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Testing Data
CytoSelect 24-well Wound Healing Assay Assay Kit
CytoSelect 24-well Wound Healing Assay
Synonyms
CytoSelect 24-well Wound Healing Assay; CytoSelect 24-well Wound Healing Assay assay kit
Preparation and Storage
Upon receipt, transfer the DAPI Fluorescence Stain to -20 degree C. Store all other components at 4 degree C.
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Related Product Information for CytoSelect 24-well Wound Healing Assay assay kit
Principle of the Assay: The CytoSelect™ 24-well Wound Healing Assay Kit contains 2 x 24-well plates each containing 12 proprietary treated plastic inserts. The inserts create a wound field with a defined gap of 0.9mm for measuring the migratory and proliferation rates of cells. Migratory cells are able to extend protrusions and ultimately invade and close the wound field. Cell proliferation and migration rates can be determined using manual fixing and microscopic imaging. A fixing solution is provided for stopping cells at specific time points. Cell stain and DAPI stain are also provided for viewing results with light and fluorescence microscopy.
Background/Introduction: Wounded tissue initiates a complex and structured series of events in order to repair the damaged region. These events may include increased vascularization by angiogenic factors, an increase in cell proliferation and extracellular matrix deposition, and infiltration by inflammatory immune cells as part of the process to destroy necrotic tissue. The wound healing process begins as cells polarize toward the wound, initiate protrusion, migrate, and close the wound area. These processes reflect the behavior of individual cells as well as the entire tissue complex. Wound healing assays have been employed by researchers for years to study cell polarization, tissue matrix remodeling, or estimate cell proliferation and migration rates of different cells and culture conditions. Wound healing assays have been used to study cell polarity and actin cytoskeletal structure regulation through the role of Rho family GTPases, microtubule and Golgi apparatus orientation, the role of p53 in cell migration, as well as other physiological processes. These assays typically involve culturing a confluent cell monolayer and then displacing or destroying a group of cells by scratching a line through the monolayer. The open gap created by this "wound" is then inspected microscopically over time as the cells move in and fill the damaged area. This "healing" effect can take several hours to several days depending on the cell type, conditions, and the surface area of the "wounded" region. The disadvantage of these "scratch wound" assays is the lack of a defined wound surface area, or gap between cells. These wounds are varying sizes and widths, which inhibits consistent results and creates variation from well to well. In addition, the "scratch wound" assay often causes damage to the cells at the edge of the wound, which can prevent cell migration into the wound site and healing. Our CytoSelect™ Wound Healing Assay Kit overcomes this inconsistency by providing proprietary treated inserts that can generate a defined wound field or gap. Cells are cultured until they form a monolayer around the insert. The insert is removed, leaving a precise 0.9 mm open "wound field" between the cells. Cells can be treated and monitored at this point for migration and proliferation into the wound field. Progression of these events can be measured by imaging samples fixed at specific time points or time-lapse microscopy. CytoSelect™ Wound Healing Assay Kit includes proprietary "wound field" inserts to assay the migratory and wound healing characteristics of cells. The kit contains sufficient reagents for the evaluation of 24 samples. The insert is optimal for use with most cell types and experimental conditions. The 0.9 mm wound field generated is compatible for use with most microscopes and imaging systems.
Background/Introduction: Wounded tissue initiates a complex and structured series of events in order to repair the damaged region. These events may include increased vascularization by angiogenic factors, an increase in cell proliferation and extracellular matrix deposition, and infiltration by inflammatory immune cells as part of the process to destroy necrotic tissue. The wound healing process begins as cells polarize toward the wound, initiate protrusion, migrate, and close the wound area. These processes reflect the behavior of individual cells as well as the entire tissue complex. Wound healing assays have been employed by researchers for years to study cell polarization, tissue matrix remodeling, or estimate cell proliferation and migration rates of different cells and culture conditions. Wound healing assays have been used to study cell polarity and actin cytoskeletal structure regulation through the role of Rho family GTPases, microtubule and Golgi apparatus orientation, the role of p53 in cell migration, as well as other physiological processes. These assays typically involve culturing a confluent cell monolayer and then displacing or destroying a group of cells by scratching a line through the monolayer. The open gap created by this "wound" is then inspected microscopically over time as the cells move in and fill the damaged area. This "healing" effect can take several hours to several days depending on the cell type, conditions, and the surface area of the "wounded" region. The disadvantage of these "scratch wound" assays is the lack of a defined wound surface area, or gap between cells. These wounds are varying sizes and widths, which inhibits consistent results and creates variation from well to well. In addition, the "scratch wound" assay often causes damage to the cells at the edge of the wound, which can prevent cell migration into the wound site and healing. Our CytoSelect™ Wound Healing Assay Kit overcomes this inconsistency by providing proprietary treated inserts that can generate a defined wound field or gap. Cells are cultured until they form a monolayer around the insert. The insert is removed, leaving a precise 0.9 mm open "wound field" between the cells. Cells can be treated and monitored at this point for migration and proliferation into the wound field. Progression of these events can be measured by imaging samples fixed at specific time points or time-lapse microscopy. CytoSelect™ Wound Healing Assay Kit includes proprietary "wound field" inserts to assay the migratory and wound healing characteristics of cells. The kit contains sufficient reagents for the evaluation of 24 samples. The insert is optimal for use with most cell types and experimental conditions. The 0.9 mm wound field generated is compatible for use with most microscopes and imaging systems.
