Epigenetic and senescence markers indicate an accelerated ageing-like state in women with preeclamptic pregnancies

Preeclampsia is a pregnancy-specific hypertensive disorder characterized by proteinuria and/or multisystem involvement. Disease-specific therapy has yet to be developed due to the lack of understanding of underlying mechanism(s). We postulate that accelerated ageing in general, and particularly cell...

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Vydáno v:	EBioMedicine Ročník 70; s. 103536
Hlavní autoři:	Suvakov, Sonja, Ghamrawi, Ranine, Cubro, Hajrunisa, Tu, Haitao, White, Wendy M., Tobah, Yvonne S. Butler, Milic, Natasa M., Grande, Joseph P., Cunningham, Julie M., Chebib, Fouad T., Prata, Larissa G.P. Langhi, Zhu, Yi, Tchkonia, Tamara, Kirkland, James L., Nath, Karl A., Milosavljevic, Aleksandar, Garovic, Vesna D.
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	Netherlands Elsevier B.V 01.08.2021 Elsevier
Témata:	Adipose Tissue - metabolism Adult Advanced Basic Science ageing Biomarkers - metabolism Cells, Cultured Cellular Senescence Cyclin-Dependent Kinase Inhibitor p16 - metabolism Dasatinib - pharmacology Epigenesis, Genetic epigenetic clock Female Humans Internal Medicine Kidney - metabolism Klotho Proteins - metabolism Mesenchymal Stem Cells - drug effects Mesenchymal Stem Cells - metabolism Pre-Eclampsia - genetics Pre-Eclampsia - metabolism Pre-Eclampsia - pathology preeclampsia Pregnancy Protein Kinase Inhibitors - pharmacology Research Paper senescence senescence ageing preeclampsia epigenetic clock
ISSN:	2352-3964, 2352-3964
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Abstract	Preeclampsia is a pregnancy-specific hypertensive disorder characterized by proteinuria and/or multisystem involvement. Disease-specific therapy has yet to be developed due to the lack of understanding of underlying mechanism(s). We postulate that accelerated ageing in general, and particularly cellular senescence, play a role in its pathophysiology. We compared women with preeclampsia vs. normotensive pregnancies with respect to epigenetic markers of ageing and markers of senescence in tissues/organs affected by preeclampsia (blood, urine, adipose tissue, and kidney). We demonstrate that preeclamptic compared to normotensive pregnant women: (i) undergo accelerated epigenetic ageing during pregnancy, as demonstrated by an “epigenetic clock”; (ii) exhibit higher levels/expression of senescence-associated secretory phenotype factors in blood and adipose tissue; (iii) display increased expression of p16INK4A in adipose tissue and renal sections, and (iv) demonstrate decreased levels of urinary α-Klotho (an anti-ageing protein) at the time of delivery. Finally, we provide data indicating that pre-treatment with dasatinib, a senolytic agent, rescues the angiogenic potential of mesenchymal stem cells (MSC) obtained from preeclamptic pregnancies, and promotes angiogenesis, even under pro-inflammatory conditions. Taken together, our results identify senescence as one of the mechanisms underpinning the pathophysiology of preeclampsia. Therapeutic strategies that target senescent cells may offer novel mechanism-based treatments for preeclampsia. This work was supported by NIH grants, R01 HL136348, R37 AG013925, P01 AG062413, R01 DK11916, generous gifts from the Connor Fund, Robert J. and Theresa W. Ryan and from The George G. Beasley family, the Noaber Foundation, and the Henry and Emma Meyer Professorship in Molecular Genetics.
