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BioMimetic Therapeutics 3d biomimetic model
High-resolution representative image of collagen gels used for <t>contractility</t> experiments without a circle around the periphery of the gel.
3d Biomimetic Model, supplied by BioMimetic Therapeutics, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/3d+biomimetic+model/pmc12187138-135-13-27?v=BioMimetic+Therapeutics
Average 90 stars, based on 1 article reviews
3d biomimetic model - by Bioz Stars, 2026-07
90/100 stars

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1) Product Images from "TRPV4 activation by TGFβ2 enhances cellular contractility and drives ocular hypertension"

Article Title: TRPV4 activation by TGFβ2 enhances cellular contractility and drives ocular hypertension

Journal: eLife

doi: 10.7554/eLife.104894

High-resolution representative image of collagen gels used for contractility experiments without a circle around the periphery of the gel.
Figure Legend Snippet: High-resolution representative image of collagen gels used for contractility experiments without a circle around the periphery of the gel.

Techniques Used:

( A ) Representative longitudinal 24-well plate scans of collagen type I hydrogels seeded with primary TM (pTM) subjected to the different treatments (dashed lines outline size of contracted constructs). ( B ) Longitudinal quantification of hydrogel construct size compared to the control group at the 0 min time point. ( C ) Detailed comparisons between groups at each experimental time point. n = 6 hydrogels/group. One-way ANOVA with Tukey’s multiple comparisons test, data in ( B, C ) show individual data points over mean ± SD. One pTM strain shown: TGFβ2-induced contractility induction, HC-06-mediated rescue of hypercontractility, and GSK101-induced transient (15 min) contraction were consistent across (3/3) pTM strains tested . **p < 0.01, ***p < 0.001, ****p < 0.0001.
Figure Legend Snippet: ( A ) Representative longitudinal 24-well plate scans of collagen type I hydrogels seeded with primary TM (pTM) subjected to the different treatments (dashed lines outline size of contracted constructs). ( B ) Longitudinal quantification of hydrogel construct size compared to the control group at the 0 min time point. ( C ) Detailed comparisons between groups at each experimental time point. n = 6 hydrogels/group. One-way ANOVA with Tukey’s multiple comparisons test, data in ( B, C ) show individual data points over mean ± SD. One pTM strain shown: TGFβ2-induced contractility induction, HC-06-mediated rescue of hypercontractility, and GSK101-induced transient (15 min) contraction were consistent across (3/3) pTM strains tested . **p < 0.01, ***p < 0.001, ****p < 0.0001.

Techniques Used: Construct, Control

Chronic exposure to TGFβ2 induces upregulation of functional TRPV4 channels alongside the autoinhibitory canonical modulator SMAD7. TRPV4-mediated Ca 2+ influx, canonical, and non-canonical TGFβ2 signaling stimulate the Rho/ROCK pathway to augment cytoskeletal contractility and stimulate extracellular matrix (ECM) release. Actomyosin contractility promotes outflow resistance and drives OHT and underpins a vicious feedforward TRPV4-dependent loop that maintains OHT. This figure was created using BioRender.com .
Figure Legend Snippet: Chronic exposure to TGFβ2 induces upregulation of functional TRPV4 channels alongside the autoinhibitory canonical modulator SMAD7. TRPV4-mediated Ca 2+ influx, canonical, and non-canonical TGFβ2 signaling stimulate the Rho/ROCK pathway to augment cytoskeletal contractility and stimulate extracellular matrix (ECM) release. Actomyosin contractility promotes outflow resistance and drives OHT and underpins a vicious feedforward TRPV4-dependent loop that maintains OHT. This figure was created using BioRender.com .

Techniques Used: Functional Assay



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Image Search Results


High-resolution representative image of collagen gels used for contractility experiments without a circle around the periphery of the gel.

Journal: eLife

Article Title: TRPV4 activation by TGFβ2 enhances cellular contractility and drives ocular hypertension

doi: 10.7554/eLife.104894

Figure Lengend Snippet: High-resolution representative image of collagen gels used for contractility experiments without a circle around the periphery of the gel.

