Qualitative analysis of contribution of intracellular skeletal changes to cellular elasticity

Effects of Visfatin on Intracellular Mechanics and Catabolism in Human Primary Chondrocytes through Glycogen Synthase Kinase 3β Inactivation

“…In that case, the surrounding mechanical microenvironment of chondrocytes is also altered, making the dynamic regulation of intracellular mechanics necessary for the cells to change their phenotype to adapt to unusual mechanical loading and pressure [ 31 ]. Interestingly, although our finding indicated that visfatin-treated chondrocytes had decreased intracellular mechanics, which was supported by some other studies, other research team reported the opposite observation, i.e., that the chondrocytes in OA are stiffer than the healthy ones [ 16 , 17 , 18 , 22 ]. Possible interpretations for the changes in intracellular mechanics and those different observations have been proposed as follows: (i) chondrocytes become stiffer or softer in accordance with the complex stress in the environment; (ii) chondrocytes must reactivate themselves to synthesize more anabolic factors to repair damage; (iii) chondrocytes mostly communicate with a weak and low-strength matrix [ 31 ].…”

“…In the cartilage, although three types of cytoskeletal networks have all been indicated as controlling the intracellular mechanics, the microfilament network has been recognized as the predominant one [ 20 ]. Many previous studies also demonstrated the importance of the microfilament network in regulating the viscoelasticity and stiffness properties of chondrocytes, including cells treated with interleukin-1β-/tumor necrosis factor α and cytoskeleton destabilizer agents [ 17 , 18 , 22 ]. However, the microtubule network was found to have little effect on the biophysical behaviors of chondrocytes in these studies [ 17 , 18 , 22 ].…”

“…Many previous studies also demonstrated the importance of the microfilament network in regulating the viscoelasticity and stiffness properties of chondrocytes, including cells treated with interleukin-1β-/tumor necrosis factor α and cytoskeleton destabilizer agents [ 17 , 18 , 22 ]. However, the microtubule network was found to have little effect on the biophysical behaviors of chondrocytes in these studies [ 17 , 18 , 22 ]. These findings are different from ours.…”

“…In addition to these extracellular mechanical modulations, data have suggested that the intracellular biophysical behavior of chondrocytes might also be vital for cartilage health and degeneration pathogenesis [ 15 , 16 , 17 ]. It has been shown that the intracellular mechanics of chondrocytes isolated from normal cartilage and OA cartilage are different [ 16 , 18 , 19 ]. These differences might result in a stiffer or softer cytoplasmic environment in chondrocytes according to various stimuli.…”

“…The dynamic deformations of the cells responding to various stimuli are mainly controlled by the three-dimensional stress fiber networks formed by the cytoskeletal proteins, i.e., actin (microfilaments), tubulin (microtubules), and vimentin (intermediate filaments) [ 20 ]. Hence, the architecture and polymerization status of the cytoskeleton have been directly associated with the intracellular mechanics changes of cells [ 17 , 18 , 19 ]. In the cartilage, the cytoskeleton has been indicated to serve as a mechanical communicator between the extracellular matrix and chondrocytes [ 21 ].…”