Distribution of Cytoskeletal Components in Endothelial Cells in the Guinea Pig Renal Artery

Katoh, Kazuo; Noda, Yasuko

doi:10.1155/2012/439349

Cited by 7 publications

(6 citation statements)

References 30 publications

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“…However, the drugs inhibiting F-actin dynamics increased NF-κB activation under low pulsatility flow whereas the drugs inhibiting microtubule dynamics did not. This observation showed that pretreatment of cells with ultralow concentrations of taxol or nocodazole, which were at least more than 3000 times lower than that previously used in flow studies 33,44,45 , reduced NF-κB activation under high pulsatility flow without affecting that activation in cells under normal flow conditions. Gene expression results further showed that drug effects on pro-inflammatory ICAM-1 mRNA expression in PAECs under high pulsatility flow were similar to their effects on NF-κB activation (Figure 4B).…”

Section: Resultsmentioning

confidence: 74%

High Pulsatility Flow Induces Acute Endothelial Inflammation Through Overpolarizing Cells to Activate NF-κB

Yan

Stenmark

et al. 2012

Cardiovasc Eng Tech

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Large artery stiffening and small artery inflammation are both well-known pathological features of pulmonary and systemic hypertension, but the relationship between them has been seldom explored. We previously demonstrated that stiffening-induced high pulsatility flow stimulated a pro-inflammatory response in distal pulmonary artery endothelial cells (PAEC). Herein, we hypothesized that high pulsatility flow activated PAEC pro-inflammatory responses are mediated through cell structural remodeling and cytoskeletal regulation of NF-κB translocation. To test this hypothesis, cells were exposed to low and high pulsatility flows with the same mean physiological flow shear stress. Results showed that unidirectional, high pulsatility flow led to continuous, high-level NF-κB activation, whereas low pulsatility flow induced only transient, minor NF-κB activation. Compared to cell shape under the static condition, low pulsatility flow induced cell elongation with a polarity index of 1.7, while high pulsatility flow further increased the cell polarity index to a value greater than 3. To explore the roles of cytoskeletal proteins in transducing high flow pulsatility into NF-κB activation, PAECs were treated with drugs that reduce the synthesis-breakdown dynamics of F-actin or microtubules (cytochalasin D, phalloidin, nocodazole, and taxol) prior to flow. Results showed that these pre-treatments suppressed NF-κB activation induced by high pulsatility flow, but drugs changing dynamics of F-actin enhanced NF-κB activation even under low pulsatility flow. Taxol was further circulated in the flow to examine its effect on cells. Results showed that circulating taxol (10nM) reduced PAEC polarity, NF-κB activation, gene expression of pro-inflammatory molecules (ICAM-1 and VCAM-1), and monocyte adhesion on the PAECs under high pulsatility flow. Therefore, taxol effectively reduced high pulsatility flow-induced PAEC overpolarization and pro-inflammatory responses via inhibiting cytoskeletal remodeling. This study suggests that stabilizing microtubule dynamics might bea potential therapeutic means of reducing endothelial inflammation caused by high pulsatility flow.

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Section: Resultsmentioning

confidence: 74%

High Pulsatility Flow Induces Acute Endothelial Inflammation Through Overpolarizing Cells to Activate NF-κB

Yan

Stenmark

et al. 2012

Cardiovasc Eng Tech

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“…Focal adhesions are structures that penetrate the cell membrane and serve as a connection between the inside of the cell and its substrate (glass or plastic surface in the case of cultured cells). The focal adhesions are directly connected to stress fibers on the inside of the cell, and can transmit signals, such as electrical stimuli, from the external environment into the cell, and are therefore considered to be signaling sites [5,14,18]. Therefore, it is likely that the focal adhesions and their associated contractile structures, the stress fibers, play important roles as receptors for electrical stimuli in cells cultured in the laboratory.…”

Section: Discussionmentioning

confidence: 99%

Effects of Electrical Stimulation on the Signal Transduction-Related Proteins, c-Src and Focal Adhesion Kinase, in Fibroblasts

