Interaction Between a Putative Mechanosensory Membrane Channel and a Collagen

Liu, Jingdong; Schrank, Bertold; Waterston, Robert H.

doi:10.1126/science.273.5273.361

Cited by 140 publications

(125 citation statements)

References 30 publications

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“…Taken together these observations suggest that integrin-mediated changes in signal transduction that regulate sodium channel activity may be a common mechanism for shear stress-dependent regulation of ERK1/2. Alternatively, the voltage-gated sodium channel may possess extracellular matrix-binding domains that interact with the matrix (26). Mechanotransduction may then occur by changes in channel conformation mediated by physical forces transmitted through the cytoskeleton to the matrix.…”

Section: Discussionmentioning

confidence: 99%

“…2) For changes in cell-cell and cell matrixinteraction,shearstressactivatesERK1/2ina␤ 1 integrindependent manner (47) and stimulates phosphorylation of PE-CAM-1 (53), which is involved in cell-cell interactions. Changes in sodium may influence these interactions and/or there may be direct interactions between the sodium channel and matrix components (26). 3) For regulation of cell volume, water balance is regulated primarily through Na ϩ content.…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies indicate that a sodium channel mediates mechanosensing in Caenorhabditis elegans (26). Iso-osmotic substitution of 130 mM N-methyl-D-glucamine chloride for 130 mM NaCl increased ERK1/2 stimulation by shear stress (1.89 Ϯ 0.10-fold maximum) in HUVEC ( Fig.…”

Section: Shear Stress-mediated Erk1/2 Activation Is Independent Ofmentioning

confidence: 99%

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Shear Stress-mediated Extracellular Signal-regulated Kinase Activation Is Regulated by Sodium in Endothelial Cells

Traub

Ishida

et al. 1999

Journal of Biological Chemistry

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Fluid shear stress is an important regulator of endothelial cell (EC) function. To determine whether mechanosensitive ion channels participate in the EC response to shear stress, we characterized the role of ion transport in shear stress-mediated extracellular signalregulated kinase (ERK1/2) stimulation. Replacement of all extracellular Na ؉ with either N-methyl-D-glucamine or choline chloride increased the ERK1/2 stimulation in response to shear stress by 1.89 ؎ 0.1-fold. The Na ؉ effect was concentration-dependent (maximal effect, <12.5 mM) and was specific for shear stress-mediated ERK1/2 activation as epidermal growth factor-stimulated ERK1/2 activation was unaffected by removal of extracellular Na ؉ . Shear stress-mediated ERK1/2 activation was potentiated by the voltage-gated sodium channel antagonist, tetrodotoxin (100 nM), to a magnitude similar to that achieved with extracellular Na ؉ withdrawal. Transfection of Chinese hamster ovary cells with a rat brain type IIa voltage-gated sodium channel completely inhibited shear stress-mediated ERK1/2 activation in these cells. Inhibition was reversed by performing the experiment in sodium-free buffer or by including tetrodotoxin in the buffer. Western blotting of bovine and human EC lysates with SP19 antibody detected a 250-kDa protein consistent with the voltage-gated sodium channel. Degenerate polymerase chain reaction of cDNA from primary human EC yielded transcripts whose sequences were identical to the sodium channel SCN4a and SCN8a ␣ subunit genes. These results indicate that shear stress-mediated ERK1/2 activation is regulated by extracellular sodium and demonstrate that ion transport via Na ؉ channels modulates EC responses to shear stress.Mechanical stimuli are important modulators of cellular function in tissues, particularly in the cardiovascular system. A key physical force experienced by EC 1 by virtue of their unique location in the vascular wall is fluid shear stress created by the frictional force of blood flow (1). Changes in fluid shear stress have been shown to regulate EC function, including permeability of plasma lipoproteins, adhesion of leukocytes, and release of pro-and antithrombotic factors, growth factors, and vasoactive substances (reviewed in Refs. 1 and 2). These hemodynamically regulated events may contribute to the pathogenesis of vascular disease as atherosclerotic plaques are preferentially localized to areas of the vascular system that experience turbulent flow and low time-averaged shear stress (3, 4).Our laboratory has previously reported that ERK1/2 are activated by shear stress in EC (5). Whereas the mechanisms responsible for growth factor-mediated stimulation of ERK1/2 have been well characterized (6), the upstream signaling pathway that leads to activation of ERK1/2 by shear stress remains undefined. Of particular interest are the primary plasma membrane mechanisms by which the physical force of shear stress can be transduced into biochemical signals. Several candidate mechanotransducers have been proposed including G p...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Shear Stress-mediated Extracellular Signal-regulated Kinase Activation Is Regulated by Sodium in Endothelial Cells

