Epithelial-Mesenchymal Transformation in the Embryonic Heart

2007 ◽  
pp. 40-55 ◽  
Author(s):  
Raymond B. Runyan ◽  
Ronald L. Heimark ◽  
Todd D. Camenisch ◽  
Scott E. Klewer
Keyword(s):  
Embryonic Heart ◽  
Mesenchymal Transformation

scholarly journals Extracellular Fibrillar Structure of Latent TGFβ Binding Protein-1: Role in TGFβ-dependent Endothelial-Mesenchymal Transformation during Endocardial Cushion Tissue Formation in Mouse Embryonic Heart

1997 ◽  
Vol 136 (1) ◽  
pp. 193-204 ◽  
Author(s):  
Yuji Nakajima ◽  
Kohei Miyazono ◽  
Mitsuyasu Kato ◽  
Masao Takase ◽  
Toshiyuki Yamagishi ◽  
...  
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Binding Protein ◽  
Three Dimensional ◽  
Collagen Gel ◽  
Embryonic Heart ◽  
Fibrillar Structure ◽  
Endocardial Cushion ◽  
Tissue Formation ◽  
Mesenchymal Transformation

Transforming growth factor-β (TGFβ) is a dimeric peptide growth factor which regulates cellular differentiation and proliferation during development. Most cells secrete TGFβ as a large latent TGFβ complex containing mature TGFβ, latency associated peptide, and latent TGFβ-binding protein (LTBP)-1. The biological role of LTBP-1 in development remains unclear. Using a polyclonal antiserum specific for LTBP-1 (Ab39) and three-dimensional collagen gel culture assay of embryonic heart, we examined the tissue distribution of LTBP-1 and its functional role during the formation of endocardial cushion tissue in the mouse embryonic heart. Mature TGFβ protein was required at the onset of the endothelial-mesenchymal transformation to initiate endocardial cushion tissue formation. Double antibody staining showed that LTBP-1 colocalized with TGFβ1 as an extracellular fibrillar structure surrounding the endocardial cushion mesenchymal cells. Immunogold electronmicroscopy showed that LTBP-1 localized to 40–100 nm extracellular fibrillar structure and 5–10-nm microfibrils. The anti–LTBP-1 antiserum (Ab39) inhibited the endothelial-mesenchymal transformation in atrio-ventricular endocardial cells cocultured with associated myocardium on a three-dimensional collagen gel lattice. This inhibitory effect was reversed by administration of mature TGFβ proteins in culture. These results suggest that LTBP-1 exists as an extracellular fibrillar structure and plays a role in the storage of TGFβ as a large latent TGFβ complex.

scholarly journals Generation of Smad7-Crerecombinase mice: A useful tool for the study of epithelial-mesenchymal transformation within the embryonic heart

genesis ◽  
2009 ◽  
Vol 47 (7) ◽  
pp. 469-475 ◽  
Author(s):  
Paige Snider ◽  
Sunyong Tang ◽  
Goldie Lin ◽  
Jian Wang ◽  
Simon J. Conway
Keyword(s):  
Embryonic Heart ◽  
Mesenchymal Transformation

Paeonol Inhibits Prostate Cancer Cell Invasion and Epithelial-Mesenchymal Transformation by Inactivation of STAT3 Pathway

2020 ◽  
Vol 19 (1) ◽  
pp. 15-20
Author(s):  
Junyi Xiang ◽  
Feng Huang ◽  
Renhua Huang ◽  
Jingzhan Su ◽  
Yulong Liu
Keyword(s):  
Prostate Cancer ◽  
Treatment Options ◽  
Surrogate Marker ◽  
Cytotoxic Agents ◽  
Potential Candidate ◽  
Dependent Manner ◽  
Ablation Therapy ◽  
Androgen Ablation ◽  
Mesenchymal Transformation ◽  
Dose Dependent

Prostate cancer is one of the leading causes of death in men all over the world. Treatment options such as androgen ablation therapy and cytotoxic agents have many undesirable side effects, narrow therapeutic windows, or other limitations. In this research, we have explored the effects of paeonol on prostate cancer and its mechanism of action. Our results have shown that paeonol reduced the viability of prostate cancer cells in a dose-dependent manner. The wound-healing assay, a surrogate marker of tumor metastasis, showed that the relative wound width of 10 µM group was less than that of 50 µM paeonol-treated cells. Besides, the results of the transwell assay also showed that the number of migrated cells was significantly lower after treatment with 50 µM paeonol compared to the 10 µM group. The Western blot results showed that paeonol treatment induced a decrease in the mesenchymal markers (vimentin and N-cadherin), while the epithelial marker (E-cadherin) increased in a dose-dependent manner suggesting that paeonol effectively inhibits the epithelial-mesenchymal transformation in PC3 cells. Furthermore, the expression of STAT3 and p-STAT3 was also decreased after paeonol treatment, which indicated that the STAT3 signaling pathway was inhibited by paeonol. To conclude, the results summarized in this paper suggest that paeonol could be a potential candidate in the treatment of prostate cancer.

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