Stress Fiber Formation is Required for Matrix Reorganization in a Corneal Myofibroblast Cell Line

Mar, Penny K.; Roy, Partha; Yin, Helen L.; Cavanagh, Harrison D; Jester, James V.

doi:10.1006/exer.2000.0967

Cited by 18 publications

(11 citation statements)

References 36 publications

(32 reference statements)

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“…Interestingly, changes of gastric fibroblast morphology, observed after their incubation in the presence of Hp , indicate that TGF‐β secreted by fibroblasts can also affect these cells in an autocrine/paracrine manner. In particular, Hp ‐infected fibroblasts displayed α‐SMA upregulation, accompanied by the reorganization of cortical actin and diffusible actin distribution in fibroblasts, Apparently, they acquired the phenotype of cancer‐associated fibroblasts, which can participate in the initiation, promotion, and progression of GC, perturbing not only the biochemical but also the biomechanical homeostasis of the tumor microenvironment . Close associations of GC with the growth factor‐producing activity of organ‐specific fibroblasts have already been reported .…”

Section: Discussionmentioning

confidence: 86%

Helicobacter pylori‐activated gastric fibroblasts induce epithelial‐mesenchymal transition of gastric epithelial cells in vitro in a TGF‐β‐dependent manner

et al. 2019

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Background: Colonization of the gastric mucosa with Helicobacter pylori (Hp) leads to the cascade of pathologic events including local inflammation, gastric ulceration, and adenocarcinoma formation. Paracrine loops between tissue cells and Hp contribute to the formation of gastric cancerous loci; however, the specific mechanisms underlying existence of these loops remain unknown. We determined the phenotypic properties of gastric fibroblasts exposed to Hp (cagA+vacA+) infection and their influence on normal epithelial RGM-1 cells. Materials and Methods: RGM-1 cells were cultured in the media conditioned with Hpactivated gastric fibroblasts. Their morphology and phenotypical changes associated with epithelial-mesenchymal transition (EMT) were assessed by Nomarski and fluorescence microscopy and Western blot analysis. Motility pattern of RGM-1 cells was examined by time-lapse video microscopy and transwell migration assay. The content of TGF-β in Hp-activated fibroblast-conditioned media was determined by ELISA. Results: The supernatant from Hp-activated gastric fibroblasts caused the EMT-like phenotypic diversification of RGM-1 cells. The formation of fibroblastoid cell sub-populations, the disappearance of their collective migration, an increase in transmigration potential with downregulation of E-cadherin and upregulation of N-cadherin proteins, prominent stress fibers, and decreased proliferation were observed. The fibroblast (CAF)-like transition was manifested by increased secretome TGF-β level, α-SMA protein expression, and its incorporation into stress fibers, and the TGF-βR1 kinase inhibitor reduced the rise in Snail, Twist, and E-cadherin mRNA and increased E-cadherin expression induced by CAFs. Conclusion: Gastric fibroblasts which are one of the main targets for Hp infection contribute to the paracrine interactions between Hp, gastric fibroblasts, and epithelial cells. TGF-β secreted by Hp-activated gastric fibroblasts prompting their differentiation toward CAF-like phenotype promotes the EMT-related phenotypic shifts in normal gastric epithelial cell populations. This mechanism may serve as the prerequisite for GC development. K E Y W O R D S cadherin, epithelial-mesenchymal transition, fibroblasts, Helicobacter pylori, transforming growth factor beta | 3 of 14 KRZYSIEK-MACZKA Et Al. | Isolation of conditioned mediaGastric fibroblasts were co-cultured with Hp (cagA+vacA+) strain for 72 hours. Then, the Hp was washed out from fibroblasts and the medium was changed into DMEM with 10% FBS and antibiotics. The culture dishes were maintained in a humidified atmosphere of 5% CO 2 at 37°C for 4 hours, and then, the incubatory fluid was again replaced with fresh portion of the medium. Fibroblasts were then left in fresh medium for 96 hours. After 96 hours, the supernatant was collected. The same procedure was applied to the control, noninfected fibroblast culture.

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Section: Discussionmentioning

confidence: 86%

Helicobacter pylori‐activated gastric fibroblasts induce epithelial‐mesenchymal transition of gastric epithelial cells in vitro in a TGF‐β‐dependent manner

et al. 2019

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“…In such a view, our data, demonstrating that the diode laser induced inhibition of fibroblast–myofibroblast transition, appear intriguing and of potential clinical interest. In particular, our results have shown that diode laser stimulation of TGF‐β1‐treated NIH/3T3 fibroblasts, affects multiple processes associated with fibroblast differentiation, namely (i) inhibition of the assembly of stress fibers; by these structures, the myofibroblast is capable to remodel and contract the ECM and also to adapt its activity to changes in the mechanical microenvironment as occur in fibrotic tissue ; (ii) reduction of α‐sma and type‐1 collagen expression; (iii) modification of plasmamembrane passive properties and ion currents typically expressed by myofibroblasts. In particular, laser stimulation counteracted the tendency of TGF‐β1 to induce a depolarization of RPM, strictly correlated with the proliferation and contractile properties of myofibroblasts , causing a hyperpolarization of this parameter, and attenuated inwardly rectifying K + currents (I Kir ), which usually increase in the transition to myofibroblasts and are determinant of RMP and thus of myofibroblast contractility .…”

