Gsmtx 4

Manufactured by Merck Group

Sourced in United States

GsMTx-4 is a peptide derived from the venom of the tarantula Grammostola spatulata. It functions as a mechanosensitive ion channel blocker, specifically inhibiting the opening of stretch-activated cation channels. This compound is used as a research tool to study the role of mechanosensitive ion channels in various biological processes.

Automatically generated - may contain errors

Lab products found in correlation

6 protocols using gsmtx 4

Mechanical Stretch Modulation of hPDLC Cytoskeleton

Check if the same lab product or an alternative is used in the 5 most similar protocols

Human periodontal ligament cells (hPDLCs) were plated in BioFlex culture plates (type I collagen-coated; Flexcell International Corporation) and divided into four groups. The first was a control group, in which cells were loaded onto a Flexcell tension system (FX-5000T, Flexcell International Corporation) without any treatment. The second were cells in the cytoD group, which were pretreated with cytoD (Sigma-Aldrich; Merck KGaA) at a concentration of 5 µg/ml to depolymerize F-actin in the cells and incubated at 37°C for 20 min, cells were refreshed by addition of fresh culture medium without cytoD. For the third (GSK205) and fourth (GsMTx4) groups, fresh medium respectively containing 30 µM GSK205 (cat. no. 616522; Merck KGaA) and 500 nM GsMTx4 (cat. no. ab141871; Abcam) were added separately before cell loading to suppress the TRPV4 and Piezo1 channels, and cells were subjected to these compounds during loading Next, the plates were set on the FX-5000T. Then, 15% stretch was applied onto the cells for 4, 8 and 12 h. According to the study of Lu et al (9 (link)) on three different cell types, a stretch time duration of <3 sec fails to initiate calcium influx. Consequently, a 0.25-Hz square waveform of periodic loading, which persisted for 3 sec with a 1-sec release, was selected for the present study.

Shen Y., Pan Y., Guo S., Sun L., Zhang C, & Wang L. (2020). The roles of mechanosensitive ion channels and associated downstream MAPK signaling pathways in PDLC mechanotransduction. Molecular Medicine Reports, 21(5), 2113-2122.

+ Open protocol

+ Expand

Modulating Neuron Cultures with Inhibitors

Check if the same lab product or an alternative is used in the 5 most similar protocols

Neurons were seeded at DIV0 and cultured in cell culture medium until DIV1. At DIV1, the medium was supplemented with Nocodazole (Sigma-Aldrich, Burlington, Massachusetts, US, #SML1665; 1.8 ng mL⁻¹) or Cycloexamide (Sigma-Aldrich, Burlington, Massachusetts, US, #C7698; 30 ng mL⁻¹) or Brefaldin-A (Sigma-Aldrich, Burlington, Massachusetts, US, #B5936; 0.05 μg ml⁻¹) or GsMTx-4 (Sigma-Aldrich, Burlington, Massachusetts, US, #SML3140; 500 nM) until DIV3 (Nocodazole, Brefaldin-A, or GsMTx-4) or DIV6 (Cycloexamide).

Falconieri A., De Vincentiis S., Cappello V., Convertino D., Das R., Ghignoli S., Figoli S., Luin S., Català-Castro F., Marchetti L., Borello U., Krieg M, & Raffa V. (2022). Axonal plasticity in response to active forces generated through magnetic nano-pulling. Cell Reports, 42(1), 111912.

+ Open protocol

+ Expand

Astrocyte Response to TGFβ2 Treatment

Check if the same lab product or an alternative is used in the 5 most similar protocols

ONH astrocytes were seeded at 1 × 10⁴ cells/cm² on sterilized glass coverslips in 24-well culture plates (Thermo Fisher Scientific, Waltham, MA). After 24 h, cells were treated with increasing doses of TGFβ2 (vehicle control, 1.25 ng/ml, 2.5 ng/ml, and 5 ng/ml; R&D Systems, Minneapolis, MN) for 48 h. In a separate set of experiments, cells underwent the following treatments for 48 h: (1) vehicle control, (2) TGFβ2 (5 ng/ml), (3) TGFβ2 (5 ng/ml) + GsMTx4 (500 nM; Sigma-Aldrich), or (4) GsMTx4 (500 nM).

Kirschner A., Strat A.N., Yablonski J., Yoo H., Bagué T., Li H., Zhao J., Bollinger K.E., Herberg S, & Ganapathy P.S. (2021). Mechanosensitive channel inhibition attenuates TGFβ2-induced actin cytoskeletal remodeling and reactivity in mouse optic nerve head astrocytes. Experimental eye research, 212, 108791.

