scholarly journals Author Correction: Investigating the nature of active forces in tissues reveals how contractile cells can form extensile monolayers

2021 ◽  
Author(s):  
Lakshmi Balasubramaniam ◽  
Amin Doostmohammadi ◽  
Thuan Beng Saw ◽  
Gautham Hari Narayana Sankara Narayana ◽  
Romain Mueller ◽  
...  
Keyword(s):  
2006 ◽  
Vol 97 (12) ◽  
Author(s):  
A. Zemel ◽  
I. B. Bischofs ◽  
S. A. Safran
Keyword(s):  

2003 ◽  
Vol 284 (6) ◽  
pp. H2325-H2334 ◽  
Author(s):  
Tom Karkanis ◽  
Shaohua Li ◽  
J. Geoffrey Pickering ◽  
Stephen M. Sims

Inwardly rectifying K+ (KIR) currents are present in some, but not all, vascular smooth muscles. We used patch-clamp methods to examine plasticity of this current by comparing contractile and proliferative phenotypes of a clonal human vascular smooth muscle cell line. Hyperpolarization of cells under voltage clamp elicited a large inward current that was selective for K+ and blocked by Ba2+. Current density was greater in proliferative compared with contractile cells (−4.5 ± 0.9 and −1.4 ± 0.3 pA/pF, respectively; P < 0.001). RT-PCR of mRNA from proliferative cells identified transcripts for Kir2.1 and Kir2.2 but not Kir2.3 potassium channels. Western blot analysis demonstrated greater expression of Kir2.1 protein in proliferative cells, consistent with the higher current density. Proliferative cells displayed a more negative membrane potential than contractile cells (−71 ± 2 and −35 ± 4 mV, respectively; P < 0.001). Ba2+ depolarized all cells, whereas small increases in extracellular K+ concentration elicited hyperpolarization only in contractile cells. Ba2+ inhibited [3H]thymidine incorporation, indicating a possible role for KIR channels in the regulation of proliferation. The phenotype-dependent plasticity of KIR channels may have relevance to vascular remodeling.


2006 ◽  
Vol 69 (2) ◽  
pp. 359-369 ◽  
Author(s):  
M DIEZMARQUES ◽  
M RUIZTORRES ◽  
M GRIERA ◽  
S LOPEZONGIL ◽  
M SAURA ◽  
...  

Science ◽  
1966 ◽  
Vol 153 (3741) ◽  
pp. 1271-1273 ◽  
Author(s):  
M. H. Ross ◽  
I. R. Long

Development ◽  
1979 ◽  
Vol 53 (1) ◽  
pp. 75-90
Author(s):  
Elizabeth L. Wee ◽  
Bruce S. Babiarz ◽  
Stephen Zimmerman ◽  
Ernest F. Zimmerman

Previous studies have localized non-muscle contractile systems in the posterior (region 2) and the anterior (region 3) ends of mouse palates at the time of shelf movement. In order to determine whether these contractile systems function in shelf rotation, effects of pharmacologic agents have been analyzed in embryo culture. First, it was shown that the posterior end of the palate rotates before the anterior end, and its rotation in culture was proportionally greater as development of the embryo progressed. Generally, the posterior end of the palate was more easily inhibited in embryo culture than the anterior end. Serotonin at 10–−8 M to 10–−5 M was shown to significantly stimulate rotation atthe anterior end of the palate after 2 h in embryo culture. The effect on the posterior palate was less pronounced. To investigate further the role of this neurotransmitter on palate shelf rotation, serotonin antagonists were employed. Methysergide (10–−4 M) inhibited anterior shelf rotation to 12% of control values (P &lt; 0·005), while not significantly affecting the posterior end. Ergotamine (10–−6 M) significantly inhibited the stimulation induced by 10–−5 M serotonin (P &lt; 0·025). Cyproheptadine (10–−9 M) partially inhibited anterior and posterior shelf rotation in embryo culture. When injected into the pregnant dam, cyproheptadine partially inhibited shelf rotation and fusion. The palate was examined histologically after embryo culture. In the presence of 10–−4 M methysergide, the elongated contractile cells in region 3 at the anterior and midpalatal mesenchyme were prevented from rounding. Thus, serotonin may be regulating rotation of the anterior end of the palate by an effect on a cell-mediated process.


Author(s):  
James S. Lowe ◽  
Peter G. Anderson
Keyword(s):  

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