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The addition of Angiotensin II (ANGII) led to VSMC contraction as evidenced by an increased traction force exerted on the microposts under the cell.
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In mesenchymal stem cells (MSC), cell spreading leads to RhoA activation of Rho-activated kinase (ROCK), myosin light chain kinase phosphorylation, elevated myosin contractility, increased traction forces to the external environment, and differentiation to an osteoblast phenotype.
Flexion of the knee joint from 90° to 119° generates an increasing traction force on the wire, but further traction force is required to release the irreversible bone segment transport.
Rather than stiffening, solidifying, and increasing traction forces above prestretch baseline values, as would be predicted from a reinforcement response, in most physiological circumstances the human airway smooth muscle cell promptly softens, fluidizes, and decreases traction force, with subsequent slow recoveries that approach but never exceed baseline values.
As an acute response to such stretches the cytoskeleton can stiffen, increase traction forces and reinforce, as reported by some, or can soften and fluidize, as reported more recently by our laboratory, but in any given circumstance it remains unknown which response might prevail or why.
Our data support the finding that upregulation of β1-integrin clustering using stiff polyacrylamide substrata increases traction forces in fibroblasts and inhibits morphological differentiation in MECs, whereas using β1-integrin mutants with increased integrin self-association increases cell-generated forces and spreading on soft substrata in MECs (Paszek et al, 2005).
Brumback et al also reported that adduction at the hip increased the traction force.
Notably, these mutant cells exert an increased cell traction force, an early cellular response during TGF β1-induced EMT.
Most of the probands (12/17) gradually increased the traction force up to the individually accepted maximum and then completely released all traction and started a second attempt.
Our investigation further showed that TAK1-deficient cancer cells exhibited an increased cell traction force, one of the earliest cellular response during EMT.
Indeed, TID substantially increased the traction force of hPSC-CMs as well as their sarcomeric structural organization, showing that all core aspects of cell function were enhanced.
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