Involvement of Mechanical Stretch in the Gelatinolytic Activity of the Fibrous Sclera of Chicks, In Vitro

2002 ◽  
Vol 46 (1) ◽  
pp. 24-30 ◽  
Author(s):  
H Fujikura
2021 ◽  
Vol 22 (9) ◽  
pp. 4297
Author(s):  
Matthew Thomas Ferreira ◽  
Juliano Andreoli Miyake ◽  
Renata Nascimento Gomes ◽  
Fábio Feitoza ◽  
Pollyana Bulgarelli Stevannato ◽  
...  

Prostaglandin E2 (PGE2) is known to increase glioblastoma (GBM) cell proliferation and migration while cyclooxygenase (COX) inhibition decreases proliferation and migration. The present study investigated the effects of COX inhibitors and PGE2 receptor antagonists on GBM cell biology. Cells were grown with inhibitors and dose response, viable cell counting, flow cytometry, cell migration, gene expression, Western blotting, and gelatin zymography studies were performed. The stimulatory effects of PGE2 and the inhibitory effects of ibuprofen (IBP) were confirmed in GBM cells. The EP2 and EP4 receptors were identified as important mediators of the actions of PGE2 in GBM cells. The concomitant inhibition of EP2 and EP4 caused a significant decrease in cell migration which was not reverted by exogenous PGE2. In T98G cells exogenous PGE2 increased latent MMP2 gelatinolytic activity. The inhibition of COX1 or COX2 caused significant alterations in MMP2 expression and gelatinolytic activity in GBM cells. These findings provide further evidence for the importance of PGE2 signalling through the EP2 and the EP4 receptor in the control of GBM cell biology. They also support the hypothesis that a relationship exists between COX1 and MMP2 in GBM cells which merits further investigation as a novel therapeutic target for drug development.


2015 ◽  
Vol 37 (5) ◽  
pp. 1817-1829 ◽  
Author(s):  
Kai Huang ◽  
Zhi-Qiang Yan ◽  
Dan Zhao ◽  
Si-Guo Chen ◽  
Li-Zhi Gao ◽  
...  

Background/Aims: Physiological mechanical stretch in vivo helps to maintain the quiescent contractile differentiation of vascular smooth muscle cells (VSMCs), but the underlying mechanisms are still unclear. Here, we investigated the effects of SIRT1 in VSMC differentiation in response to mechanical cyclic stretch. Methods and Results: Rat VSMCs were subjected to 10%-1.25Hz-cyclic stretch in vitro using a FX-4000T system. The data indicated that the expression of contractile markers, including α-actin, calponin and SM22α, was significantly enhanced in VSMCs that were subjected to cyclic stretch compared to the static controls. The expression of SIRT1 and FOXO3a was increased by the stretch, but the expression of FOXO4 was decreased. Decreasing SIRT1 by siRNA transfection attenuated the stretch-induced expression of contractile VSMC markers and FOXO3a. Furthermore, increasing SIRT1 by either treatment with activator resveratrol or transfection with a plasmid to induce overexpression increased the expression of FOXO3a and contractile markers, and decreased the expression of FOXO4 in VSMCs. Similar trends were observed in VSMCs of SIRT1 (+/-) knockout mice. The overexpression of FOXO3a promoted the expression of contractile markers in VSMCs, while the overexpression of FOXO4 demonstrated the opposite effect. Conclusion: Our results indicated that physiological cyclic stretch promotes the contractile differentiation of VSMCs via the SIRT1/FOXO pathways and thus contributes to maintaining vascular homeostasis.


