Mechanical Stress Stimuli Research Articles

Air-Processed Efficient Perovskite Solar Cells With Full Lifecycle Management.

Despite the outstanding power conversion efficiency of perovskite solar cells (PSCs) realized over the years, the entire lifecycle from preparation and operation to discarding of PSCs still needs to be carefully considered when it faces the upcoming large-scale production and deployment. In this study, bio-derived chitin-based polymers are employed to realize the full lifecycle regulation of air-processed PSCs by forming multiple coordinated and hydrogen bonds to stabilize the lead iodide and organic salt precursor inks, accelerating the solid-liquid reaction and crystallization of two-step deposition process, then achieving the high crystalline and oriented perovskites with less notorious charge defects in the open air. The air-prepared PSCs exhibit a decent efficiency of 25.18% with high preparation reproducibility and improved operational stability toward the harsh environment and mechanical stress stimuli. The modified PSCs display negligible fatigue behavior with keeping 92% of its initial efficiency after operating for 32 diurnal cycles (ISOS-LC-1 protocol). Meanwhile, closed-loop lead management of end-of-life PSCs including suppression of lead leakage, toxicity evaluation of broken devices, and recycling of lead iodide components are comprehensively investigated. This work sheds light on a promising avenue to realize the entire lifecycle regulation of air-processed efficient and stable PSCs.

3D Cell Culture: Recent Development in Materials with Tunable Stiffness.

It is widely accepted that three-dimensional cell culture systems simulate physiological conditions better than traditional 2D systems. Although extracellular matrix components strongly modulate cell behavior, several studies underlined the importance of mechanosensing in the control of different cell functions such as growth, proliferation, differentiation, and migration. Human tissues are characterized by different degrees of stiffness, and various pathologies (e.g., tumor or fibrosis) cause changes in the mechanical properties through the alteration of the extracellular matrix structure. Additionally, these modifications have an impact on disease progression and on therapy response. Hence, the development of platforms whose stiffness could be modulated may improve our knowledge of cell behavior under different mechanical stress stimuli. In this review, we have analyzed the mechanical diversity of healthy and diseased tissues, and we have summarized recently developed materials with a wide range of stiffness.

A New Hope in Spinal Degenerative Diseases: Piezo1.

As a newly discovered mechanosensitive ion channel protein, the piezo1 protein participates in the transmission of mechanical signals on the cell membrane and plays a vital role in mammalian biomechanics. Piezo1 has attracted widespread attention since it was discovered in 2010. In recent years, studies on piezo1 have gradually increased and deepened. In addition to the discovery that piezo1 is expressed in the respiratory, cardiovascular, gastrointestinal, and urinary systems, it is also stably expressed in cells such as mesenchymal stem cells (MSCs), osteoblasts, osteoclasts, chondrocytes, and nucleus pulposus cells that constitute vertebral bodies and intervertebral discs. They can all receive external mechanical stimulation through the piezo1 protein channel to affect cell proliferation, differentiation, migration, and apoptosis to promote the occurrence and development of lumbar degenerative diseases. Through reviewing the relevant literature of piezo1 in the abovementioned cells, this paper discusses the effect of piezo1 protein expression under mechanical stress stimuli on spinal degenerative disease, providing the molecular basis for the pathological mechanism of spinal degenerative disease and also a new basis, ideas, and methods for the prevention and treatment of this degenerative disease.

Intermittent compressive stress regulates Notch target gene expression via transforming growth factor-β signaling in murine pre-osteoblast cell line

