Tissue Regeneration from Mechanical Stretching of Cell–Cell Adhesion

Esfahani, Amir Monemian; Rosenbohm, Jordan; Reddy, K. Sharan Teja; Jin, Xiaowei; Bouzid, Tasneem; Riehl, Brandon D.; Kim, Eunju; Lim, Jung Yul; Yang, Ruiguo

doi:10.1089/ten.tec.2019.0098

Cited by 26 publications

(16 citation statements)

References 121 publications

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“…Mechanical stretch has been shown to induce a spectrum of physiological transformations in many cell types, and activate intracellular biochemical signals and alter gene expression. [ 34 ] The most widely reported effects are stress fiber reorganization in endothelial cells [ 35 ] and in muscles cells [ 36 ] through Rho‐dependent stress fiber assembly from myosin light chain phosphorylation. [ 37,38 ] The cytoskeleton reorganization represents an important mechanism for cells to adapt to an increased mechanical stress and for preparation for cell proliferation.…”

Section: Discussionmentioning

confidence: 99%

Modulation of Mechanical Stress Mitigates Anti‐Dsg3 Antibody‐Induced Dissociation of Cell–Cell Adhesion

et al. 2021

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the presence of autoantibodies (autoAbs) directed against keratinocyte surface antigens, [2] primarily the desmosomal cadherins desmoglein 3 (Dsg3) and Dsg1. [3,4] Binding of these autoAbs leads to desmosome internalization, keratin retraction, cell dissociation, and ultimately blister formation. [5] Several signaling pathways induced by autoAb binding in PV have been identified, including protein kinase C (PKC), [6,7] p38 mitogen-activated protein kinase (MAPK), [8,9] and Rho GTPases family proteins such as RhoA. [10,11] Nevertheless, there remain large gaps in knowledge concerning the precise mechanisms through which autoAb-binding induces blister formation. [12] The bulk of research in PV to date has focused on immune mechanisms upstream of autoAb binding (i.e., antibody specificity, B-cell and T-cell functions). Consequently, therapeutic interventions in PV have mostly relied on nonspecific immunosuppression, which is often accompanied by detrimental longterm side effects. [13] However, the biophysical aspects of the cell behavior after autoAb binding are only recently being explored thanks to the advancement of innovative technologies applied to fundamental biological questions at the cellular level. [14-16] There is already compelling evidence that mechanical stress in adhesive junctions plays a significant role in dictating the fate of cell-cell attachment. [17,18] We posit that mechanical It is becoming increasingly clear that mechanical stress in adhesive junctions plays a significant role in dictating the fate of cell-cell attachment under physiological conditions. Targeted disruption of cell-cell junctions leads to multiple pathological conditions, among them the life-threatening autoimmune blistering disease pemphigus vulgaris (PV). The dissociation of cellcell junctions by autoantibodies is the hallmark of PV, however, the detailed mechanisms that result in tissue destruction remain unclear. Thus far, research and therapy in PV have focused primarily on immune mechanisms upstream of autoantibody binding, while the biophysical aspects of the cellcell dissociation process leading to acantholysis are less well studied. In work aimed at illuminating the cellular consequences of autoantibody attachment, it is reported that externally applied mechanical stress mitigates antibodyinduced monolayer fragmentation and inhibits p38 MAPK phosphorylation activated by anti-Dsg3 antibody. Further, it is demonstrated that mechanical stress applied externally to cell monolayers enhances cell contractility via RhoA activation and promotes the strengthening of cortical actin, which ultimately mitigates antibody-induced cell-cell dissociation. The study elevates understanding of the mechanism of acantholysis in PV and shifts the paradigm of PV disease development from a focus solely on immune pathways to highlight the key role of physical transformations at the target cell.