2001 ◽  
Vol 123 (3) ◽  
pp. 247-255 ◽  
Author(s):  
Donna M. Geddes ◽  
Robert S. Cargill

An in vitro model for neural trauma was characterized and validated. The model is based on a novel device that is capable of applying high strain rate, homogeneous, and equibiaxial deformation to neural cells in culture. The deformation waveform is fully arbitrary and controlled via closed-loop feedback. Intracellular calcium [Ca2+]i alterations were recorded in real time throughout the imposed strain with an epifluorescent microscopy system. Peak change in [Ca2+]i, recovery of [Ca2+]i, and percent responding NG108-15 cells were shown to be dependent on strain rate (1−1 to 10−1) and magnitude (0.1 to 0.3 Green’s Strain). These measures were also shown to depend significantly on the interaction between strain rate and magnitude. This model for neural trauma is a robust system that can be used to investigate the cellular tolerance and response to traumatic brain injury.


2018 ◽  
Vol 205 (4) ◽  
pp. 189-196 ◽  
Author(s):  
Yu Feng ◽  
Xiang-Yang Tian ◽  
Peng Sun ◽  
Ze-Peng Cheng ◽  
Reng-Fei Shi

Mechanical stretch may cause myoblasts to either proliferate or undergo apoptosis. Identifying the molecular events that switch the fate of a stretched cell from proliferation to apoptosis is practically important in the field of regenerative medicine. A recent study on vascular smooth muscle cells illustrated that identification of these events may be achieved by addressing the stretch-induced opposite cellular outcomes simultaneously within a single investigation. To define conditions or a model in which both proliferation and apoptosis can be studied at the same time, we exposed in vitro cultured C2C12 myoblasts to a cyclic mechanical stretch regimen of 15% elongation at a stretching frequency of 1 Hz for 0, 2, 4, 6, or 8 h every day, consecutively, for 3 days. Both proliferation and apoptosis were observed. Moreover, as the duration of the stretch was prolonged, cell proliferation increased until it peaked at the optimal stretching duration. Afterwards, apoptosis gradually prevailed. Therefore, we established a model in which stretch-induced cell proliferation and apoptosis can be studied simultaneously.


2002 ◽  
Vol 283 (6) ◽  
pp. F1192-F1199 ◽  
Author(s):  
David J. Galvin ◽  
R. William G. Watson ◽  
James I. Gillespie ◽  
Hugh Brady ◽  
John M. Fitzpatrick

Our understanding of the pathophysiology of the overactive bladder is poor. It has been proposed that localized contractions result in the abnormal stretching of bladder smooth muscle. We hypothesize that stretch regulates the cellular processes that determine tissue size. The purpose of this study was to investigate the effect of stretch on apoptosis, proliferation, cell hypertrophy, and growth factor production in human bladder smooth muscle cells in vitro. Normal human detrusor muscle was obtained from patients undergoing radical cystectomy for invasive bladder cancer, and primary cultures were established. Cells were mechanically stretched on flexible plates at a range of pressures and times. Apoptosis was assessed by propidium iodide incorporation and flow cytometry. Radiolabeled thymidine and amino acid incorporation were used to assess proliferation and cell hypertrophy. ELISA and RT-PCR were used to assess growth factor production. Mechanical stretch inhibits apoptosis in a time- and dose-dependent manner and was associated with increases in the antiapoptotic proteins heat shock protein-70 and cIAP-1. Stretch also increases smooth muscle cell proliferation and hypertrophy, but hypertrophy is the more dominant response. These changes were associated with increases in IGF-1 and basic FGF and a decrease in transforming growth factor-β1. Mechanical stretch regulates apoptosis, proliferation, and cell hypertrophy in human bladder smooth muscle cells.


2000 ◽  
Vol 279 (6) ◽  
pp. H3124-H3130 ◽  
Author(s):  
Michael J. Yost ◽  
David Simpson ◽  
Kimberly Wrona ◽  
Stephen Ridley ◽  
Harry J. Ploehn ◽  
...  

