EGF Suppresses the Initiation and Drives the Reversion of TGF-β1-induced Transition in Hepatic Oval Cells Showing the Plasticity of Progenitor Cells

2015 ◽  
Vol 230 (10) ◽  
pp. 2362-2370 ◽  
Author(s):  
Ping Wang ◽  
AI-Ting Yang ◽  
Min Cong ◽  
Tian-Hui Liu ◽  
Dong Zhang ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Oval Cells ◽  
Hepatic Oval Cells ◽  
Tgf Β1

scholarly journals Diabetic Impairment of Nitric Oxide Generation in CD34 + Hematopoietic Stem/ Progenitor Cells is mediated by TGF‐β1/TSP‐1/CD47 pathway

2021 ◽  
Vol 35 (S1) ◽  
Author(s):  
Jesmin Jahan ◽  
Brian Meissner ◽  
Ildamaris Montes de Oca ◽  
C. Yang‐Lopez ◽  
Julio Quiroz‐Olvera ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Progenitor Cells ◽  
Hematopoietic Stem ◽  
Tgf Β1

Biphasic effect of pioglitazone on isolated human endothelial progenitor cells: Involvement of peroxisome proliferator-activated receptor-γ and transforming growth factor-β1

2007 ◽  
Vol 97 (06) ◽  
pp. 988-997 ◽  
Author(s):  
Mihail Hristov ◽  
Denis Gümbel ◽  
Teresa Tejerina ◽  
Santiago Redondo ◽  
Christian Weber
Keyword(s):  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Peroxisome Proliferator ◽  
Endothelial Progenitor ◽  
Peroxisome Proliferator Activated Receptor ◽  
Ppar Γ ◽  
Patients With Diabetes ◽  
Tgf Β1

SummaryEndothelial progenitor cells (EPCs) have been implicated in vascular repair and found to be functionally impaired in patients with diabetes. We evaluated the effects of the anti-diabetic drug pioglitazone on human EPC function and the involvement of PPAR-γ and TGF-β1. EPCs in culture were characterized at day 7 by the development of colony-forming units (CFUs) and flow cytometry assessment of differentiation marker (DiI-ac-LDL/lectin, KDR and CD31). Adhesion on fibronectin and fibrinogen in flow was analyzed as functional parameter. Treatment with pioglitazone for 72 hours increased the number of EPC-CFUs, DiI-ac-LDL+/lectin+, CD31+ and KDR+ EPCs at 1 μM but not at 10 μM. Since pioglitazone did not significantly alter proliferation and apoptosis in cultured EPCs, the increase in EPC number was most likely attributable to augmented adhesion and differentiation. Indeed, pioglitazone increased EPC adhesion in flow at 1 μM, an effect prevented by PPAR-γ and β2-integrin blockade. In contrast, pioglitazone did not promote EPC adhesion at 10 μM; however, increased adhesion became evident by co-incubation with a blocking TGF-β1 antibody. As determined by ELISA, pioglitazone induced a persistent increase in TGF-β1 secretion only at 10 μM when a significantly elevated expression of endoglin, the accessory receptor forTGF-β1, was also observed. Taken together, pioglitazone exerts biphasic effects on the function of isolated EPCs, causing a PPAR-γ-dependent stimulation at 1 μM and a TGF-β1-mediated suppression at 10 μM. These results may help to define optimal therapeutic doses of pioglitazone for improving endothelial dysfunction.

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