Product Categories/Family for CytoSelect 24-well Wound Healing Assay assay kit
References
1. Ridley AJ, Schwartz MA, Burridge K, Firtel RA, Ginsberg MH, Borisy G, Parsons JT, Horwitz AR. (2003) Science 302, 1704-9.
2. Horwitz R, Webb D. (2003) Curr Biol. 13, R756-9.
3. Lauffenburger DA, Horwitz AF. (1996) Cell 84, 359-369.
1. Otsubo, T. et al. (2015). Aberrant DNA hypermethylation reduces the expression of the desmosome-related molecule periplakin in esophageal squamous cell carcinoma. Cancer Med.. doi: 10.1002/cam4.369.
2. Kawai, T. et al. (2015). Secretomes from bone marrow-derived mesenchymal stromal cells enhance periodontal tissue regeneration. Cytotherapy. doi: 10.1016/j.jcyt.2014.11.009.
3. Niu, F. et al. (2014). Tat 101-mediated enhancement of brain pericyte migration involves platelet-derived growth factor subunit B homodimer: implications for human immunodeficiency virus-associated neurocognitive disorders. J Neurosci. 34:11812-11825.4. Cui, X.G. et al. (2013). Response gene to complement 32 deficiency causes impaired placental angiogenesis in mice. Cardiovasc Res. 10.1093/cvr/cvt121.
5. Gutschner, T. et al. (2013). The noncoding RNA MALAT1 is a critical regulator of the metastasis phenotype of lung cancer cells. Cancer Res. 73:1180-1189.
6. Xing, C. et al. (2013). Reversing effect of ring finger protein 43 inhibition on malignant phenotypes of human hepatocellular carcinoma. Mol. Cancer Ther. 12:94-103.
7. Mao, R. et al. (2012). Circadian gating of epithelial-to-mesenchymal transition in breast cancer cells via melatonin-regulation of GSK3beta. Mol Endocrinol. 26:1808-1820.
8. Walsh, E.M. et al. (2012). Importance of interaction between nerve growth factor and alpha9beta1 integrin in glial tumor angiogenesis. Neuro Oncology. 10.1093/neuonc/nos119.
9. Hirata, H. et al. (2012). MicroRNA-1826 targets VEGFC, Beta-catenin (CTNNB1) and MEK1 (MAP2K1) in human bladder cancer. Carcinogenesis 33:41-48.
10. Wang, J.N. et al. (2011). Response gene to complement 32 promotes vascular lesion formation through stimulation of smooth muscle cell proliferation and migration. Arterioscler Thromb Vasc Biol. 31:e19-e26.
11. Oommen, S. et al. (2011). Vascular Endothelial Growth Factor A (VEGF-A) induces endothelial and cancer cell migration through direct binding to integrin alpha9beta1: identification of a specific alpha9beta1 binding site. J. Biol. Chem. 286:1083-1092.
12. Buckley, S. et al. (2011). The milieu of damaged alveolar epithelial type 2 cells stimulates alveolar wound repair by endogenous and exogenous progenitors. Am. J. Respir. Cell Mol. Biol. 45:1212-1221.
13. Tao, Y. et al. (2011). Treatment of breast cancer cells with DNA demethylating agents leads to a release of Pol II stalling at genes with DNA-hypermethylated regions upstream of TSS. Nucleic Acid Res. 10.1093/nar/gkr611.