+ Open protocol

+ Expand

Modulating Alveolar and Endothelial Cells

Check if the same lab product or an alternative is used in the 5 most similar protocols

The human alveolar epithelial cell line (A549) and the human pulmonary microvascular endothelial cell line (HPMEC) were purchased from the BNCC Biotechnology Research Institute (Beijing, China). The cells were cultured in Dulbecco’s modified Eagle’s medium (DMEM) and M199 (HyClone, Logan, UT, USA) supplemented with 10% fetal bovine serum (Gibco, Carlsbad, CA, USA), 100 U/mL penicillin, and 100 μg/mL streptomycin at 37 °C in an atmosphere of 95% air and 5% CO₂. When the cells reached 80% confluence, they were seeded into 24-well or 6-well plates for further experiments. For small interfering RNA (siRNA) transfection, the Piezo1 siRNA (Thermo Fisher Scientific, Waltham, MA, USA) and its negative control siRNA (Invitrogen) were transfected into the cells using Lipofectamine 3000 (Invitrogen, Carlsbad, CA, USA) according to the manufacturer’s instructions. Three days later, the cells were collected. HPMEC monolayers were pre-treated with different concentration of Yoda1 (Tocris/BioTechne, Bristol, UK), 5 μM GSMTx4, 10 μM Y-27632 or fasudil (Merck Millipore, Burlington, MA, USA) for 24 h before cell deformation or collection.

Zhang Y., Jiang L., Huang T., Lu D., Song Y., Wang L, & Gao J. (2021). Mechanosensitive cation channel Piezo1 contributes to ventilator-induced lung injury by activating RhoA/ROCK1 in rats. Respiratory Research, 22, 250.

+ Open protocol

+ Expand

Inhibition of Ca2+ Signaling Pathways

Check if the same lab product or an alternative is used in the 5 most similar protocols

After loading Fluo-4AM onto cells, the cells were loaded with inhibitors. To inhibit Ca²⁺ release, either thapsigargin (1 µM in HBSS, Sigma), U73122 (1 μM in HBSS, Calbiochem), or 2-APB (1 µM in HBSS, Sigma) was loaded for 30 min. To inhibit Ca²⁺ influx, extracellular Ca²⁺ was depleted with Ca²⁺-free HBSS (NaCl 130, KCl 5.4, MgCl₂ 2.6, glucose 5.5, HEPES 20, EGTA 0.1; in mM)^{21 (link)} for 30 min. To inhibit SAChs, either Gd³⁺ (1 µM in HBSS, Sigma) or GsMTx-4 (1 µM in HBSS, Sigma) was loaded. To inhibit cytoskeletons, either cytochalasin D (10 μM in HBSS, Sigma), blebbistatin (10 μM in HBSS, Sigma), or nocodazole (1 μM in HBSS, Sigma) was loaded for 30 min. Without washing away the inhibitors, the cells were irradiated with shock waves.

Takahashi T., Nakagawa K., Tada S, & Tsukamoto A. (2019). Low-energy shock waves evoke intracellular Ca2+ increases independently of sonoporation. Scientific Reports, 9, 3218.

+ Open protocol

+ Expand

Macrophage-Cementoblast Interaction Study

Check if the same lab product or an alternative is used in the 5 most similar protocols

The macrophage cell line RAW264.7 was purchased from the ATCC, and the OCCM-30 cementoblast [54 (link)] was kindly provided by Prof. M. Somerman (NIH, NIDCR, Bethesda, MD, USA). Briefly, all cells were maintained in DMEM (41965062, Gibco, New York, NY, USA) containing 10% Fetal Bovine Serum (FBS) (10270-106, Gibco) and 1% penicillin/streptomycin (A3160502, Gibco) and incubated in a humidified atmosphere of 5% CO₂ at 37 °C. The cells were seeded into 6-well plates (657160, Greiner Bio-One, Kremsmünster, Austria).) at a density of 3 × 10⁴ cells/well until confluence. The cells used were between passages 3 and 7. Mouse adiponectin was purchased from Sino Biological Inc. (Beijing, China) (Cat. No: 50636-M08H) with purity > 95% (determined via SDS-PAGE). Histone acetylation inhibitor I-BET 762 and Piezo 1 inhibitor GSMTX4 were purchased from Sigma-Aldrich (St. Louis, MO, USA) (SML1272, SML-3140).

Wang Y., Groeger S., Yong J, & Ruf S. (2023). Orthodontic Compression Enhances Macrophage M2 Polarization via Histone H3 Hyperacetylation. International Journal of Molecular Sciences, 24(4), 3117.

+ Open protocol

+ Expand

About PubCompare

Our mission is to provide scientists with the largest repository of trustworthy protocols and intelligent analytical tools, thereby offering them extensive information to design robust protocols aimed at minimizing the risk of failures.

We believe that the most crucial aspect is to grant scientists access to a wide range of reliable sources and new useful tools that surpass human capabilities.

However, we trust in allowing scientists to determine how to construct their own protocols based on this information, as they are the experts in their field.

Ready to get started?

Revolutionizing how scientists
search and build protocols!