scholarly journals In vitro effect of transforming growth factor-B1 (TGF-B1) on gene expression in human flexor digitorum profundus tendon cells

2016 ◽  
Vol 05 (03) ◽  
Author(s):  
Subhash C. Juneja
Keyword(s):  
Gene Expression ◽  
Growth Factor ◽  
Transforming Growth Factor ◽  
Flexor Digitorum Profundus ◽  
Tendon Cells ◽  
Flexor Digitorum ◽  
Vitro Effect ◽  
Flexor Digitorum Profundus Tendon

Supplementary Core Sutures Increase Resistance to Gapping for Flexor Digitorum Profundus Tendon to Bone Surface Repair – An in vitro Biomechanical Analysis

2005 ◽  
Vol 30 (3) ◽  
pp. 288-293 ◽  
Author(s):  
N. KUSANO ◽  
M. A. ZAEGEL ◽  
J. D. PLACZEK ◽  
R. H. GELBERMAN ◽  
M. J. SILVA
Keyword(s):  
Biomechanical Analysis ◽  
Flexor Digitorum Profundus ◽  
Gap Formation ◽  
Bone Anchor ◽  
Anchor Group ◽  
Insertion Sites ◽  
Flexor Digitorum ◽  
Flexor Digitorum Profundus Tendon ◽  
Repair Techniques

We evaluated the effects of two types of supplementary core sutures on the tensile properties and resistance to gap formation of flexor digitorum profundus (FDP) tendon-bone repairs. Forty-five human cadaver FDP tendons were sharply released from their insertion sites and repaired to bone utilizing one of three repair techniques: four-strand modified Becker core suture (Becker only), modified Becker plus a figure-of-eight supplementary core suture (Becker plus figure-of-eight), and modified Becker plus a supplementary core suture using a bone anchor (Becker plus anchor). Ultimate (maximum) force did not differ between repair groups. However, addition of a supplementary suture significantly increased repair-site stiffness and the 1, 2 and 3 mm gap forces, while decreasing the gap at 20 N compared to the Becker only suture ( P<0.05). The only difference between the two supplementary suture groups was that the Becker plus anchor group had increased stiffness compared to the Becker plus figure-of-eight group. In conclusion, a supplementary figure-of-eight suture and a supplementary suture using a bone anchor provide enhanced resistance to gap formation for FDP tendon–bone repairs.

scholarly journals Limited role for transforming growth factor–β pathway activation-mediated escape from VEGF inhibition in murine glioma models

2016 ◽  
Vol 18 (12) ◽  
pp. 1610-1621 ◽  
Author(s):  
Davide Mangani ◽  
Michael Weller ◽  
Emad Seyed Sadr ◽  
Edith Willscher ◽  
Katharina Seystahl ◽  
...  
Keyword(s):  
Gene Expression ◽  
Growth Factor ◽  
Transforming Growth Factor ◽  
Single Agent ◽  
Immune Response Gene ◽  
Tumor Control ◽  
Vegf Inhibition ◽  
Murine Glioma

AbstractBackgroundThe vascular endothelial growth factor (VEGF) and transforming growth factor (TGF)–β pathways regulate key biological features of glioblastoma. Here we explore whether the TGF-β pathway, which promotes angiogenesis, invasiveness, and immunosuppression, acts as an escape pathway from VEGF inhibition.MethodsThe role of the TGF-β pathway in escape from VEGF inhibition was assessed in vitro and in vivo and by gene expression profiling in syngeneic mouse glioma models.ResultsWe found that TGF-β is an upstream regulator of VEGF, whereas VEGF pathway activity does not alter the TGF-β pathway in vitro. In vivo, single-agent activity was observed for the VEGF antibody B20-4.1.1 in 3 and for the TGF-β receptor 1 antagonist LY2157299 in 2 of 4 models. Reduction of tumor volume and blood vessel density, but not induction of hypoxia, correlated with benefit from B20-4.1.1. Reduction of phosphorylated (p)SMAD2 by LY2157299 was seen in all models but did not predict survival. Resistance to B20 was associated with anti-angiogenesis escape pathway gene expression, whereas resistance to LY2157299 was associated with different immune response gene signatures in SMA-497 and GL-261 on transcriptomic profiling. The combination of B20 with LY2157299 was ineffective in SMA-497 but provided prolongation of survival in GL-261, associated with early suppression of pSMAD2 in tumor and host immune cells, prolonged suppression of angiogenesis, and delayed accumulation of tumor infiltrating microglia/macrophages.ConclusionsOur study highlights the biological heterogeneity of murine glioma models and illustrates that cotargeting of the VEGF and TGF-β pathways might lead to improved tumor control only in subsets of glioblastoma.