In vitro mechanical cell stimulators are used for the study of the effect of mechanical stimulation on anchorage-dependent cells. We developed a new mechanical cell stimulator, which uses stepper motor technology and computer control to achieve a high degree of accuracy and repeatability. This device also uses high-performance plastic components that have been shown to be noncytotoxic, dimensionally stable, and resistant to chemical degradation from common culture laboratory chemicals. We show that treatment with glow discharge for 25 s at 20 mA is sufficient to modify the surface of the rubber to allow proper adhesion for polymerization of aligned collagen. We show through finite element analysis that the middle area of the membrane, away from the clamped ends, is predictable, homogeneous, and has negligible shear strain. To test the efficacy of the mechanical stretch, we examined the effect of mechanical stimulation on the production of β1-integrin by neonatal rat cardiac fibroblasts. Mechanical stimulation was tested in the range of 0–12% stretch and 0–10-cycles/min stretch frequency. The fibroblasts respond with an increase in β1-integrin at 3% stretch and a decrease at 6 and 12% stretch. Stretch frequency was found to not significantly effect the concentration of β1-integrin. These studies yield a new and improved mechanical cell stimulator and demonstrate that mechanical stimulation has an effect on the expression of β1-integrin.


2000 ◽  
Vol 89 (5) ◽  
pp. 2078-2084 ◽  
Author(s):  
Mingyao Liu ◽  
Martin Post

Growth and maturation of fetal lungs are regulated by both humoral and physical factors. Mechanical stretch stimulates fetal lung cell proliferation and affects fetal lung maturation by influencing the production of extracellular matrix molecules and the expression of specific genes of fetal lung cells. These effects are mediated through special signal transduction pathways in fetal lung cells. Various in vivo and in vitro model systems have been developed to investigate the mechanotransduction process. The diversity and discrepancy of these studies have raised many questions. We will briefly summarize mechanical force-induced signals in fetal lung cell proliferation and differentiation and then discuss several important issues related to these studies.


1996 ◽  
Vol 270 (5) ◽  
pp. C1284-C1292 ◽  
Author(s):  
H. H. Vandenburgh ◽  
R. Solerssi ◽  
J. Shansky ◽  
J. W. Adams ◽  
S. A. Henderson

Adherent cultures of neonatal rat cardiomyocytes were subjected to progressive, unidirectional lengthening for 2-4 days in serum-containing medium. This mechanical stretch (25% increase in initial length each day) simulates the eccentric mechanical load placed on in vivo heart cells by increases in postnatal blood pressure and volume. The in vitro mechanical stimuli initiated a number of morphological alterations in the confluent cardiomyocyte population which were similar to those occurring during in vivo heart growth. These include cardiomyocyte organization into parallel arrays of rod-shaped cells, increased cardiomyocyte binucleation, and cardiomyocyte hypertrophy by longitudinal cell growth. Stretch stimulated DNA synthesis in the noncardiomyocyte population but not in the cardiomyocytes. Myosin heavy chain (MHC) content increased 62% over 4 days of stretch and included increased accumulation of both fetal beta-MHC and adult alpha-MHC isoforms. This new model of stretch-induced cardiomyocyte hypertrophy may assist in examining some of the complex mechanogenic growth processes that occur in the rapidly enlarging neonatal heart.


Author(s):  
Chen-rei Wan ◽  
Seok Chung ◽  
Ryo Sudo ◽  
Roger D. Kamm

Embryonic stem cell derived cardiomyocytes are deemed an attractive treatment option for myocardial infarction. Their clinical efficacy, however, has not been unequivocally demonstrated. There is a need for better understanding and characterization of the cardiogenesis process. A microfluidic platform in vitro is used to dissect and better understand the differentiation process. Through this study, we find that while embryoid bodies (EBs) flatten out in a well plate system, differentiated EBs self-assemble into complex 3D structures. The beating regions of EBs are also different. Most beating areas are observed in a ring pattern on 2D well plates around the center, self-assembled beating large 3D aggregates are found in microfluidic devices. Furthermore, inspired by the natural mechanical environment of the heart, we applied uniaxial cyclic mechanical stretch to EBs. Results suggest that prolonged mechanical stimulation acts as a negative regulator of cardiogenesis. From this study, we conclude that the culture environments can influence differentiation of embryonic stem cells into cardiomycytes, and that the use of microfluidic systems can provide new insights into the differentiation process.


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