2. Horwitz R, Webb D. (2003) Curr Biol. 13, R756-9.
3. Lauffenburger DA, Horwitz AF. (1996) Cell 84, 359-369.
1. Otsubo, T. et al. (2015). Aberrant DNA hypermethylation reduces the expression of the desmosome-related molecule periplakin in esophageal squamous cell carcinoma. Cancer Med.. doi: 10.1002/cam4.369.
2. Kawai, T. et al. (2015). Secretomes from bone marrow-derived mesenchymal stromal cells enhance periodontal tissue regeneration. Cytotherapy. doi: 10.1016/j.jcyt.2014.11.009.
3. Niu, F. et al. (2014). Tat 101-mediated enhancement of brain pericyte migration involves platelet-derived growth factor subunit B homodimer: implications for human immunodeficiency virus-associated neurocognitive disorders. J Neurosci. 34:11812-11825.4. Cui, X.G. et al. (2013). Response gene to complement 32 deficiency causes impaired placental angiogenesis in mice. Cardiovasc Res. 10.1093/cvr/cvt121.
5. Gutschner, T. et al. (2013). The noncoding RNA MALAT1 is a critical regulator of the metastasis phenotype of lung cancer cells. Cancer Res. 73:1180-1189.
6. Xing, C. et al. (2013). Reversing effect of ring finger protein 43 inhibition on malignant phenotypes of human hepatocellular carcinoma. Mol. Cancer Ther. 12:94-103.
7. Mao, R. et al. (2012). Circadian gating of epithelial-to-mesenchymal transition in breast cancer cells via melatonin-regulation of GSK3beta. Mol Endocrinol. 26:1808-1820.
8. Walsh, E.M. et al. (2012). Importance of interaction between nerve growth factor and alpha9beta1 integrin in glial tumor angiogenesis. Neuro Oncology. 10.1093/neuonc/nos119.
9. Hirata, H. et al. (2012). MicroRNA-1826 targets VEGFC, Beta-catenin (CTNNB1) and MEK1 (MAP2K1) in human bladder cancer. Carcinogenesis 33:41-48.
10. Wang, J.N. et al. (2011). Response gene to complement 32 promotes vascular lesion formation through stimulation of smooth muscle cell proliferation and migration. Arterioscler Thromb Vasc Biol. 31:e19-e26.
11. Oommen, S. et al. (2011). Vascular Endothelial Growth Factor A (VEGF-A) induces endothelial and cancer cell migration through direct binding to integrin alpha9beta1: identification of a specific alpha9beta1 binding site. J. Biol. Chem. 286:1083-1092.
12. Buckley, S. et al. (2011). The milieu of damaged alveolar epithelial type 2 cells stimulates alveolar wound repair by endogenous and exogenous progenitors. Am. J. Respir. Cell Mol. Biol. 45:1212-1221.
13. Tao, Y. et al. (2011). Treatment of breast cancer cells with DNA demethylating agents leads to a release of Pol II stalling at genes with DNA-hypermethylated regions upstream of TSS. Nucleic Acid Res. 10.1093/nar/gkr611.
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Product Notes
The CytoSelect 24-well Wound Healing Assay (Catalog #AAA168434) is an Assay Kit and is intended for research purposes only. The product is available for immediate purchase. It is sometimes possible for the material contained within the vial of "CytoSelect 24-well Wound Healing Assay, Assay Kit" to become dispersed throughout the inside of the vial, particularly around the seal of said vial, during shipment and storage. We always suggest centrifuging these vials to consolidate all of the liquid away from the lid and to the bottom of the vial prior to opening. Please be advised that certain products may require dry ice for shipping and that, if this is the case, an additional dry ice fee may also be required.Precautions
All products in the AAA Biotech catalog are strictly for research-use only, and are absolutely not suitable for use in any sort of medical, therapeutic, prophylactic, in-vivo, or diagnostic capacity. By purchasing a product from AAA Biotech, you are explicitly certifying that said products will be properly tested and used in line with industry standard. AAA Biotech and its authorized distribution partners reserve the right to refuse to fulfill any order if we have any indication that a purchaser may be intending to use a product outside of our accepted criteria.Disclaimer
Though we do strive to guarantee the information represented in this datasheet, AAA Biotech cannot be held responsible for any oversights or imprecisions. AAA Biotech reserves the right to adjust any aspect of this datasheet at any time and without notice. It is the responsibility of the customer to inform AAA Biotech of any product performance issues observed or experienced within 30 days of receipt of said product. To see additional details on this or any of our other policies, please see our Terms & Conditions page.Item has been added to Shopping Cart
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