The role of heterogeneous nuclear ribonucleoproteins (hnRNP) in cellular senescence is yet to be defined. Cellular senescence is a terminal growth arrest in somatic cells. It is thought to be the consequence of telomeric shortening that acts as a DNA damage signal. Conversely, cells induced into premature senescence (SIPS) by oxidative stress, is independent of telomere attrition. Premature senescence has been proposed to be physiologically relevant as it can be induced by treatment with chemotherapeutic agents. In particular, we are studying the roles of hnRNP A1 and A2 in the maintenance of the senescence phenotype. hnRNPs are a family of RNA binding proteins that play key roles in various metabolic functions of the RNA such as splicing. hnRNP A1 in addition to its biochemical functions in RNA metabolism can bind to mRNAs for transport through the nuclear envelope. Our studies have shown that the protein level of hnRNP A1 is lower in senescent cells than in young cells. Thus, we have hypothesized that the altered expression of hnRNP A1 potentially modulates gene expression profiles and may maintain the senescent phenotype. We have observed that varying the levels of hnRNP A1 alters the expression levels of p21, p16 and ARF, all cell cycle regulators. To determine if this is the case during stress induced premature senescence (SIPS), IMR-90 fibroblast diploid normal lung cells were treated with a sub-lethal concentration of hydrogen peroxide that has been shown to induce premature senescence. To determine if hnRNPs may play a role in vivo, we measured their expression in rat hippocampal lysates isolated from rats treated with a combination of the chemotherapeutic drugs, doxorubicin and cyclophosphamide. We have shown here that stress induced premature senescence is not modulated in the same hnRNP dependent fashion as replicative senescence and possibly independent of p38MAPK.
","abstract_html":"<p>The role of heterogeneous nuclear ribonucleoproteins (hnRNP) in cellular senescence is yet to be defined. Cellular senescence is a terminal growth arrest in somatic cells. It is thought to be the consequence of telomeric shortening that acts as a DNA damage signal. Conversely, cells induced into premature senescence (SIPS) by oxidative stress, is independent of telomere attrition. Premature senescence has been proposed to be physiologically relevant as it can be induced by treatment with chemotherapeutic agents. In particular, we are studying the roles of hnRNP A1 and A2 in the maintenance of the senescence phenotype. hnRNPs are a family of RNA binding proteins that play key roles in various metabolic functions of the RNA such as splicing. hnRNP A1 in addition to its biochemical functions in RNA metabolism can bind to mRNAs for transport through the nuclear envelope. Our studies have shown that the protein level of hnRNP A1 is lower in senescent cells than in young cells. Thus, we have hypothesized that the altered expression of hnRNP A1 potentially modulates gene expression profiles and may maintain the senescent phenotype. We have observed that varying the levels of hnRNP A1 alters the expression levels of p21, p16 and ARF, all cell cycle regulators. To determine if this is the case during stress induced premature senescence (SIPS), IMR-90 fibroblast diploid normal lung cells were treated with a sub-lethal concentration of hydrogen peroxide that has been shown to induce premature senescence. To determine if hnRNPs may play a role <em>in vivo</em>, we measured their expression in rat hippocampal lysates isolated from rats treated with a combination of the chemotherapeutic drugs, doxorubicin and cyclophosphamide. We have shown here that stress induced premature senescence is not modulated in the same hnRNP dependent fashion as replicative senescence and possibly independent of p38MAPK.</p>","abstract_has_math":false,"creators":["Pechenyy, Yuriy"],"institution":null,"degree_name":"Master of Science (M.S.)","degree_level":"Thesis","degree_discipline":"Biology","degree_department":null,"school":null,"contributors":["Karen Hubbard","Mark Pezzano","Tadmiri Venkatesh"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2018,"date_issued":"2018-01-01T08:00:00Z","date_published":"2018-01-01T08:00:00Z","updated_at":"2026-07-24T01:57:14Z","subjects":["Aging","Fibroblast","hnRNP","A1","Premature","Senescence","Cancer Biology","Cell Biology"],"languages":[],"rights":[],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"https://academicworks.cuny.edu/cc_etds_theses/722","outbound_label":"Repository record","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Karen Hubbard","Mark Pezzano","Tadmiri Venkatesh"]},{"key":"dc:creator","label":"Author","values":["Pechenyy, Yuriy"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.available","label":"Dc Date Available","values":["2018-05-15T07:00:00Z"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Biology"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Thesis"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Master of Science (M.S.)"