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Molecular and Cellular Response of Co-cultured Cells toward Cobalt Chloride (CoCl(2))-Induced Hypoxia
[Image: see text] Cobalt chloride (CoCl(2)) is a well-known hypoxia mimetic mediator that induces hypoxia-like responses. CoCl(2), a mediator confirmed to alleviate hypoxia-inducible factor-1 (HIF-1), has been associated with a variety of hypoxic responses. HIF-1 is the foremost transcriptionfactor...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
American Chemical
Society
2019
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6921254/ https://www.ncbi.nlm.nih.gov/pubmed/31867478 http://dx.doi.org/10.1021/acsomega.9b01474 |
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author | Tripathi, Vinay Kumar Subramaniyan, Sivakumar Allur Hwang, Inho |
author_facet | Tripathi, Vinay Kumar Subramaniyan, Sivakumar Allur Hwang, Inho |
author_sort | Tripathi, Vinay Kumar |
collection | PubMed |
description | [Image: see text] Cobalt chloride (CoCl(2)) is a well-known hypoxia mimetic mediator that induces hypoxia-like responses. CoCl(2), a mediator confirmed to alleviate hypoxia-inducible factor-1 (HIF-1), has been associated with a variety of hypoxic responses. HIF-1 is the foremost transcriptionfactor that is particularly activated during hypoxia and regulates various genes. Therefore, this study aimed to investigate the cellular and molecular responses of the co-cultured cells under the influence of the CoCl(2)-induced hypoxic condition. Mono- and co-cultured C2C12 and 3T3-L1 cells were exposed to CoCl(2), and a significant induction in HIF-1, reactive oxygen species and lipid peroxidase and a reduction in glutathione and catalase were observed. The expressions of proapoptotic genes like Bax, p53, caspase-9, and caspase-3 were notably increased, whereas the antiapoptotic gene, i.e., Bcl2, was downregulated during hypoxia in mono- as well as co-cultured C2C12 cells. However, the co-cultured C2C12 cells show significantly lower induction in oxidative stress and expression of apoptotic genes in comparison to monocultured C2C12 cells. Whereas, the co-cultured 3T3-L1 cells show comparatively higher oxidative stress and apoptotic event in comparison to monocultured 3T3-L1 cells. The reason may be the communication between the cells and some soluble factors that help in cell survival/death from hypoxia. Moreover, it may also be due to the fact that fat and muscle cells interact and communicate via proximity and mutual ability when growing together. Therefore, the co-culture system provides a unique approach to intercellular communication between the two different cell types. |
format | Online Article Text |
id | pubmed-6921254 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | American Chemical
Society |
record_format | MEDLINE/PubMed |
spelling | pubmed-69212542019-12-20 Molecular and Cellular Response of Co-cultured Cells toward Cobalt Chloride (CoCl(2))-Induced Hypoxia Tripathi, Vinay Kumar Subramaniyan, Sivakumar Allur Hwang, Inho ACS Omega [Image: see text] Cobalt chloride (CoCl(2)) is a well-known hypoxia mimetic mediator that induces hypoxia-like responses. CoCl(2), a mediator confirmed to alleviate hypoxia-inducible factor-1 (HIF-1), has been associated with a variety of hypoxic responses. HIF-1 is the foremost transcriptionfactor that is particularly activated during hypoxia and regulates various genes. Therefore, this study aimed to investigate the cellular and molecular responses of the co-cultured cells under the influence of the CoCl(2)-induced hypoxic condition. Mono- and co-cultured C2C12 and 3T3-L1 cells were exposed to CoCl(2), and a significant induction in HIF-1, reactive oxygen species and lipid peroxidase and a reduction in glutathione and catalase were observed. The expressions of proapoptotic genes like Bax, p53, caspase-9, and caspase-3 were notably increased, whereas the antiapoptotic gene, i.e., Bcl2, was downregulated during hypoxia in mono- as well as co-cultured C2C12 cells. However, the co-cultured C2C12 cells show significantly lower induction in oxidative stress and expression of apoptotic genes in comparison to monocultured C2C12 cells. Whereas, the co-cultured 3T3-L1 cells show comparatively higher oxidative stress and apoptotic event in comparison to monocultured 3T3-L1 cells. The reason may be the communication between the cells and some soluble factors that help in cell survival/death from hypoxia. Moreover, it may also be due to the fact that fat and muscle cells interact and communicate via proximity and mutual ability when growing together. Therefore, the co-culture system provides a unique approach to intercellular communication between the two different cell types. American Chemical Society 2019-12-02 /pmc/articles/PMC6921254/ /pubmed/31867478 http://dx.doi.org/10.1021/acsomega.9b01474 Text en Copyright © 2019 American Chemical Society This is an open access article published under an ACS AuthorChoice License (http://pubs.acs.org/page/policy/authorchoice_termsofuse.html) , which permits copying and redistribution of the article or any adaptations for non-commercial purposes. |
spellingShingle | Tripathi, Vinay Kumar Subramaniyan, Sivakumar Allur Hwang, Inho Molecular and Cellular Response of Co-cultured Cells toward Cobalt Chloride (CoCl(2))-Induced Hypoxia |
title | Molecular and Cellular
Response of Co-cultured Cells
toward Cobalt Chloride (CoCl(2))-Induced Hypoxia |
title_full | Molecular and Cellular
Response of Co-cultured Cells
toward Cobalt Chloride (CoCl(2))-Induced Hypoxia |
title_fullStr | Molecular and Cellular
Response of Co-cultured Cells
toward Cobalt Chloride (CoCl(2))-Induced Hypoxia |
title_full_unstemmed | Molecular and Cellular
Response of Co-cultured Cells
toward Cobalt Chloride (CoCl(2))-Induced Hypoxia |
title_short | Molecular and Cellular
Response of Co-cultured Cells
toward Cobalt Chloride (CoCl(2))-Induced Hypoxia |
title_sort | molecular and cellular
response of co-cultured cells
toward cobalt chloride (cocl(2))-induced hypoxia |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6921254/ https://www.ncbi.nlm.nih.gov/pubmed/31867478 http://dx.doi.org/10.1021/acsomega.9b01474 |
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