Mechanobiology: A landscape for reinterpreting stem cell heterogeneity and regenerative potential in diseased tissues

Tassinari, Riccardo; Olivi, Elena; Cavallini, Claudia; Taglioli, Valentina; Zannini, Chiara; Marcuzzi, Martina; Fedchenko, Oleksandra; Ventura, Carlo

doi:10.1016/j.isci.2022.105875

Cited by 5 publications

(3 citation statements)

References 132 publications

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“…Thus, understanding the molecular basis of such pathways is critical in elucidating the molecular mechanisms governing cellular functions in physiology and pathology [ 9 , 10 , 11 , 12 , 13 , 14 ]. Plasma membrane proteins (e.g., ion channels, integrins, cadherins) and intracellular proteins (e.g., focal adhesion complexes, cytoskeleton components, nucleoskeleton components, soluble proteins) are organized in molecular complexes that are spatially juxtaposed to act as players for the mechanosensing and/or mechanotransduction pathways [ 6 , 15 ]. However, how the pathway(s) is (are) activated by one or more physical cues and the protein(s) involved in propagating the signal cascade are still unclear.…”

Section: Introductionmentioning

confidence: 99%

Tight Regulation of Mechanotransducer Proteins Distinguishes the Response of Adult Multipotent Mesenchymal Cells on PBCE-Derivative Polymer Films with Different Hydrophilicity and Stiffness

Argentati

Morena

Guidotti

et al. 2023

Cells

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Mechanotransduction is a molecular process by which cells translate physical stimuli exerted by the external environment into biochemical pathways to orchestrate the cellular shape and function. Even with the advancements in the field, the molecular events leading to the signal cascade are still unclear. The current biotechnology of tissue engineering offers the opportunity to study in vitro the effect of the physical stimuli exerted by biomaterial on stem cells and the mechanotransduction pathway involved in the process. Here, we cultured multipotent human mesenchymal/stromal cells (hMSCs) isolated from bone marrow (hBM-MSCs) and adipose tissue (hASCs) on films of poly(butylene 1,4-cyclohexane dicarboxylate) (PBCE) and a PBCE-based copolymer containing 50 mol% of butylene diglycolate co-units (BDG50), to intentionally tune the surface hydrophilicity and the stiffness (PBCE = 560 Mpa; BDG50 = 94 MPa). We demonstrated the activated distinctive mechanotransduction pathways, resulting in the acquisition of an elongated shape in hBM-MSCs on the BDG50 film and in maintaining the canonical morphology on the PBCE film. Notably, hASCs acquired a new, elongated morphology on both the PBCE and BDG50 films. We found that these events were mainly due to the differences in the expression of Cofilin1, Vimentin, Filamin A, and Talin, which established highly sensitive machinery by which, rather than hASCs, hBM-MSCs distinguished PBCE from BDG50 films.

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Section: Introductionmentioning

confidence: 99%

Tight Regulation of Mechanotransducer Proteins Distinguishes the Response of Adult Multipotent Mesenchymal Cells on PBCE-Derivative Polymer Films with Different Hydrophilicity and Stiffness

Argentati

Morena

Guidotti

et al. 2023

Cells

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“…In addition, mechanical therapies (e.g. based on shockwaves) are already known to enhance recovery for other injured tissues such as the heart, skin, and bone ( 107 ). Exploiting mechanoregulatory cues such as extracellular matrix stiffness is an established and powerful avenue to control stem cell differentiation or cancer cell behavior ( 108 ).…”

Section: Discussionmentioning

confidence: 99%

Rac1 promotes kidney collecting duct repair by mechanically coupling cell morphology to mitotic entry

Bock,

Dong,

et al. 2024

Sci. Adv.

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Prolonged obstruction of the ureter, which leads to injury of the kidney collecting ducts, results in permanent structural damage, while early reversal allows for repair. Cell structure is defined by the actin cytoskeleton, which is dynamically organized by small Rho guanosine triphosphatases (GTPases). In this study, we identified the Rho GTPase, Rac1, as a driver of postobstructive kidney collecting duct repair. After the relief of ureteric obstruction, Rac1 promoted actin cytoskeletal reconstitution, which was required to maintain normal mitotic morphology allowing for successful cell division. Mechanistically, Rac1 restricted excessive actomyosin activity that stabilized the negative mitotic entry kinase Wee1. This mechanism ensured mechanical G 2 -M checkpoint stability and prevented premature mitotic entry. The repair defects following injury could be rescued by direct myosin inhibition. Thus, Rac1-dependent control of the actin cytoskeleton integrates with the cell cycle to mediate kidney tubular repair by preventing dysmorphic cells from entering cell division.

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“…Indeed, mechanobiology is as old as living organisms. In the human body, biophysical stimuli exerted by ECM or fluids surrounding the cells are necessary for tissue development and maintenance of tissue homeostasis, morphology, and function throughout life [4][5][6]. Therefore, understanding how physical forces are applied to cells and identifying the types of proteins involved in the phenomenon is currently challenging.…”

mentioning

confidence: 99%

Mechanobiology in Cells and Tissues

Martino

2023

IJMS

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Mechanobiology: A landscape for reinterpreting stem cell heterogeneity and regenerative potential in diseased tissues

Cited by 5 publications

References 132 publications

Tight Regulation of Mechanotransducer Proteins Distinguishes the Response of Adult Multipotent Mesenchymal Cells on PBCE-Derivative Polymer Films with Different Hydrophilicity and Stiffness

Tight Regulation of Mechanotransducer Proteins Distinguishes the Response of Adult Multipotent Mesenchymal Cells on PBCE-Derivative Polymer Films with Different Hydrophilicity and Stiffness

Rac1 promotes kidney collecting duct repair by mechanically coupling cell morphology to mitotic entry

Mechanobiology in Cells and Tissues

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