Please use this identifier to cite or link to this item: http://dr.iiserpune.ac.in:8080/xmlui/handle/123456789/7511
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dc.contributor.authorGupta, Kavyaen_US
dc.contributor.authorMathew, Abraham Binoyen_US
dc.contributor.authorCHAKRAPANI, HARINATHen_US
dc.contributor.authorSaini, Deepak Kumaren_US
dc.date.accessioned2022-12-16T10:27:32Z
dc.date.available2022-12-16T10:27:32Z
dc.date.issued2023-02en_US
dc.identifier.citationBiochimica et Biophysica Acta (BBA) - Molecular Cell Research, 1870(2), 119388.en_US
dc.identifier.issn0167-4889en_US
dc.identifier.issn1879-2596en_US
dc.identifier.urihttps://doi.org/10.1016/j.bbamcr.2022.119388en_US
dc.identifier.urihttp://dr.iiserpune.ac.in:8080/xmlui/handle/123456789/7511
dc.description.abstractAging involves the time-dependent deterioration of physiological functions attributed to various intracellular and extracellular factors. Cellular senescence is akin to aging and involves alteration in redox homeostasis. This is primarily marked by increased reactive oxygen/nitrogen species (ROS/RNS), inflammatory gene expression, and senescence-associated beta-galactosidase activity, all hallmarks of aging. It is proposed that gasotransmitters which include hydrogen sulfide (H2S), carbon monoxide (CO), and nitric oxide (NO), may affect redox homeostasis during senescence. H2S has been independently shown to induce DNA damage and suppress oxidative stress. While an increase in NO levels during aging is well established, the role of H2S has remained controversial. To understand the role of H2S during aging, we evaluated H2S homeostasis in non-senescent and senescent cells, using a combination of direct measurements with a fluorescent reporter dye (WSP-5) and protein sulfhydration analysis. The free intracellular H2S and total protein sulfhydration levels are high during senescence, concomitant to cystathionine gamma-lyase (CSE) expression induction. Using lentiviral shRNA-mediated expression knockdown, we identified that H2S contributed by CSE alters global gene expression, which regulates key inflammatory processes during cellular senescence. We propose that H2S decreases inflammation during cellular senescence by reducing phosphorylation of IκBα and the p65 subunit of nuclear factor kappa B (NF-κB). H2S was also found to reduce NO levels, a significant source of nitrosative stress during cellular senescence. Overall, we establish H2S as a key gasotransmitter molecule that regulates inflammatory phenotype and nitrosative stress during cellular senescence.en_US
dc.language.isoenen_US
dc.publisherElsevier B.V.en_US
dc.subjectCellular senescenceen_US
dc.subjectGasotransmittersen_US
dc.subjectHydrogen sulfideen_US
dc.subjectInflammation Nitric oxideen_US
dc.subjectReactive oxygen speciesen_US
dc.subject2022-DEC-WEEK1en_US
dc.subjectTOC-DEC-2022en_US
dc.subject2023en_US
dc.titleH2S contributed from CSE during cellular senescence suppresses inflammation and nitrosative stressen_US
dc.typeArticleen_US
dc.contributor.departmentDept. of Chemistryen_US
dc.identifier.sourcetitleBiochimica et Biophysica Acta (BBA) - Molecular Cell Researchen_US
dc.publication.originofpublisherForeignen_US
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