Section: Discussionmentioning

confidence: 90%

“…Significance of difference evaluated by one-way ANOVA and Newman-Keuls multiple comparison test: Ã P < 0.05 versus CONTROL (FBS 10%), 8 P < 0.05 versus FBS2% þ TGF-b1; # P < 0.05 versus previous time; § P < 0.05 versus GdCl 3 þ TGF-b1; % P < 0.05 versus SCR-siRNA þ TGF-b1; $ P < 0.05 versus TRPC1-siRNA þ TGF-b1. remodel and contract the ECM and also to adapt its activity to changes in the mechanical microenvironment as occur in fibrotic tissue [12,52]; (ii) reduction of a-sma and type-1 collagen expression; (iii) modification of plasmamembrane passive properties and ion currents typically expressed by myofibroblasts. In particular, laser stimulation counteracted the tendency of TGF-b1 to induce a depolarization of RPM, strictly correlated with the proliferation and contractile properties of myofibroblasts [53], causing a hyperpolarization of this parameter, and attenuated inwardly rectifying K þ currents (I Kir ), which usually increase in the transition to myofibroblasts and are determinant of RMP and thus of myofibroblast contractility [17,53].…”

Section: Fig 6 Effect Of Diode Laser Irradiation On Trpc1 Expressiomentioning

confidence: 99%

Low intensity 635 nm diode laser irradiation inhibits fibroblast–myofibroblast transition reducing TRPC1 channel expression/activity: New perspectives for tissue fibrosis treatment

et al. 2015

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Low intensity irradiation with 635 ± 5 nm diode laser inhibited TGF-β1/Smad3-mediated fibroblast-myofibroblast transition and this effect involved the modulation of TRPC1 ion channels. These data contribute to support the potential anti-fibrotic effect of LLLT and may offer further informations for considering this therapy as a promising therapeutic tool for the treatment of tissue fibrosis.

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“…Our data are in agreement with previous study that IS induces generation of ROS followed by increased expression of TGF-β, in term of kidney fibrosis. α-SMA is commonly expressed in fibroblastic cells and is responsible for kidney fibrosis upon stimulation such as cytokine or mechanical damage [30], [31]. α-SMA is thought to participate in epithelial-to-mesenchymal transition (EMT), which is critical for tissue remodeling and metastasis [32], [33].…”

Section: Discussionmentioning

confidence: 99%

DPP-4 Inhibitor Attenuates Toxic Effects of Indoxyl Sulfate on Kidney Tubular Cells

et al. 2014

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Diabetic nephropathy is a common causative factor of chronic kidney disease (CKD). DPP-4 inhibitor has the ability to improve kidney function and renal microvasculature. In the present study, we investigate the deleterious effects of IS on proximal tubular cells and the protective role of DPP-4 inhibitor. Human kidney 2 (HK-2) cells were exposed to IS in the presence or absence of DPP-4 inhibitor. Effects of DPP-4 inhibitor on viability of HK-2 cells were determined by MTT assay. Reactive oxygen species (ROS) production was examined using fluorescent microscopy. Levels of cleaved caspase-3, transforming growth factor-beta (TGF-β), α-smooth muscle actin (α-SMA) and NF-kappaB p65 and phosphorylation of AKT and extracellular signal-regulated kinase (ERK) were detected by immunoblotting. Production of ROS and level of cleaved caspase-3 were increased by IS in a dose-dependent manner. The phosphorylation of AKT and ERK p65 were decreased alongside activation of NF-κB. Expression of TGF-β and α-SMA, were upregulated in IS-treated HK-2 cells. Treatment with DPP-4 inhibitor resulted in a significant increase in cell viability and a decrease of ROS production in IS-treated HK-2 cells. DPP-4 inhibitor restored IS-induced deactivations of AKT and ERK and inhibited activation of NF-κB in IS-treated HK-2 cells. Moreover, DPP-4 inhibitor could also attenuate IS-induced up-regulation of TGF-β and α-SMA expression. These findings suggest that DPP-4 inhibitor possesses anti-apoptotic activity to ameliorate the IS-induced renal damage, which may be partly attributed to regulating ROS/p38MAPK/ERK and PI3K-AKT pathways as well as downstream NF-κB signaling pathway.

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Stress Fiber Formation is Required for Matrix Reorganization in a Corneal Myofibroblast Cell Line

Cited by 18 publications

References 36 publications

Helicobacter pylori‐activated gastric fibroblasts induce epithelial‐mesenchymal transition of gastric epithelial cells in vitro in a TGF‐β‐dependent manner

Helicobacter pylori‐activated gastric fibroblasts induce epithelial‐mesenchymal transition of gastric epithelial cells in vitro in a TGF‐β‐dependent manner

Low intensity 635 nm diode laser irradiation inhibits fibroblast–myofibroblast transition reducing TRPC1 channel expression/activity: New perspectives for tissue fibrosis treatment

DPP-4 Inhibitor Attenuates Toxic Effects of Indoxyl Sulfate on Kidney Tubular Cells

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