Gliding resistance after repair of partially lacerated human flexor digitorum profundus tendon in vitro

2001 ◽  
Vol 16 (8) ◽  
pp. 696-701 ◽  
Author(s):  
Chunfeng Zhao ◽  
Peter C. Amadio ◽  
Mark E. Zobitz ◽  
Toshimitsu Momose ◽  
Paulus Couvreur ◽  
...  
Keyword(s):  
Flexor Digitorum Profundus ◽  
Flexor Digitorum ◽  
Flexor Digitorum Profundus Tendon

scholarly journals Prostaglandin F2α promotes angiogenesis and embryo–maternal interactions during implantation

Reproduction ◽  
2016 ◽  
Vol 151 (5) ◽  
pp. 539-552 ◽  
Author(s):  
Piotr Kaczynski ◽  
Mariusz P Kowalewski ◽  
Agnieszka Waclawik
Keyword(s):  
Gene Expression ◽  
Growth Factor ◽  
Reproductive Tract ◽  
Transforming Growth Factor ◽  
Prostaglandin F2α ◽  
Expression Of Genes ◽  
Interleukin 1Α ◽  
Extraembryonic Membranes ◽  
Endothelial Growth Factor

AbstractImplantation in humans and other mammals is a critical period during which high embryonic mortality rates occur. Prostaglandins (PGs) are key mediators regulating interactions between the reproductive tract and the conceptus (embryo with extraembryonic membranes). Although the significance of PGF2α as a regulator of corpus luteum regression is well established, the role of its high amounts in the uterine lumen in most mammals, regardless of placentation type, during the implantation period remains unresolved. We hypothesized that PGF2α acting as an embryonic signal mediator contributes to pregnancy establishment. Using a porcine model, we demonstrated that the conceptus and its signal (estradiol-17β) elevated endometrial expression of PGF2α receptor (PTGFR)invivoandin vitro. PTGFR protein was expressed mainly in luminal epithelial (LE) and glandular epithelial cells and blood vessels in the endometrium. PGF2α stimulated the MAPK1/3 pathway in endometrial LE cells that coincided with elevated gene expression and secretion of endometrial vascular endothelial growth factor A (VEGFA) protein. PGF2α–PTGFR and adenylyl cyclase signaling were involved in this process. PGF2α-induced VEGFA acting through its receptors stimulated proliferation of endometrial endothelial cells. Moreover, PGF2α elevated gene expression of biglycan, matrix metalloproteinase 9, transforming growth factor β3, and interleukin 1α in the endometrium. In summary, our study indicates that PGF2α participates in pregnancy establishment by promoting angiogenesis and expression of genes involved in tissue remodeling and conceptus–maternal interactions in porcine endometrium during early pregnancy.

A phorbol ester-regulated ribonuclease system controlling transforming growth factor beta 1 gene expression in hematopoietic cells

1990 ◽  
Vol 10 (11) ◽  
pp. 5983-5990
Author(s):  
R E Wager ◽  
R K Assoian
Keyword(s):  
Gene Expression ◽  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Fold Increase ◽  
Mrna Levels ◽  
Tgf Beta ◽  
Growth Factor Beta

12-Tetradecanoylphorbol-13-acetate (TPA)-induced differentiation of U937 promonocytes leads to a 30-fold increase in transforming growth factor beta 1 (TGF-beta 1) gene expression, and this effect results from a stabilized mRNA. Similar up-regulation was detected in TPA-treated K562 erythroblasts but was absent from cell lines that do not differentiate in response to TPA. Related studies in vitro showed that postnuclear extracts of U937 promonocytes contain a ribonuclease system that degrades TGF-beta 1 mRNA selectively and that this system is completely blocked by prior treatment of the cells with TPA. These data identify a new mechanism for regulating TGF-beta 1 mRNA levels and allow us to establish the overall basis for control of TGF-beta 1 gene expression by activation of protein kinase C. Our results also provide a new basis for understanding the long-term up-regulation of TGF-beta 1 gene expression that can accompany hematopoietic cell differentiation.

scholarly journals A phorbol ester-regulated ribonuclease system controlling transforming growth factor beta 1 gene expression in hematopoietic cells.

1990 ◽  
Vol 10 (11) ◽  
pp. 5983-5990 ◽  
Author(s):  
R E Wager ◽  
R K Assoian
Keyword(s):  
Gene Expression ◽  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Fold Increase ◽  
Mrna Levels ◽  
Tgf Beta ◽  
Growth Factor Beta

12-Tetradecanoylphorbol-13-acetate (TPA)-induced differentiation of U937 promonocytes leads to a 30-fold increase in transforming growth factor beta 1 (TGF-beta 1) gene expression, and this effect results from a stabilized mRNA. Similar up-regulation was detected in TPA-treated K562 erythroblasts but was absent from cell lines that do not differentiate in response to TPA. Related studies in vitro showed that postnuclear extracts of U937 promonocytes contain a ribonuclease system that degrades TGF-beta 1 mRNA selectively and that this system is completely blocked by prior treatment of the cells with TPA. These data identify a new mechanism for regulating TGF-beta 1 mRNA levels and allow us to establish the overall basis for control of TGF-beta 1 gene expression by activation of protein kinase C. Our results also provide a new basis for understanding the long-term up-regulation of TGF-beta 1 gene expression that can accompany hematopoietic cell differentiation.

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