Traub

Ishida

et al. 1999

Journal of Biological Chemistry

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“…These results suggest that MEC-6 is a subunit of the mechanosensory complex required for proper channel localization, formation, and function. Because it is widely expressed in other tissues and required for degeneration caused by gain-of-function mutations in other degenerins, MEC-6 may play similar roles in other DEG/ENaC channels [16,30,50,73].…”

Section: Proteins Required For Mechanosensationmentioning

confidence: 99%

Touch sensitivity in Caenorhabditis elegans

Bounoutas

Chalfie

2007

Pflugers Arch - Eur J Physiol

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The nematode Caenorhabditis elegans was the first organism for which touch insensitive mutants were obtained. The study of the genes defective in these mutants has led to the identification of components of a mechanosensory complex needed for specific cells to sense gentle touch to the body. Multiple approaches using genetics, cell biology, biochemistry, and electrophysiology have characterized a channel complex, containing two DEG/ENaC pore-forming subunits and several other proteins, that transduces the touch response. Other mechanical responses, sensed by other cells using a variety of other components, are less well understood in C. elegans. Many of these other senses may use TRP channels, although DEG/ENaC channels have also been implicated.

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“…Mechanical hyperalgesia is enhanced, and heat hyperalgesia is unchanged after carrageenan inflammation of the paw (Price et al, 2001). ASIC3 is a member of the DEG/ ENaC family that is known to mediate mechanical responsiveness in Caenorhabditis elegens including those sensations related to deep tissue, proprioception and muscle stretch (Driscoll and Chalfie, 1991;Huang and Chalfie, 1994;Liu et al, 1996;Tavernarakis et al, 1997). Further, ASIC3 plays a role in normal visceral mechanosensation to stretch and in mechanical sensitization of primary afferents after visceral inflammation (Jones et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

ASIC3 in muscle mediates mechanical, but not heat, hyperalgesia associated with muscle inflammation

Sluka

Radhakrishnan

Benson

et al. 2007

Pain

166

160

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Peripheral initiators of muscle pain are virtually unknown, but likely key to development of chronic pain after muscle insult. The current study tested the hypothesis that ASIC3 in muscle is necessary for development of cutaneous mechanical, but not heat hyperalgesia induced by muscle inflammation. Using mechanical and heat stimuli, we assessed behavioral responses in ASIC3−/− and ASIC3+/+ mice after induction of carrageenan muscle inflammation. ASIC3−/−mice did not develop cutaneous mechanical hyperalgesia after muscle inflammation when compared to ASIC3+/ + mice; heat hyperalgesia developed similarly between groups. We then tested if the phenotype could be rescued in ASIC3−/− mice by using a recombinant herpes virus vector to express ASIC3 in skin (where testing occurred) or muscle (where inflammation occurred). Infection of mouse DRG neurons with ASIC3-encoding virus resulted in functional expression of ASICs. Injection of ASIC3-encoding virus into muscle or skin of ASIC3−/− mice resulted in ASIC3 mRNA in DRG and protein expression in DRG and the peripheral injection site. Injection of ASIC3-encoding virus into muscle, but not skin, resulted in development of mechanical hyperalgesia similar to that observed in ASIC3+/+ mice. Thus, ASIC3 in primary afferent fibers innervating muscle is critical to development of hyperalgesia that results from muscle insult.

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Interaction Between a Putative Mechanosensory Membrane Channel and a Collagen

Cited by 140 publications

References 30 publications

Shear Stress-mediated Extracellular Signal-regulated Kinase Activation Is Regulated by Sodium in Endothelial Cells

Shear Stress-mediated Extracellular Signal-regulated Kinase Activation Is Regulated by Sodium in Endothelial Cells

Touch sensitivity in Caenorhabditis elegans

ASIC3 in muscle mediates mechanical, but not heat, hyperalgesia associated with muscle inflammation

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