Article Snippet: The present study extends those observations by revealing the TRPV4 -dependence of TM contractility (the agonist GSK101 induced, and the antagonist HC-06 suppressed, contractility in a 3D biomimetic model) and by establishing TRPV4 as an obligatory effector of OHT under physiological (circadian rhythmicity) as well as pathological conditions.

Techniques:

( A ) Representative longitudinal 24-well plate scans of collagen type I hydrogels seeded with primary TM (pTM) subjected to the different treatments (dashed lines outline size of contracted constructs). ( B ) Longitudinal quantification of hydrogel construct size compared to the control group at the 0 min time point. ( C ) Detailed comparisons between groups at each experimental time point. n = 6 hydrogels/group. One-way ANOVA with Tukey’s multiple comparisons test, data in ( B, C ) show individual data points over mean ± SD. One pTM strain shown: TGFβ2-induced contractility induction, HC-06-mediated rescue of hypercontractility, and GSK101-induced transient (15 min) contraction were consistent across (3/3) pTM strains tested . **p < 0.01, ***p < 0.001, ****p < 0.0001.

Journal: eLife

Article Title: TRPV4 activation by TGFβ2 enhances cellular contractility and drives ocular hypertension

doi: 10.7554/eLife.104894

Figure Lengend Snippet: ( A ) Representative longitudinal 24-well plate scans of collagen type I hydrogels seeded with primary TM (pTM) subjected to the different treatments (dashed lines outline size of contracted constructs). ( B ) Longitudinal quantification of hydrogel construct size compared to the control group at the 0 min time point. ( C ) Detailed comparisons between groups at each experimental time point. n = 6 hydrogels/group. One-way ANOVA with Tukey’s multiple comparisons test, data in ( B, C ) show individual data points over mean ± SD. One pTM strain shown: TGFβ2-induced contractility induction, HC-06-mediated rescue of hypercontractility, and GSK101-induced transient (15 min) contraction were consistent across (3/3) pTM strains tested . **p < 0.01, ***p < 0.001, ****p < 0.0001.

Article Snippet: The present study extends those observations by revealing the TRPV4 -dependence of TM contractility (the agonist GSK101 induced, and the antagonist HC-06 suppressed, contractility in a 3D biomimetic model) and by establishing TRPV4 as an obligatory effector of OHT under physiological (circadian rhythmicity) as well as pathological conditions.

Techniques: Construct, Control

Chronic exposure to TGFβ2 induces upregulation of functional TRPV4 channels alongside the autoinhibitory canonical modulator SMAD7. TRPV4-mediated Ca 2+ influx, canonical, and non-canonical TGFβ2 signaling stimulate the Rho/ROCK pathway to augment cytoskeletal contractility and stimulate extracellular matrix (ECM) release. Actomyosin contractility promotes outflow resistance and drives OHT and underpins a vicious feedforward TRPV4-dependent loop that maintains OHT. This figure was created using BioRender.com .

Journal: eLife

Article Title: TRPV4 activation by TGFβ2 enhances cellular contractility and drives ocular hypertension

doi: 10.7554/eLife.104894

Figure Lengend Snippet: Chronic exposure to TGFβ2 induces upregulation of functional TRPV4 channels alongside the autoinhibitory canonical modulator SMAD7. TRPV4-mediated Ca 2+ influx, canonical, and non-canonical TGFβ2 signaling stimulate the Rho/ROCK pathway to augment cytoskeletal contractility and stimulate extracellular matrix (ECM) release. Actomyosin contractility promotes outflow resistance and drives OHT and underpins a vicious feedforward TRPV4-dependent loop that maintains OHT. This figure was created using BioRender.com .

Article Snippet: The present study extends those observations by revealing the TRPV4 -dependence of TM contractility (the agonist GSK101 induced, and the antagonist HC-06 suppressed, contractility in a 3D biomimetic model) and by establishing TRPV4 as an obligatory effector of OHT under physiological (circadian rhythmicity) as well as pathological conditions.

Techniques: Functional Assay