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Section: Discussionmentioning

confidence: 99%

Modulation of Mechanical Stress Mitigates Anti‐Dsg3 Antibody‐Induced Dissociation of Cell–Cell Adhesion

et al. 2021

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“…Mechanical forces regulate the development and correct function of virtually every tissue in the human body by mechanisms closely related to cell division. [43][44][45] The ability of cells to respond to soluble mitogenic factors and to proliferate requires their extension, generating isometric tension, either by adherence to a stiff substrate or by external application of mechanical forces. [46][47][48] Similarly, in vivo stretch models have shown that mechanical stretching induces cell division at the site during tissue development.…”

Section: Eve Induction Of Adsc Proliferation In Adipose Tissuesmentioning

confidence: 99%

The Application and Mechanism of Action of External Volume Expansion in Soft Tissue Regeneration

Chen

Yuan

2021

Tissue Engineering Part B: Reviews

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The reconstruction of large-volume soft tissue defects is a major problem in plastic surgery. Many plastic surgeons have focused on external volume expansion (EVE) because of its capacity to promote regeneration of soft tissues, including breast, subcutaneous fat, and skin. EVE is a minimally invasive and less costly tissue engineering approach that has shown great clinical potential. However, many challenges still need to be addressed before such technology can become a common clinical practice. Basic in vivo and in vitro studies have been performed to determine the possible mechanisms by which EVE promotes tissue regeneration and to design optimized animal models. EVE application was found to facilitate cell proliferation and migration, enhance adipogenesis, improve angiogenesis, and provide available space for soft tissue growth. Understanding the mechanical and chemical signals associated with EVE during tissue regeneration may enable the clinical adaptation of this technology. This article reviews the clinical application of EVE techniques, describes preclinical animal models, and evaluates the possible mechanisms by which EVE induces tissue regeneration.

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“…Cell adhesion molecules are a collective term for the numerous classes of molecules that mediate contact and binding between cells and cells or between cells and the extracellular matrix (ECM) (10,11) .The adhesion molecules currently identi ed can be classi ed into integrin family, selectin family, immunoglobulin superfamily, calmodulin family according to their structural features (12)(13)(14). In addition there are a number of adhesion molecules that have not yet been categorized.…”

Section: Introductionmentioning

confidence: 99%

CERCAM is a prognostic biomarker associated with immune infiltration of macrophage M2 polarization in head and neck squamous carcinoma

Yang

Yan²,

Chen

2023

Preprint

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Purpose This study aimed to investigate the relevance of cerebral endothelial cell adhesion molecule (CERCAM) expression to head and neck squamous cell carcinoma (HNSCC) prognosis and immune infiltration by macrophage M2 polarization. Methods Timer, UALCAN and HPA databases was used to analyze the differences in mRNA and protein levels of CERCAM expression in HNSCC. The Timer database was also applied to analyze the correlation between CERCAM in HNSCC and immune infiltration. TCGA-HNSCC database was applied to analyze the correlation between CERCAM expression levels and clinicopathological features, and its diagnostic and prognostic value in HNSCC was also assessed. The cBioPortal and MethSurv databases were then applied to analyze the genetic variation and methylation status of CERCAM. In vitro cellular assays were performed to provide evidence that CERCAM promotes malignant biological behavior of tumors and promotes macrophage M2 polarization in tumors. Finally, underlying pathophysiological mechanisms of CERCAM involvement in the development of HNSCC were predicted using a bioinformatics approach. Results CERCAM is significantly overexpressed in HNSCC and correlates with poor prognostic levels and has good performance in predicting survival status in HNSCC patients. Cox regression analysis indicates that CERCAM expression levels are independent risk factors for predicting OS, DSS, and PFI. CERCAM promotes tumor malignant biological behavior and promotes macrophage M2 polarization immune infiltration in HNSCC. In addition, CERCAM promotes tumor cell adhesion in head and neck squamous carcinoma and promotes tumor progression through several oncogenic signaling pathways. Conclusion CERCAM may serve as a new diagnostic and prognostic biomarker in HNSCC and is a promising therapeutic target for HNSCC.

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Tissue Regeneration from Mechanical Stretching of Cell–Cell Adhesion

Cited by 26 publications

References 121 publications

Modulation of Mechanical Stress Mitigates Anti‐Dsg3 Antibody‐Induced Dissociation of Cell–Cell Adhesion

Modulation of Mechanical Stress Mitigates Anti‐Dsg3 Antibody‐Induced Dissociation of Cell–Cell Adhesion

The Application and Mechanism of Action of External Volume Expansion in Soft Tissue Regeneration

CERCAM is a prognostic biomarker associated with immune infiltration of macrophage M2 polarization in head and neck squamous carcinoma

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