Increased pressure alters plasma membrane dynamics and renders acute myeloid leukemia cells resistant to daunorubicin

Nirmalanandhan, Victor S.; Hurren, Rose; Cameron, William D.; Gronda, Marcela; Shamas‐Din, Aisha; You, Lidan; Minden, Mark D.; Rocheleau, Jonathan V.; Schimmer, Aaron D.

doi:10.3324/haematol.2015.129866

Cited by 7 publications

(5 citation statements)

References 11 publications

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“…As cartilage tissue and chondrocytes are reported to be incompressible under low strains ( Bachrach et al, 1998 ; Ofek et al, 2009 ), a pressure-sensing mechanism in the absence of a gas–liquid interface remains unclear. One possible mechanism is a change in plasma membrane fluidity, which could activate mechanosensitive ion channels ( Nirmalanandhan et al, 2015 ). A recent study on the endothelial cell cytoskeleton indeed showed that HP-induced cytoskeletal remodeling was mediated by mechanosensitive cation channels and a subsequent elevation in intracellular Ca 2+ ( Prystopiuk et al, 2018 ).…”

Section: Discussionmentioning

confidence: 99%

Hydrostatic pressure prevents chondrocyte differentiation through heterochromatin remodeling

Maki

Nava

Villeneuve

et al. 2021

Journal of Cell Science

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Articular cartilage protects and lubricates joints for smooth motion and transmission of loads. Owing to its high water content, chondrocytes within the cartilage are exposed to high levels of hydrostatic pressure, which has been shown to promote chondrocyte identity through unknown mechanisms. Here, we investigate the effects of hydrostatic pressure on chondrocyte state and behavior, and discover that application of hydrostatic pressure promotes chondrocyte quiescence and prevents maturation towards the hypertrophic state. Mechanistically, hydrostatic pressure reduces the amount of trimethylated H3K9 (K3K9me3)-marked constitutive heterochromatin and concomitantly increases H3K27me3-marked facultative heterochromatin. Reduced levels of H3K9me3 attenuates expression of pre-hypertrophic genes, replication and transcription, thereby reducing replicative stress. Conversely, promoting replicative stress by inhibition of topoisomerase II decreases Sox9 expression, suggesting that it enhances chondrocyte maturation. Our results reveal how hydrostatic pressure triggers chromatin remodeling to impact cell fate and function.This article has an associated First Person interview with the first author of the paper.

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Section: Discussionmentioning

confidence: 99%

Hydrostatic pressure prevents chondrocyte differentiation through heterochromatin remodeling

Maki

Nava

Villeneuve

et al. 2021

Journal of Cell Science

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“…The thirdand most likelymechanism of pressure sensing might be a phase shift in the lipid organization of the plasma membrane. It has been shown that under increasing pressure, plasma membrane dynamics shift from a fluid-liquid crystalline state into a gel-like state and that this directly affects transport across the plasma membrane (Nirmalanandhan et al, 2015). This plasma membrane phase shift is likely to affect MSCs and thereby induce the pressure-dependent signaling.…”

Section: Discussionmentioning

confidence: 99%

A two-phase response of endothelial cells to hydrostatic pressure

Prystopiuk

Fels

Simon

et al. 2018

Journal of Cell Science

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The vascular endothelium is exposed to three types of mechanical forces: blood flow-mediated shear stress, vessel diameter-dependent wall tension and hydrostatic pressure. Despite considerable variations of blood pressure during normal and pathological physiology, little is known about the acute molecular and cellular effects of hydrostatic pressure on endothelial cells. Here, we used a combination of quantitative fluorescence microscopy, atomic force microscopy and molecular perturbations to characterize the specific response of endothelial cells to application of pressure. We identified a two-phase response of endothelial cells with an initial response to acute (1 h) application of pressure (100 mmHg) followed by a different response to chronic (24 h) application. While both regimes induce cortical stiffening, the acute response is linked to Ca-mediated myosin activation, whereas the chronic cell response is dominated by increased cortical actin density and a loss in endothelial barrier function. GsMTx-4 and amiloride inhibit the acute pressure response, which suggests that the ENaC Na channel is a key player in endothelial pressure sensing. The described two-phase pressure response may participate in the differential effects of transient changes in blood pressure and hypertension.

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“…PEG is often used for its stealth functions in nanoparticle formulations because it is a hydrophilic (Bolwell et al, 1988;Crom et al, 1994;Wall and Wani, 1995;Clarke and Rivory, 1999;Lobert et al, 2000;Screnci et al, 2000;Hirschfeld et al, 2003;Forrest et al, 2006;Pommier, 2006;Yang et al, 2006;Kelland, 2007;Kreder and Dmochowski, 2007;Cai et al, 2010;Surapaneni et al, 2012;Wilson and Lippard, 2012;Yadav and Khan, 2013;Ferrati et al, 2015;Nirmalanandhan et al, 2015;Saari et al, 2015). and flexible polymer (Bergström et al, 1994).…”

Section: Mt1-mmp (A Member Of Matrix Metalloproteinase)mentioning

confidence: 99%

Lipid-Based Drug Delivery Systems in Cancer Therapy: What Is Available and What Is Yet to Come

2016

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Increased pressure alters plasma membrane dynamics and renders acute myeloid leukemia cells resistant to daunorubicin

Cited by 7 publications

References 11 publications

Hydrostatic pressure prevents chondrocyte differentiation through heterochromatin remodeling

Hydrostatic pressure prevents chondrocyte differentiation through heterochromatin remodeling

A two-phase response of endothelial cells to hydrostatic pressure

Lipid-Based Drug Delivery Systems in Cancer Therapy: What Is Available and What Is Yet to Come

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