Isoform-specific role of transforming growth factor-β2 in the regulation of proliferation and differentiation of murine adrenal chromaffin cells in vivo

2004 ◽  
Vol 78 (4) ◽  
pp. 493-498 ◽  
Author(s):  
Belal Rahhal ◽  
Nicole Dünker ◽  
Stephanie Combs ◽  
Kerstin Krieglstein
Keyword(s):  
Growth Factor ◽  
Chromaffin Cells ◽  
Transforming Growth Factor ◽  
Adrenal Chromaffin Cells ◽  
Proliferation And Differentiation ◽  
Regulation Of Proliferation ◽  
Transforming Growth Factor Β2 ◽  
Adrenal Chromaffin

In vivo effects of transforming growth factor-β2 in ovariectomized rats

1993 ◽  
Vol 22 (3) ◽  
pp. 209-220 ◽  
Author(s):  
Dike N. Kalu ◽  
Elena Salerno ◽  
Yoshikazu Higami ◽  
Chung Ching Liu ◽  
Fabrizio Ferraro ◽  
...  
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Ovariectomized Rats ◽  
Transforming Growth Factor Β2 ◽  
In Vivo Effects

scholarly journals Dominant Role of Mitochondria in Clearance of Large Ca2+ Loads from Rat Adrenal Chromaffin Cells

Neuron ◽  
1996 ◽  
Vol 16 (1) ◽  
pp. 219-228 ◽  
Author(s):  
James Herrington ◽  
Young Bae Park ◽  
Donner F Babcock ◽  
Bertil Hille
Keyword(s):  
Chromaffin Cells ◽  
Dominant Role ◽  
Adrenal Chromaffin Cells ◽  
Adrenal Chromaffin

Absence of transforming growth factor beta 1 in murine platelets reduces neointima formation without affecting arterial thrombosis

2017 ◽  
Vol 117 (09) ◽  
pp. 1782-1797 ◽  
Author(s):  
Eva Schütz ◽  
Magdalena L. Bochenek ◽  
Dennis R. Riehl ◽  
Markus Bosmann ◽  
Thomas Münzel ◽  
...  
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Smooth Muscle Actin ◽  
Arterial Injury ◽  
Neointima Formation ◽  
Proliferating Cells ◽  
The Media

SummaryPlatelet degranulation at the site of vascular injury prevents bleeding and may affect the chronic vascular wound healing response. Transforming Growth Factor (TGF)-β1 is a major component of platelet α-granules known to accumulating in thrombi. It was our aim to determine the role of TGFβ1 released from activated platelets for neointima formation following arterial injury and thrombosis. Mice with platelet-specific deletion of TGFβ1 (Plt.TGFβ-KO) underwent carotid artery injury. Immunoassays confirmed the absence of active TGFβ1 in platelet releasates and plasma of Plt.TGFβ-KO mice. Whole blood analyses revealed similar haematological parameters, and tail cut assays excluded major bleeding defects. Platelet aggregation and the acute thrombotic response to injury in vivo did not differ between Plt.TGFβ-KO and Plt.TGFβ-WT mice. Morphometric analysis revealed that absence of TGFβ1 in platelets resulted in a significant reduction of neointima formation with lower neointima area, intima-to-media ratio, and lumen stenosis. On the other hand, the media area was enlarged in mice lacking TGFβ1 in platelets and contained increased amounts of proteases involved in latent TGFβ activation, including MMP2, MMP9 and thrombin. Significantly increased numbers of proliferating cells and cells expressing the mesenchymal markers platelet-derived growth factor receptor-β or fibroblast-specific protein-1, and the macrophage antigen F4/80, were observed in the media of Plt.TGFβ-KO mice, whereas the medial smooth muscle-actin-immuno-positive area and collagen content did not differ between genotypes. Our findings support an essential role for platelet-derived TGFβ1 for the vascular remodelling response to arterial injury, apparently independent from the role of platelets in thrombosis or haemostasis.Supplementary Material to this article is available online at www.thrombosis-online.com.

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