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Aging","Fibroblast","hnRNP","A1","Premature","Senescence","Cancer Biology","Cell Biology"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://academicworks.cuny.edu/cc_etds_theses/722"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["The role of heterogeneous nuclear ribonucleoproteins (hnRNP) in cellular senescence is yet to be defined. Cellular senescence is a terminal growth arrest in somatic cells. It is thought to be the consequence of telomeric shortening that acts as a DNA damage signal. Conversely, cells induced into premature senescence (SIPS) by oxidative stress, is independent of telomere attrition. Premature senescence has been proposed to be physiologically relevant as it can be induced by treatment with chemotherapeutic agents. In particular, we are studying the roles of hnRNP A1 and A2 in the maintenance of the senescence phenotype. hnRNPs are a family of RNA binding proteins that play key roles in various metabolic functions of the RNA such as splicing. hnRNP A1 in addition to its biochemical functions in RNA metabolism can bind to mRNAs for transport through the nuclear envelope. Our studies have shown that the protein level of hnRNP A1 is lower in senescent cells than in young cells. Thus, we have hypothesized that the altered expression of hnRNP A1 potentially modulates gene expression profiles and may maintain the senescent phenotype. We have observed that varying the levels of hnRNP A1 alters the expression levels of p21, p16 and ARF, all cell cycle regulators. To determine if this is the case during stress induced premature senescence (SIPS), IMR-90 fibroblast diploid normal lung cells were treated with a sub-lethal concentration of hydrogen peroxide that has been shown to induce premature senescence. To determine if hnRNPs may play a role in vivo, we measured their expression in rat hippocampal lysates isolated from rats treated with a combination of the chemotherapeutic drugs, doxorubicin and cyclophosphamide. We have shown here that stress induced premature senescence is not modulated in the same hnRNP dependent fashion as replicative senescence and possibly independent of p38MAPK.
"]},{"key":"dc:title","label":"Title","values":["The Effect of Stress Induced Premature Senescence on the Expression of Heterogeneous RibonucleoIeoprotein"]}]}],"canonical_facts":{"dc:contributor":["Karen Hubbard","Mark Pezzano","Tadmiri Venkatesh"],"dc:creator":["Pechenyy, Yuriy"],"dc:date.available":["2018-05-15T07:00:00Z"],"dc:description.abstract":["The role of heterogeneous nuclear ribonucleoproteins (hnRNP) in cellular senescence is yet to be defined. Cellular senescence is a terminal growth arrest in somatic cells. It is thought to be the consequence of telomeric shortening that acts as a DNA damage signal. Conversely, cells induced into premature senescence (SIPS) by oxidative stress, is independent of telomere attrition. Premature senescence has been proposed to be physiologically relevant as it can be induced by treatment with chemotherapeutic agents. In particular, we are studying the roles of hnRNP A1 and A2 in the maintenance of the senescence phenotype. hnRNPs are a family of RNA binding proteins that play key roles in various metabolic functions of the RNA such as splicing. hnRNP A1 in addition to its biochemical functions in RNA metabolism can bind to mRNAs for transport through the nuclear envelope. Our studies have shown that the protein level of hnRNP A1 is lower in senescent cells than in young cells. Thus, we have hypothesized that the altered expression of hnRNP A1 potentially modulates gene expression profiles and may maintain the senescent phenotype. We have observed that varying the levels of hnRNP A1 alters the expression levels of p21, p16 and ARF, all cell cycle regulators. To determine if this is the case during stress induced premature senescence (SIPS), IMR-90 fibroblast diploid normal lung cells were treated with a sub-lethal concentration of hydrogen peroxide that has been shown to induce premature senescence. To determine if hnRNPs may play a role in vivo, we measured their expression in rat hippocampal lysates isolated from rats treated with a combination of the chemotherapeutic drugs, doxorubicin and cyclophosphamide. We have shown here that stress induced premature senescence is not modulated in the same hnRNP dependent fashion as replicative senescence and possibly independent of p38MAPK.
"],"dc:identifier":["https://academicworks.cuny.edu/cc_etds_theses/722"],"dc:subject":["Aging","Fibroblast","hnRNP","A1","Premature","Senescence","Cancer Biology","Cell Biology"],"dc:title":["The Effect of Stress Induced Premature Senescence on the Expression of Heterogeneous RibonucleoIeoprotein"],"thesis:degree_discipline":["Biology"],"thesis:degree_level":["Thesis"],"thesis:degree_name":["Master of Science (M.S.)"]},"updated_at":"2026-07-24T01:57:14Z"}