scholarly journals Oestrogen signalling in white adipose progenitor cells inhibits differentiation into brown adipose and smooth muscle cells

2014 ◽  
Vol 5 (1) ◽  
Author(s):  
Kfir Lapid ◽  
Ajin Lim ◽  
Deborah J. Clegg ◽  
Daniel Zeve ◽  
Jonathan M. Graff
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Progenitor Cells ◽  
Muscle Cells ◽  
Brown Adipose ◽  
Oestrogen Signalling

scholarly journals Time-Course Analysis on the Differentiation of Bone Marrow-Derived Progenitor Cells Into Smooth Muscle Cells During Neointima Formation

2010 ◽  
Vol 30 (10) ◽  
pp. 1890-1896 ◽  
Author(s):  
Jan-Marcus Daniel ◽  
Wiebke Bielenberg ◽  
Philipp Stieger ◽  
Soenke Weinert ◽  
Harald Tillmanns ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Progenitor Cells ◽  
Time Course ◽  
Muscle Cells ◽  
Neointima Formation

scholarly journals Smooth Muscle Cells in Atherosclerosis Originate From the Local Vessel Wall and Not Circulating Progenitor Cells in ApoE Knockout Mice

2006 ◽  
Vol 26 (12) ◽  
pp. 2696-2702 ◽  
Author(s):  
Jacob F. Bentzon ◽  
Charlotte Weile ◽  
Claus S. Sondergaard ◽  
Johnny Hindkjaer ◽  
Moustapha Kassem ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Progenitor Cells ◽  
Knockout Mice ◽  
Vessel Wall ◽  
Muscle Cells ◽  
Apoe Knockout Mice

scholarly journals S100B is required for maintaining an intermediate state with double-positive Sca-1+ progenitor and vascular smooth muscle cells during neointimal formation

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Yan Wu ◽  
Xin Liu ◽  
Ling-Yun Guo ◽  
Lei Zhang ◽  
Fei Zheng ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Progenitor Cells ◽  
Vascular Smooth Muscle Cells ◽  
Intermediate State ◽  
Muscle Cells ◽  
Neointimal Formation ◽  
Double Positive ◽  
Vessel Injury

Abstract Introduction Accumulation of vascular smooth muscle cells (VSMCs) within the neointimal region is a hallmark of atherosclerosis and vessel injury. Evidence has shown that Sca-1-positive (Sca-1+) progenitor cells residing in the vascular adventitia play a crucial role in VSMC assemblages and intimal lesions. However, the underlying mechanisms, especially in the circumstances of vascular injury, remain unknown. Methods and results The neointimal formation model in rats was established by carotid artery balloon injury using a 2F-Forgaty catheter. Most Sca-1+ cells first appeared at the adventitia of the vascular wall. S100B expressions were highest within the adventitia on the first day after vessel injury. Along with the sequentially increasing trend of S100B expression in the intima, media, and adventitia, respectively, the numbers of Sca-1+ cells were prominently increased at the media or neointima during the time course of neointimal formation. Furthermore, the Sca-1+ cells were markedly increased in the tunica media on the third day of vessel injury, SDF-1α expressions were obviously increased, and SDF-1α levels and Sca-1+ cells were almost synchronously increased within the neointima on the seventh day of vessel injury. These effects could effectually be reversed by knockdown of S100B by shRNA, RAGE inhibitor (SPF-ZM1), or CXCR4 blocker (AMD3100), indicating that migration of Sca-1+ cells from the adventitia into the neointima was associated with S100B/RAGE and SDF-1α/CXCR4. More importantly, the intermediate state of double-positive Sca-1+ and α-SMA cells was first found in the neointima of injured arteries, which could be substantially abrogated by using shRNA for S100B or blockade of CXCR4. S100B dose-dependently regulated SDF-1α expressions in VSMCs by activating PI3K/AKT and NF-κB, which were markedly abolished by PI3K/AKT inhibitor wortmannin and enhanced by p65 blocker PDTC. Furthermore, S100B was involved in human umbilical cord-derived Sca-1+ progenitor cells’ differentiation into VSMCs, especially in maintaining the intermediate state of double-positive Sca-1+ and α-SMA. Conclusions S100B triggered neointimal formation in rat injured arteries by maintaining the intermediate state of double-positive Sca-1+ progenitor and VSMCs, which were associated with direct activation of RAGE by S100B and indirect induction of SDF-1α by activating PI3K/AKT and NF-κB.

scholarly journals O2 Level Controls Hematopoietic Circulating Progenitor Cells Differentiation into Endothelial or Smooth Muscle Cells

PLoS ONE ◽  
2009 ◽  
Vol 4 (5) ◽  
pp. e5514 ◽  
Author(s):  
Nicolas Berthelemy ◽  
Halima Kerdjoudj ◽  
Pierre Schaaf ◽  
Christine Prin-Mathieu ◽  
Patrick Lacolley ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Progenitor Cells ◽  
Muscle Cells

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.

Differentiation of Multipotent Adult Progenitor Cells into Functional Endothelial and Smooth Muscle Cells

2006 ◽  
Vol 75 (1) ◽  
Author(s):  
Aernout Luttun ◽  
Jeffrey J. Ross ◽  
Catherine Verfaillie ◽  
Xabier L. Aranguren ◽  
Felipe Prósper
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Progenitor Cells ◽  
Muscle Cells ◽  
Multipotent Adult Progenitor Cells

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.

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