Katoh

2022

Life

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Electrical stimulation of the skin and muscles, e.g., in the fields of rehabilitation medicine and acupuncture, is known to locally increase blood flow and metabolism, and thus have beneficial health effects. However, little is known about the changes in cellular morphology or regulation of the localization of specific proteins in response to electrical stimuli. The present study was performed to examine the effects of electrical stimulation on the cytoskeletal system of cultured fibroblasts. Following application of electrical stimulation to cultured fibroblastic cells for a period of about 2 h, the stress fibers in the cells became thicker and the cells showed a contracted appearance. Cells were subjected to periodic electrical stimulation for 0 (unstimulated control), 2, 5, or 20 h. The stress fibers showed an increase in thickness within 2 h, and became gradually thicker until 20 h. In addition, the focal adhesions and stress fibers were enlarged after 2 h of continuous stimulation, and both stress fibers and focal adhesions became larger and thicker after 20 h of periodic stimulation. Cells showed increased staining of focal adhesions with anti-phosphotyrosine antibody (PY-20) after electrical stimulation. Cells also showed increased staining of tyrosine-phosphorylated focal adhesion kinase (FAK) (pY397) and tyrosine-phosphorylated c-Src (pY418), indicating that electrical stimulation affected signal transduction-related proteins.

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“…The stress fibers that comprise the actomyosin system observed in various cultured cells are cytoskeletal structures that are commonly found at sites involved in the generation of contractile force both in vivo and in vitro, and they are exposed to sustained mechanical stimulation applied by blood flow in endothelial cells in the aortae or veins [68,69]. In addition, focal adhesions are structures involved in connecting cells to the substrates on the basal plane, and focal adhesions and the ends of the stress fibers are connected on the plasma membrane via focal adhesion-associated proteins.…”

Section: Morphology Change and Elongation Of Fak Knockout Cellsmentioning

confidence: 99%

“…Two types of stress fibers were identified: those located at the peripheral portion of the cell, which are called peripheral stress fibers, and those located at the central portion of the cell, called central stress fibers [70,71]]. The activation of ROCK controls the formation of stress fibers and focal adhesions in the central part of cultured fibroblasts [69,71]. Local accumulation and the activation of FAK are thought to be important for the formation and destruction of focal adhesions, and the activation of FAK regulates the organization of newly formed stress fibers and focal adhesions by ROCK [35].…”

Section: Morphology Change and Elongation Of Fak Knockout Cellsmentioning

confidence: 99%

FAK-Dependent Cell Motility and Cell Elongation

Katoh

2020

Cells

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Fibroblastic cells show specific substrate selectivity for typical cell–substrate adhesion. However, focal adhesion kinase (FAK) contributes to controlling the regulation of orientation and polarity. When fibroblasts attach to micropatterns, tyrosine-phosphorylated proteins and FAK are both detected along the inner border between the adhesive micropatterns and the nonadhesive glass surface. FAK likely plays important roles in regulation of cell adhesion to the substrate, as FAK is a tyrosine-phosphorylated protein that acts as a signal transduction molecule at sites of cell–substrate attachment, called focal adhesions. FAK has been suggested to play a role in the attachment of cells at adhesive micropatterns by affecting cell polarity. Therefore, the localization of FAK might play a key role in recognition of the border of the cell with the adhesive micropattern, thus regulating cell polarity and the cell axis. This review discusses the regulation and molecular mechanism of cell proliferation and cell elongation by FAK and its associated signal transduction proteins.

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Distribution of Cytoskeletal Components in Endothelial Cells in the Guinea Pig Renal Artery

Cited by 7 publications

References 30 publications

High Pulsatility Flow Induces Acute Endothelial Inflammation Through Overpolarizing Cells to Activate NF-κB

High Pulsatility Flow Induces Acute Endothelial Inflammation Through Overpolarizing Cells to Activate NF-κB

Effects of Electrical Stimulation on the Signal Transduction-Related Proteins, c-Src and Focal Adhesion Kinase, in Fibroblasts

FAK-Dependent Cell Motility and Cell Elongation

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