scholarly journals Characteristics of epidemiological and molecular relationships between allergic diseases and helminth disorders in Opisthorchis endemic region

2008 ◽  
Vol 7 (4) ◽  
pp. 37-44
Author(s):  
L. M. Ogorodova ◽  
O. S. Fyodorova ◽  
M. B. Freidin ◽  
M. B. Vasil’yeva ◽  
N. A. Cherevko ◽  
...  
Keyword(s):  
Transforming Growth Factor Beta ◽  
Molecular Mechanisms ◽  
Transforming Growth Factor ◽  
Phenotypic Variability ◽  
Allergic Diseases ◽  
Endemic Region ◽  
Gene Differential Expression ◽  
Atopic Bronchial Asthma ◽  
Growth Factor Beta ◽  
Molecular Relationships

To elucidate the molecular mechanisms of O. felineus impact into phenotypic variability of allergic diseases in the opisthorchis endemic region, we studied 104 patients with opisthorchosis, 92 patients with atopic bronchial asthma, 52 patients with a combination of both diseases, and 120 healthy persons. Standard clinical, immunological, and genetic methods were used. An association of opisthorchis invasion with the improvement of lung function signs and bronchial hyperreactivity was found. It was established, that IL-4-dependent mechanisms of atopy were suppressed by O. felineus antigens, in particular due to hyperproduction of IL-10 and transforming growth factor-beta. However, IL-5-dependant mechanisms were supported. A phenomenology of the cytokine gene differential expression was established, disclosing the molecular basis of the immune system function in diseases with polar immune response in the helminth endemic region.

The Role of TGF-β Signaling Regulatory MicroRNAs in the Pathogenesis of Colorectal Cancer

2019 ◽  
Vol 24 (39) ◽  
pp. 4611-4618 ◽  
Author(s):  
Reyhaneh Moradi-Marjaneh ◽  
Majid Khazaei ◽  
Gordon A. Ferns ◽  
Seyed H. Aghaee-Bakhtiari
Keyword(s):  
Colorectal Cancer ◽  
Signaling Pathway ◽  
Transforming Growth Factor Beta ◽  
Molecular Mechanisms ◽  
Transforming Growth Factor ◽  
Growth Factor Beta ◽  
And Migration ◽  
Multiple Signaling ◽  
Tgf Β1

Colorectal cancer (CRC) is one of the most common cancers globally and is associated with a high mortality rate. The transforming growth factor beta (TGF-β) signaling pathway plays an important role in normal intestinal tissue function, but has also been implicated in the development of CRC. MicroRNAs (miRNAs) have also recently emerged as important regulators of cancer development and progression. They act by targeting multiple signaling pathways including the TGF-β signaling pathway. There is growing evidence demonstrating that miRNAs target various components of the TGF-β signaling pathway, including TGF-β1, TGF-β2, regulatory SMADs (SMAD1, 2, 3, 5 and 9), co-mediator SMAD4, inhibitory SMADs (SMAD6 and 7) and the TGF-β receptors, and thereby alter the proliferation and migration of CRC cells. In this review, we summarize the data concerning the interaction between TGF-β signaling pathway and miRNAs with the aim to better understanding the CRC molecular mechanisms and hence better management of this disease.

scholarly journals P.106 Thrombospondin 1 mediates transforming growth factor beta induced premature senescence in primary glioblastoma cells

2016 ◽  
Vol 43 (S2) ◽  
pp. S45-S45
Author(s):  
R Kumar ◽  
I Lorimer
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Molecular Mechanisms ◽  
Transforming Growth Factor ◽  
Global Gene Expression ◽  
Premature Senescence ◽  
Primary Glioblastoma ◽  
Thrombospondin 1 ◽  
Growth Factor Beta ◽  
Novel Therapeutic Strategies

Background: Glioblastoma is the most common primary malignant brain tumor. Primary Glioblastoma (PriGO) cells are key drivers of glioblastoma. Senescence is the irreversible growth arrest of cells with continued metabolic activity. Recently, I discovered PriGO cells undergo premature senescence in response to Fetal Bovine Serum (FBS). Determining the underlying molecular mechanisms may allow development of novel therapeutic strategies to decrease the malignant potential of glioblastoma. Methods: Global gene expression changes in PriGO cells treated with serum were analyzed and compared to untreated cells. Senescence was determined by the Senescence-Associated-Beta-Galactosidase (SA-B-Gal) assay. Results: PriGO cells treated with serum demonstrated increased expression of genes in the Transforming Growth Factor Beta (TGF-B) pathway, such as Thrombospondin 1 (TSP1), compared to untreated cells. TGF-B treatment of PriGO cells significantly increased senescence compared to untreated cells. Treatment of PriGO cells with serum and the TGF-B inhibitor SB431542 led to a decrease in senescence compared to serum only treated cells. Treatment of PriGO cells with serum and the TSP1 inhibitor LSKL led to a reduction in senescence compared to serum only treated cells. Conclusions: Our data identifies TGF-B as an important component of serum responsible for inducing senescence in PriGO cells. Furthermore, TGF-B induced senescence in PriGO cells is in part mediated by TSP1.

scholarly journals Molecular Mechanisms Controlling Bone Formation during Fracture Healing and Distraction Osteogenesis

