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LncRNA UCA1 enhances NRF2 expression through the m6A pathway to mitigate oxidative stress and ferroptosis in aging cardiomyocytes.

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Title: LncRNA UCA1 enhances NRF2 expression through the m6A pathway to mitigate oxidative stress and ferroptosis in aging cardiomyocytes.
Authors: Jiao, Kunli1 (AUTHOR), Cheng, Jiahao2 (AUTHOR), Wang, Qi2 (AUTHOR), Hao, Mingxiu2 (AUTHOR) haomingxiu1981@126.com
Source: Journal of Bioenergetics & Biomembranes. Dec2024, Vol. 56 Issue 6, p607-617. 11p.
Subjects: Cytology, Life sciences, Cellular aging, Protein expression, Nuclear factor E2 related factor
Abstract: To explore the regulatory mechanism of lncRNA UCA1 and NRF2 in cardiomyocyte aging. In this study, we explored how lncRNA UCA1 regulates NRF2 and its effect on cardiomyocyte aging. H9c2 cardiomyocytes were cultured and treated with H2O2 to simulate cardiomyocyte aging in vitro. The expression levels of lncRNA UCA1 and NRF2 in cells were detected using qRT-PCR. Cell viability was assessed using the CCK8 assay, and cell aging was detected via Sa-β-gal staining. The levels of oxidative stress markers (SOD, MDA, ROS) and the expressions of ferroptosis-related proteins (ACSL4, TFR1, FTH1, GPX4) were measured. The regulatory mechanism between UCA1 and NRF2 was investigated using RIP-qPCR. Additionally, changes in m6A modification levels and the expression of m6A modification-related proteins in cells after UCA1 overexpression were analyzed by western blot. Our results indicate that H2O2 treatment significantly downregulated the expression of lncRNA UCA1 and NRF2. UCA1 overexpression promoted H9c2 cell proliferation, inhibited cell aging, increased SOD activity and the expression of FTH1 and GPX4 proteins, and decreased MDA and ROS content as well as ACSL4 and TFR1 protein expression. RIP-qPCR verified that UCA1 can promote the expression of NRF2 in cells. Overexpression of UCA1 significantly increased the expression of the demethylase FTO, leading to a reduction in m6A modification levels. Furthermore, there was significant enrichment between FTO and NRF2, and overexpression of FTO improved the expression of NRF2 protein in cells. Taken together, lncRNA UCA1 inhibits oxidative stress and ferroptosis, thereby preventing cardiomyocyte aging. This protective effect is likely mediated by increasing the expression of demethylase FTO and reducing m6A modification, which promotes the expression of NRF2. [ABSTRACT FROM AUTHOR]
Copyright of Journal of Bioenergetics & Biomembranes is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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  Data: LncRNA UCA1 enhances NRF2 expression through the m<superscript>6</superscript>A pathway to mitigate oxidative stress and ferroptosis in aging cardiomyocytes.
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  Data: <searchLink fieldCode="AR" term="%22Jiao%2C+Kunli%22">Jiao, Kunli</searchLink><relatesTo>1</relatesTo> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Cheng%2C+Jiahao%22">Cheng, Jiahao</searchLink><relatesTo>2</relatesTo> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Wang%2C+Qi%22">Wang, Qi</searchLink><relatesTo>2</relatesTo> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Hao%2C+Mingxiu%22">Hao, Mingxiu</searchLink><relatesTo>2</relatesTo> (AUTHOR)<i> haomingxiu1981@126.com</i>
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  Data: <searchLink fieldCode="JN" term="%22Journal+of+Bioenergetics+%26+Biomembranes%22">Journal of Bioenergetics & Biomembranes</searchLink>. Dec2024, Vol. 56 Issue 6, p607-617. 11p.
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  Data: <searchLink fieldCode="DE" term="%22Cytology%22">Cytology</searchLink><br /><searchLink fieldCode="DE" term="%22Life+sciences%22">Life sciences</searchLink><br /><searchLink fieldCode="DE" term="%22Cellular+aging%22">Cellular aging</searchLink><br /><searchLink fieldCode="DE" term="%22Protein+expression%22">Protein expression</searchLink><br /><searchLink fieldCode="DE" term="%22Nuclear+factor+E2+related+factor%22">Nuclear factor E2 related factor</searchLink>
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: To explore the regulatory mechanism of lncRNA UCA1 and NRF2 in cardiomyocyte aging. In this study, we explored how lncRNA UCA1 regulates NRF2 and its effect on cardiomyocyte aging. H9c2 cardiomyocytes were cultured and treated with H2O2 to simulate cardiomyocyte aging in vitro. The expression levels of lncRNA UCA1 and NRF2 in cells were detected using qRT-PCR. Cell viability was assessed using the CCK8 assay, and cell aging was detected via Sa-β-gal staining. The levels of oxidative stress markers (SOD, MDA, ROS) and the expressions of ferroptosis-related proteins (ACSL4, TFR1, FTH1, GPX4) were measured. The regulatory mechanism between UCA1 and NRF2 was investigated using RIP-qPCR. Additionally, changes in m6A modification levels and the expression of m6A modification-related proteins in cells after UCA1 overexpression were analyzed by western blot. Our results indicate that H2O2 treatment significantly downregulated the expression of lncRNA UCA1 and NRF2. UCA1 overexpression promoted H9c2 cell proliferation, inhibited cell aging, increased SOD activity and the expression of FTH1 and GPX4 proteins, and decreased MDA and ROS content as well as ACSL4 and TFR1 protein expression. RIP-qPCR verified that UCA1 can promote the expression of NRF2 in cells. Overexpression of UCA1 significantly increased the expression of the demethylase FTO, leading to a reduction in m6A modification levels. Furthermore, there was significant enrichment between FTO and NRF2, and overexpression of FTO improved the expression of NRF2 protein in cells. Taken together, lncRNA UCA1 inhibits oxidative stress and ferroptosis, thereby preventing cardiomyocyte aging. This protective effect is likely mediated by increasing the expression of demethylase FTO and reducing m6A modification, which promotes the expression of NRF2. [ABSTRACT FROM AUTHOR]
– Name: AbstractSuppliedCopyright
  Label:
  Group: Ab
  Data: <i>Copyright of Journal of Bioenergetics & Biomembranes is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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        Value: 10.1007/s10863-024-10045-8
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        Type: general
      – SubjectFull: Life sciences
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      – SubjectFull: Cellular aging
        Type: general
      – SubjectFull: Protein expression
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      – SubjectFull: Nuclear factor E2 related factor
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      – TitleFull: LncRNA UCA1 enhances NRF2 expression through the m6A pathway to mitigate oxidative stress and ferroptosis in aging cardiomyocytes.
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            NameFull: Jiao, Kunli
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            NameFull: Cheng, Jiahao
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            NameFull: Wang, Qi
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            – D: 01
              M: 12
              Text: Dec2024
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