Stretch and Shear Interactions Affect Intercellular Junction Protein Expression and Turnover in Endothelial Cells

Berardi, Danielle E.; Tarbell, John M.

doi:10.1007/s12195-009-0073-7

Cited by 27 publications

(20 citation statements)

References 55 publications

(88 reference statements)

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“…Leader cells have been observed in collective migration during cancer cell invasion, vascular sprouting, wound closure, and embryogenesis (36,37). Furthermore, there is some evidence that mechanical forces can modulate coordinated migration in vascular morphogenesis: It has been shown that forces exerted by flowing fluids can induce changes in endothelial junction structure (38), differentiation of vascular wall cells (39), and tip cell formation (40). Interestingly, our leader cells are morphologically and functionally similar to endothelial tip cells.…”

Section: Discussionmentioning

confidence: 68%

Mechanical compression drives cancer cells toward invasive phenotype

Tse

Cheng²,

Tyrrell³

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

536

451

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Uncontrolled growth in a confined space generates mechanical compressive stress within tumors, but little is known about how such stress affects tumor cell behavior. Here we show that compressive stress stimulates migration of mammary carcinoma cells. The enhanced migration is accomplished by a subset of "leader cells" that extend filopodia at the leading edge of the cell sheet. Formation of these leader cells is dependent on cell microorganization and is enhanced by compressive stress. Accompanied by fibronectin deposition and stronger cell-matrix adhesion, the transition to leader-cell phenotype results in stabilization of persistent actomyosin-independent cell extensions and coordinated migration. Our results suggest that compressive stress accumulated during tumor growth can enable coordinated migration of cancer cells by stimulating formation of leader cells and enhancing cell-substrate adhesion. This novel mechanism represents a potential target for the prevention of cancer cell migration and invasion.mechanobiology | solid stress | collective migration | metastasis

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Section: Discussionmentioning

confidence: 68%

Mechanical compression drives cancer cells toward invasive phenotype

Tse

Cheng²,

Tyrrell³

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

536

451

View full text Add to dashboard Cite

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“…Several reports have provided evidence of flow shear stress-mediated distribution of tight junction proteins, in which exposure to shear stress leads to a transient decrease (<4 hrs post shear) in VE-cadherin or occludin protein expression, as endothelial cells migrate and align in the direction of flow. 14,15,39,[55][56][57][58][59] Studies investigating the effect of shear stress on permeability of macromolecules across the endothelium also revealed that endothelial permeability is acutely sensitive to shear stress in vitro. 53 Exposure of both 1 and 10 dyne/cm 2 dramatically increased permeability of FITC-BSA after 30 and 60 minutes; however, permeability returned to pre-shear values after 120 minutes.…”

Section: Endothelial Barrier Functionmentioning

confidence: 99%

Flow shear stress regulates endothelial barrier function and expression of angiogenic factors in a 3D microfluidic tumor vascular model

Buchanan

Verbridge

Vlachos

et al. 2014

Cell Adhesion & Migration

183

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Endothelial cells lining blood vessels are exposed to various hemodynamic forces associated with blood flow. These include fluid shear, the tangential force derived from the friction of blood flowing across the luminal cell surface, tensile stress due to deformation of the vessel wall by transvascular flow, and normal stress caused by the hydrodynamic pressure differential across the vessel wall. While it is well known that these fluid forces induce changes in endothelial morphology, cytoskeletal remodeling, and altered gene expression, the effect of flow on endothelial organization within the context of the tumor microenvironment is largely unknown. Using a previously established microfluidic tumor vascular model, the objective of this study was to investigate the effect of normal (4 dyn/cm 2 ), low (1 dyn/cm 2 ), and high (10 dyn/cm 2 ) microvascular wall shear stress (WSS) on tumor-endothelial paracrine signaling associated with angiogenesis. It is hypothesized that high WSS will alter the endothelial phenotype such that vascular permeability and tumor-expressed angiogenic factors are reduced. Results demonstrate that endothelial permeability decreases as a function of increasing WSS, while co-culture with tumor cells increases permeability relative to mono-cultures. This response is likely due to shear stress-mediated endothelial cell alignment and tumor-VEGF-induced permeability. In addition, gene expression analysis revealed that high WSS (10 dyn/cm 2 ) significantly down-regulates tumor-expressed MMP9, HIF1, VEGFA, ANG1, and ANG2, all of which are important factors implicated in tumor angiogenesis. This result was not observed in tumor mono-cultures or static conditioned media experiments, suggesting a flow-mediated paracrine signaling mechanism exists with surrounding tumor cells that elicits a change in expression of angiogenic factors. Findings from this work have significant implications regarding low blood velocities commonly seen in the tumor vasculature, suggesting high shear stress-regulation of angiogenic activity is lacking in many vessels, thereby driving tumor angiogenesis.

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“…The temporal phase angle between flow and pressure generated by wave reflection in the circulation and the inertial effects of blood flow cause time lags to occur between WSS and WCS. The temporal phase angle between WSS and WCS has been referred to as the stress phase angle (SPA) (Qin et al, 2006;Berardi and Tarbell, 2009). Studies have shown that the production rates of the vasoactive agents Nitric Oxide (NO); Prostacyclin (PGI2) and Endothelin-1 (ET-1) of ECs synergistically exposed to WCS and WSS are dependent on the SPA.…”

Section: Introductionmentioning

confidence: 99%

“…In another in vitro study Qiu and Tarbell (2000) found that the highly negative SPA ( À 100 1 compared to À151) suppressed NO and PGI2 and induced ET-1 production. Further in-vitro studies have also shown that a SPA¼ À1801 for asynchronous hemodynamic condition in comparison to a SPA¼01 for synchronous hemodynamic condition represents a strong decrease in NO and PGI2 production, an increase in ET-1 production (Dancu et.al., 2004), a high rate of cell turnover and an increase in the number of leaky junctions (Berardi and Tarbell, 2009). The leaky junctions' increase causes the resistance of the leaky junction pathway to decrease the flow considerably and so the blood plasma flux through the leaky junctions increases.…”

Section: Introductionmentioning

confidence: 99%