2008 ◽  
Vol 87 (2) ◽  
pp. 107-118 ◽  
Author(s):  
Z.S. AI-Aql ◽  
A.S. Alagl ◽  
D.T. Graves ◽  
L.C. Gerstenfeld ◽  
T.A. Einhorn
Keyword(s):  
Fracture Healing ◽  
Distraction Osteogenesis ◽  
Transforming Growth Factor Beta ◽  
Bone Repair ◽  
Molecular Mechanisms ◽  
Transforming Growth Factor ◽  
Biological Activities ◽  
Fracture Repair ◽  
Relative Importance ◽  
Growth Factor Beta

Fracture healing and distraction osteogenesis have important applications in orthopedic, maxillofacial, and periodontal treatment. In this review, the cellular and molecular mechanisms that regulate fracture repair are contrasted with bone regeneration that occurs during distraction osteogenesis. While both processes have many common features, unique differences are observed in the temporal appearance and expression of specific molecular factors that regulate each. The relative importance of inflammatory cytokines in normal and diabetic healing, the transforming growth factor beta superfamily of bone morphogenetic mediators, and the process of angiogenesis are discussed as they relate to bone repair. A complete summary of biological activities and functions of various bioactive factors may be found at COPE (Cytokines & Cells Online Pathfinder Encyclopedia), http://www.copewithcytokines.de/cope.cgi .

scholarly journals Role of PDGF-A expression in the control of vascular smooth muscle cell growth by transforming growth factor-beta.

1990 ◽  
Vol 111 (1) ◽  
pp. 239-247 ◽  
Author(s):  
R A Majack ◽  
M W Majesky ◽  
L V Goodman
Keyword(s):  
Smooth Muscle ◽  
Growth Factor ◽  
Vascular Smooth Muscle ◽  
Transforming Growth Factor Beta ◽  
Molecular Mechanisms ◽  
Transforming Growth Factor ◽  
De Novo ◽  
Tgf Beta ◽  
Gene And Protein Expression ◽  
Growth Factor Beta

Transforming growth factor-beta (TGF-beta) is a multifunctional regulatory peptide that can inhibit or promote the proliferation of cultured vascular smooth muscle cells (SMCs), depending on cell density (Majack, R. A. 1987. J. Cell Biol. 105:465-471). In this study, we have examined the mechanisms underlying the growth-promoting effects of TGF-beta in confluent SMC cultures. In mitogenesis assays using confluent cells, TGF-beta was found to potentiate the stimulatory effects of serum, PDGF, and basic fibroblast growth factor (bFGF), and was shown to act individually as a mitogen for SMC. In gene and protein expression experiments, TGF-beta was found to regulate the expression of PDGF-A and thrombospondin, two potential mediators of SMC proliferative events. The induction of thrombospondin protein and mRNA was density-dependent, delayed relative to its induction by PDGF and, based on cycloheximide experiments, appeared to depend on the de novo synthesis of an intermediary protein (probably PDGF-A). The relationship between PDGF-A expression and TGF-beta-mediated mitogenesis was investigated, and it was determined that a PDGF-like activity (probably PDGF-A) was the biological mediator of the growth-stimulatory effects of TGF-beta on confluent SMC. The effects of purified homodimers of PDGF-A on SMC replication were investigated, and it was determined that PDGF-AA was mitogenic for cultured SMC, particularly when used in combination with other growth factors such as bFGF and PDGF-BB. The data suggest several molecular mechanisms that may account for the ability of TGF-beta to promote the growth of confluent SMC in culture.

scholarly journals Structural biology of the TGFβ family

2019 ◽  
Vol 244 (17) ◽  
pp. 1530-1546 ◽  
Author(s):  
Erich J Goebel ◽  
Kaitlin N Hart ◽  
Jason C McCoy ◽  
Thomas B Thompson
Keyword(s):  
Growth Factor ◽  
Signaling Pathway ◽  
Structural Biology ◽  
Transforming Growth Factor Beta ◽  
Molecular Mechanisms ◽  
Transforming Growth Factor ◽  
Biological Processes ◽  
Tgfβ Signaling ◽  
Growth Factor Beta ◽  
Tgfβ Signaling Pathway

The transforming growth factor beta (TGFβ) signaling pathway orchestrates a wide breadth of biological processes, ranging from bone development to reproduction. Given this, there has been a surge of interest from the drug development industry to modulate the pathway – at several points. This review discusses and provides additional context for several layers of the TGFβ signaling pathway from a structural biology viewpoint. The combination of structural techniques coupled with biophysical studies has provided a foundational knowledge of the molecular mechanisms governing this high impact, ubiquitous pathway, underlying many of the current therapeutic pursuits. This work seeks to consolidate TGFβ-related structural knowledge and educate other researchers of the apparent gaps that still prove elusive. We aim to highlight the importance of these structures and provide the contextual information to understand the contribution to the field, with the hope of advancing the discussion and exploration of the TGFβ signaling pathway. Impact statement The transforming growth factor beta (TGFβ) signaling pathway is a multifacetted and highly regulated pathway, forming the underpinnings of a large range of biological processes. Here, we review and consolidate the key steps in TGFβ signaling using literature rooted in structural and biophysical techniques, with a focus on molecular mechanisms and gaps in knowledge. From extracellular regulation to ligand–receptor interactions and intracellular activation cascades, we hope to provide an introductory base for understanding the TGFβ pathway as a whole.

Sign in / Sign up

Export Citation Format

Share Document