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 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 Elevated transforming growth factor-beta 1 (TGF-β1) levels in human fracture healing

Injury ◽  
2011 ◽  
Vol 42 (8) ◽  
pp. 833-837 ◽  
Author(s):  
Kambiz Sarahrudi ◽  
Anita Thomas ◽  
Mehdi Mousavi ◽  
Georg Kaiser ◽  
Julia Köttstorfer ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fracture Healing ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Growth Factor Beta ◽  
Tgf Β1

scholarly journals Transforming growth factor-beta and the initiation of chondrogenesis and osteogenesis in the rat femur.

1990 ◽  
Vol 110 (6) ◽  
pp. 2195-2207 ◽  
Author(s):  
M E Joyce ◽  
A B Roberts ◽  
M B Sporn ◽  
M E Bolander
Keyword(s):  
Growth Factor ◽  
Bone Formation ◽  
Fracture Healing ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Tgf Beta ◽  
Intramembranous Bone ◽  
Growth Factor Beta ◽  
Beta 2 ◽  
Intramembranous Bone Formation

We have investigated the ability of exogenous transforming growth factor-beta (TGF-beta) to induce osteogenesis and chondrogenesis, critical events in both bone formation and fracture healing. Daily injections of TGF-beta 1 or 2 into the subperiosteal region of newborn rat femurs resulted in localized intramembranous bone formation and chondrogenesis. After cessation of the injections, endochondral ossification occurred, resulting in replacement of cartilage with bone. Gene expression of type II collagen and immunolocalization of types I and II collagen were detected within the TGF-beta-induced cartilage and bone. Moreover, injection of TGF-beta 2 stimulated synthesis of TGF-beta 1 in chondrocytes and osteoblasts within the newly induced bone and cartilage, suggesting positive autoregulation of TGF-beta. TGF-beta 2 was more active in vivo than TGF-beta 1, stimulating formation of a mass that was on the average 375% larger at a comparable dose (p less than 0.001). With either TGF-beta isoform, the dose of the growth factor determined which type of tissue formed, so that the ratio of cartilage formation to intramembranous bone formation decreased as the dose was lowered. For TGF-beta 1, reducing the daily dose from 200 to 20 ng decreased the cartilage/intramembranous bone formation ratio from 3.57 to zero (p less than 0.001). With TGF-beta 2, the same dose change decreased the ratio from 3.71 to 0.28 (p less than 0.001). These data demonstrate that mesenchymal precursor cells in the periosteum are stimulated by TGF-beta to proliferate and differentiate, as occurs in embryologic bone formation and early fracture healing.

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