AbstractList	Background: Preeclampsia is a pregnancy-specific hypertensive disorder characterized by proteinuria and/or multisystem involvement. Disease-specific therapy has yet to be developed due to the lack of understanding of underlying mechanism(s). We postulate that accelerated ageing in general, and particularly cellular senescence, play a role in its pathophysiology. Methods: We compared women with preeclampsia vs. normotensive pregnancies with respect to epigenetic markers of ageing and markers of senescence in tissues/organs affected by preeclampsia (blood, urine, adipose tissue, and kidney). Findings: We demonstrate that preeclamptic compared to normotensive pregnant women: (i) undergo accelerated epigenetic ageing during pregnancy, as demonstrated by an “epigenetic clock”; (ii) exhibit higher levels/expression of senescence-associated secretory phenotype factors in blood and adipose tissue; (iii) display increased expression of p16INK4A in adipose tissue and renal sections, and (iv) demonstrate decreased levels of urinary α-Klotho (an anti-ageing protein) at the time of delivery. Finally, we provide data indicating that pre-treatment with dasatinib, a senolytic agent, rescues the angiogenic potential of mesenchymal stem cells (MSC) obtained from preeclamptic pregnancies, and promotes angiogenesis, even under pro-inflammatory conditions. Interpretation: Taken together, our results identify senescence as one of the mechanisms underpinning the pathophysiology of preeclampsia. Therapeutic strategies that target senescent cells may offer novel mechanism-based treatments for preeclampsia. Funding: This work was supported by NIH grants, R01 HL136348, R37 AG013925, P01 AG062413, R01 DK11916, generous gifts from the Connor Fund, Robert J. and Theresa W. Ryan and from The George G. Beasley family, the Noaber Foundation, and the Henry and Emma Meyer Professorship in Molecular Genetics. Preeclampsia is a pregnancy-specific hypertensive disorder characterized by proteinuria and/or multisystem involvement. Disease-specific therapy has yet to be developed due to the lack of understanding of underlying mechanism(s). We postulate that accelerated ageing in general, and particularly cellular senescence, play a role in its pathophysiology. We compared women with preeclampsia vs. normotensive pregnancies with respect to epigenetic markers of ageing and markers of senescence in tissues/organs affected by preeclampsia (blood, urine, adipose tissue, and kidney). We demonstrate that preeclamptic compared to normotensive pregnant women: (i) undergo accelerated epigenetic ageing during pregnancy, as demonstrated by an “epigenetic clock”; (ii) exhibit higher levels/expression of senescence-associated secretory phenotype factors in blood and adipose tissue; (iii) display increased expression of p16INK4A in adipose tissue and renal sections, and (iv) demonstrate decreased levels of urinary α-Klotho (an anti-ageing protein) at the time of delivery. Finally, we provide data indicating that pre-treatment with dasatinib, a senolytic agent, rescues the angiogenic potential of mesenchymal stem cells (MSC) obtained from preeclamptic pregnancies, and promotes angiogenesis, even under pro-inflammatory conditions. Taken together, our results identify senescence as one of the mechanisms underpinning the pathophysiology of preeclampsia. Therapeutic strategies that target senescent cells may offer novel mechanism-based treatments for preeclampsia. This work was supported by NIH grants, R01 HL136348, R37 AG013925, P01 AG062413, R01 DK11916, generous gifts from the Connor Fund, Robert J. and Theresa W. Ryan and from The George G. Beasley family, the Noaber Foundation, and the Henry and Emma Meyer Professorship in Molecular Genetics. AbstractBackgroundPreeclampsia is a pregnancy-specific hypertensive disorder characterized by proteinuria and/or multisystem involvement. Disease-specific therapy has yet to be developed due to the lack of understanding of underlying mechanism(s). We postulate that accelerated ageing in general, and particularly cellular senescence, play a role in its pathophysiology. MethodsWe compared women with preeclampsia vs. normotensive pregnancies with respect to epigenetic markers of ageing and markers of senescence in tissues/organs affected by preeclampsia (blood, urine, adipose tissue, and kidney). FindingsWe demonstrate that preeclamptic compared to normotensive pregnant women: (i) undergo accelerated epigenetic ageing during pregnancy, as demonstrated by an “epigenetic clock”; (ii) exhibit higher levels/expression of senescence-associated secretory phenotype factors in blood and adipose tissue; (iii) display increased expression