially influenced by ECM rigidity, but is ultimately superseded by TGF-β1. This suggests that targeting TGF-β signaling pathways in cardiac fibroblasts may have therapeutic potential for attenuating fibrosis, even in rigid microenvironments. Additionally, our approach can be leveraged to engineer more precise multi-cellular human cardiac tissue models.

scholarly journals Comparison of Transforming Growth Factor-Beta 1 Concentration in Preeclampsia and Normal Pregnancy Women

2017 ◽  
Vol 9 (1) ◽  
pp. 49 ◽  
Author(s):  
Yusrawati Yusrawati ◽  
Dyka Aidina ◽  
Eti Yerizel
Keyword(s):  
Growth Factor ◽  
Pregnant Women ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Normal Pregnancy ◽  
Mean Difference ◽  
Blood Samples ◽  
The Mean ◽  
Growth Factor Beta ◽  
Tgf Β1

BACKGROUND: According to the theory of endothelial dysfunction, the pathogenesis of preeclampsia is associated with the imbalance of angiogenic and anti-angiogenic factors. Transforming growth factor-beta 1 (TGF-β1) has also proposed as a proangiogenic factor that influences preeclampsia. This study was conducted to compare a mean difference of TGF-β1 between preeclampsia and normal pregnancy.METHODS: This study was an observational crosssectional study with 25 subjects of pregnant women with preeclampsia and 25 subjects of normotensive pregnant women. The study was conducted in Dr. Reksodiwiryo Hospital, Bhayangkara Hospital, and Dr. Rasidin Hospital in Padang, Indonesia from October 2015 to January 2016. For the determination of TGF-β1 concentration, peripheral Abstract venous blood samples were taken. The blood samples wereanalyzed by enzyme-linked immunosorbent assay (ELISA) in Biomedical Laboratory, Faculty of Medicine, Andalas University. The mean difference was statically analyzed by independent samples T-test.RESULTS: The mean difference of TGF-β1 was lower in preeclampsia group than normal pregnancy group (2.02±0.99 ng/mL vs. 3.24±2.67 ng/mL; p<0.05).CONCLUSION: The TGF-β1 concentration was lower in pregnant women with preeclampsia. Thus, it may have a role as a marker in preeclampsia.KEYWORDS: preeclampsia, normal pregnancy, transforming growth factor-beta1, TGF-β1

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