ObjectiveDifferent mechanical stimuli regulate behaviors of various cell types, including osteoblasts, osteocytes, and periodontal ligament fibroblasts. Notch signaling participates in the mechanical stress-regulated cell responses. The present study investigated the regulation of Notch target gene and sclerostin (Sost) expression in murine pre-osteoblast cell line (MC3T3-E1) under intermittent compressive stress. MethodsMC3T3-E1 were subjected to the intermittent compressive force under the computerized controlled machine. In some experiments, cells were pretreated with chemical inhibitors for Notch and transforming growth factor (TGF)-β signaling prior to mechanical stimuli. To evaluate role of Notch signaling in MC3T3-E1 cells under unloaded condition, cells were seeded on indirect immobilized Notch ligand (Jagged1). Gene expression was determined using real-time quantitative polymerase chain reaction. ResultsThe intermittent compressive stress significantly upregulated Notch target gene expression (Hes Family BHLH transcription factor 1; Hes1 and Hairy/enhancer-of-split related with YRPW motif protein1; Hey1). The intermittent stress-induced Hes1 and Hey1 mRNA expression could be inhibited by a γ-secretase inhibitor (DAPT) or a TGF-β superfamily type I activing receptor-like kinase receptors inhibitor (SB431542). The results imply that intermittent compressive stress regulates Notch signaling via TGF-β pathway. Further, the intermittent compressive stress reduced Sost mRNA expression and this phenomenon could be rescued by a DAPT pretreatment, implying the involvement of Notch signaling. However, activation of Notch signaling under the unloaded condition resulted in the increase of Sost expression and the reduction of osteogenic marker genes. ConclusionsThese results imply the involvement of Notch signaling in the homeostasis maintaining of osteogenic cells under mechanical stress stimuli.

A novel computational remodelling algorithm for the probabilistic evolution of collagen fibre dispersion in biaxially strained vascular tissue.

In this work, we constructed a novel collagen fibre remodelling algorithm that incorporates the complex nature of random evolution acting on single fibres causing macroscopic fibre dispersion. The proposed framework is different from the existing remodelling algorithms, in that the microscopic random force on cellular scales causing a rotational-type Brownian motion alone is considered as an aspect of vascular tissue remodelling. A continuum mechanical framework for the evolution of local dispersion and how it could be used for modeling the evolution of internal radius of biaxially strained artery structures under constant internal blood pressure are presented. A linear evolution form for the statistical fibre dispersion is employed in the model. The random force component of the evolution, which depends on the mechanical stress stimuli, is described by a single parameter. Although the mathematical form of the proposed model is simple, there is a strong link between the microscopic evolution of collagen dispersion on the cellular level and its effects on the macroscopic visible world through mechanical variables. We believe that the proposed algorithm utilizes a better understanding of the relationship between the evolution rates of mean fibre direction and fibre dispersion. The predictive capability of the algorithm is presented using experimental data. The model has been simulated by solving a single-layered axisymmetric artery (adventitia) deformation problem. The algorithm performed well for estimating the quantitative features of experimental anisotropy, the mean fibre direction vector and the dispersion (κ) measurements under strain-dependent evolution assumptions.

Gating of Pannexin 1‐Mediated ATP Release Channels by Mechanical Stress Stimuli

Most cells release ATP to extracellular compartments wherein ATP acts as a signaling molecule to regulate responses such as vasodilation and inflammatory activation. Pannexin‐1 (Panx1) hemichannels have been proposed as major conduits for ATP efflux in response to proapoptotic stimulation or mechanical deformation of the plasma membrane. Recent studies have demonstrated that caspase‐mediated cleavage of the Panx1 C‐terminus is a novel gating mechanism for this channel in apoptotic cells. In this study we examine the possible role of caspases or other proteases in the acute ATP release induced by non‐apoptotic mechanical stress stimuli in rat C6 glioma cells (which lack native Panx1) versus C6 cells stably transfected with Panx1 (C6‐Panx1). C6 cells were mechanically stimulated by medium exchange or by thrombin (which triggers rapid reorganization of the actin cytoskeleton) to elicit acute ATP release. Only minor ATP release was observed in control C6 cells in response to either medium exchange or thrombin addition. In contrast, medium exchange triggered robust ATP release from C6‐Panx1 cells. Current experiments are testing whether thrombin triggers similar ATP release in C6‐Panx1 cells and whether proteolysis of Panx1 mediates gating of these ATP release channels in response to mechanical stimulation.