of p16 INK4A in adipose tissue and renal sections, and (iv) demonstrate decreased levels of urinary α-Klotho (an anti-ageing protein) at the time of delivery. Finally, we provide data indicating that pre-treatment with dasatinib, a senolytic agent, rescues the angiogenic potential of mesenchymal stem cells (MSC) obtained from preeclamptic pregnancies, and promotes angiogenesis, even under pro-inflammatory conditions. InterpretationTaken together, our results identify senescence as one of the mechanisms underpinning the pathophysiology of preeclampsia. Therapeutic strategies that target senescent cells may offer novel mechanism-based treatments for preeclampsia. FundingThis work was supported by NIH grants, R01 HL136348, R37 AG013925, P01 AG062413, R01 DK11916, generous gifts from the Connor Fund, Robert J. and Theresa W. Ryan and from The George G. Beasley family, the Noaber Foundation, and the Henry and Emma Meyer Professorship in Molecular Genetics. Preeclampsia is a pregnancy-specific hypertensive disorder characterized by proteinuria and/or multisystem involvement. Disease-specific therapy has yet to be developed due to the lack of understanding of underlying mechanism(s). We postulate that accelerated ageing in general, and particularly cellular senescence, play a role in its pathophysiology.BACKGROUNDPreeclampsia is a pregnancy-specific hypertensive disorder characterized by proteinuria and/or multisystem involvement. Disease-specific therapy has yet to be developed due to the lack of understanding of underlying mechanism(s). We postulate that accelerated ageing in general, and particularly cellular senescence, play a role in its pathophysiology.We compared women with preeclampsia vs. normotensive pregnancies with respect to epigenetic markers of ageing and markers of senescence in tissues/organs affected by preeclampsia (blood, urine, adipose tissue, and kidney).METHODSWe compared women with preeclampsia vs. normotensive pregnancies with respect to epigenetic markers of ageing and markers of senescence in tissues/organs affected by preeclampsia (blood, urine, adipose tissue, and kidney).We demonstrate that preeclamptic compared to normotensive pregnant women: (i) undergo accelerated epigenetic ageing during pregnancy, as demonstrated by an "epigenetic clock"; (ii) exhibit higher levels/expression of senescence-associated secretory phenotype factors in blood and adipose tissue; (iii) display increased expression of p16INK4A in adipose tissue and renal sections, and (iv) demonstrate decreased levels of urinary α-Klotho (an anti-ageing protein) at the time of delivery. Finally, we provide data indicating that pre-treatment with dasatinib, a senolytic agent, rescues the angiogenic potential of mesenchymal stem cells (MSC) obtained from preeclamptic pregnancies, and promotes angiogenesis, even under pro-inflammatory conditions.FINDINGSWe demonstrate that preeclamptic compared to normotensive pregnant women: (i) undergo accelerated epigenetic ageing during pregnancy, as demonstrated by an "epigenetic clock"; (ii) exhibit higher levels/expression of senescence-associated secretory phenotype factors in blood and adipose tissue; (iii) display increased expression of p16INK4A in adipose tissue and renal sections, and (iv) demonstrate decreased levels of urinary α-Klotho (an anti-ageing protein) at the time of delivery. Finally, we provide data indicating that pre-treatment with dasatinib, a senolytic agent, rescues the angiogenic potential of mesenchymal stem cells (MSC) obtained from preeclamptic pregnancies, and promotes angiogenesis, even under pro-inflammatory conditions.Taken together, our results identify senescence as one of the mechanisms underpinning the pathophysiology of preeclampsia. Therapeutic strategies that target senescent cells may offer novel mechanism-based treatments for preeclampsia.INTERPRETATIONTaken together, our results identify senescence as one of the mechanisms underpinning the pathophysiology of preeclampsia. Therapeutic strategies that target senescent cells may offer novel mechanism-based treatments for preeclampsia.This work was supported by NIH grants, R01 HL136348, R37 AG013925, P01 AG062413, R01 DK11916, generous gifts from the Connor Fund, Robert J. and Theresa W. Ryan and from The George G. Beasley family, the Noaber Foundation, and the Henry and Emma Meyer Professorship in Molecular Genetics.FUNDINGThis work was supported by NIH grants, R01 HL136348, R37 AG013925, P01 AG062413, R01 DK11916, generous gifts from the Connor Fund, Robert J. and Theresa W. Ryan and from The George G. Beasley family, the Noaber Foundation, and the Henry and Emma Meyer Professorship in Molecular Genetics. