scholarly journals TGF-β-Operated Growth Inhibition and Translineage Commitment into Smooth Muscle Cells of Periodontal Ligament-Derived Endothelial Progenitor Cells through Smad- and p38 MAPK-Dependent Signals

2012 ◽  
Vol 8 (7) ◽  
pp. 1062-1074 ◽  
Author(s):  
Mariko Yoshida ◽  
Naoto Okubo ◽  
Naoyuki Chosa ◽  
Tomokazu Hasegawa ◽  
Miho Ibi ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Growth Inhibition ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
P38 Mapk ◽  
Periodontal Ligament ◽  
Muscle Cells ◽  
Endothelial Progenitor

EFFECTS OF STRETCHED VASCULAR ENDOTHELIAL CELLS AND SMOOTH MUSCLE CELLS ON DIFFERENTIATION OF ENDOTHELIAL PROGENITOR CELLS

2013 ◽  
Vol 13 (02) ◽  
pp. 1350050 ◽  
Author(s):  
ZHI-QIANG YAN ◽  
YU-QING LI ◽  
BIN-BIN CHENG ◽  
QING-PING YAO ◽  
LI-ZHI GAO ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Vascular Endothelial Cells ◽  
Cyclic Strain ◽  
Muscle Cells ◽  
Endothelial Progenitor ◽  
Vessel Injury

Differentiation of endothelial progenitor cells (EPCs) plays important roles in endothelial repair after vessel injury. Endothelial cells (ECs), vascular smooth muscle cells (VSMCs), and mechanical forces, including cyclic strain and shear stress, synergistically form the microenvironment of EPCs. However, the synergistic effect of cyclic strain, ECs, and VSMCs on the differentiation of EPCs remains unclear. In the present study, EPCs were indirectly co-cultured with stretched ECs or VSMCs that were subjected to 5%, 1.25-Hz cyclic strain by using FX-4000T Strain Unit. Then, Western blot and real-time PCR were used to examine expressions of EC marker, i.e., vascular cell adhesion molecule (VCAM), CD31, von Willebrand factor (vWF); VSMC markers, i.e., α-actin, Calponin, and SM22α; and signaling molecules, i.e., p-Akt and p-ERK. In static, co-cultured ECs increased expression of VCAM and phosphorylation of Akt and ERK in EPCs compared to that in EPCs cultured alone. In EPCs, co-cultured VSMCs decreased expressions of CD31 and vWF, but increased expressions of Calponin and SM22α. Stretched ECs reduced expressions of CD31 and vWF, enhanced Calponin and SM22α, and repressed phosphorylations of Akt and ERK in EPCs. Stretched VSMCs decreased CD31, increased Calponin and SM22α expressions, and repressed phosphorylation of Akt and ERK in EPCs. Our results suggest that ECs promoted EPC differentiation into ECs in static. VSMCs in static, as well as stretched ECs and stretched VSMCs, promoted EPC differentiation into VSMCs. Phosphorylation of Akt and ERK might be involved in EPC differentiation, mediated by the stretched ECs and VSMCs.

Endothelial Progenitor Cells Modulate the Phenotype of Smooth Muscle Cells and Increase Their Neointimal Accumulation Following Vascular Injury

2021 ◽  
Author(s):  
Sebastian F. Mause ◽  
Elisabeth Ritzel ◽  
Annika Deck ◽  
Felix Vogt ◽  
Elisa A. Liehn
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Progenitor Cells ◽  
Conditioned Medium ◽  
Endothelial Progenitor Cells ◽  
Vascular Injury ◽  
Muscle Cells ◽  
Neointima Formation ◽  
Endothelial Progenitor ◽  
Direct Cell

Abstract Background Smooth muscle cells (SMCs) are the main driver of neointima formation and restenosis following vascular injury. In animal models, endothelial progenitor cells (EPCs) accelerate endothelial regeneration and reduce neointima formation after arterial injury; however, EPC-capture stents do not reduce target vessel failure compared with conventional stents. Here we examined the influence of EPCs on features of SMCs pivotal for their impact on injury-induced neointima formation including proliferation, migration, and phenotype switch. Methods and Results EPCs, their conditioned medium, and EPC-derived microparticles induced proliferation of SMCs while limiting their apoptosis. In transwell membrane experiments and scratch assays, EPCs stimulated migration of SMCs and accelerated their recovery from scratch-induced injury. Treatment of SMCs with an EPC-derived conditioned medium or microparticles triggered transformation of SMCs toward a synthetic phenotype. However, co-cultivation of EPCs and SMCs enabling direct cell–cell contacts preserved their original phenotype and protected from the transformative effect of SMC cholesterol loading. Adhesion of EPCs to SMCs was stimulated by SMC injury and reduced by blocking CXCR2 and CCR5. Interaction of EPCs with SMCs modulated their secretory products and synergistically increased the release of selected chemokines. Following carotid wire injury in athymic mice, injection of EPCs resulted not only in reduced neointima formation but also in altered cellular composition of the neointima with augmented accumulation of SMCs. Conclusion EPCs stimulate proliferation and migration of SMCs and increase their neointimal accumulation following vascular injury. Furthermore, EPCs context-dependently modify the SMC phenotype with protection from the transformative effect of cholesterol when a direct cell–cell contact is established.

Paclitaxel and sirolimus differentially affect growth and motility of endothelial progenitor cells and coronary artery smooth muscle cells

2011 ◽  
Vol 7 (K) ◽  
pp. K32-K42 ◽  
Author(s):  
Yvonne Clever ◽  
Bodo Cremers ◽  
Bastian Krauß ◽  
Michael Böhm ◽  
Ulrich Speck ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Coronary Artery ◽  
Smooth Muscle Cells ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Muscle Cells ◽  
Endothelial Progenitor

Expression of TGF-beta1 in Smooth Muscle Cells Regulates Endothelial Progenitor Cells Migration and Differentiation1

2005 ◽  
Vol 125 (2) ◽  
pp. 151-156 ◽  
Author(s):  
Chuhong Zhu ◽  
Dajun Ying ◽  
Dinghua Zhou ◽  
Jianhong Mi ◽  
Wei Zhang ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Muscle Cells ◽  
Endothelial Progenitor
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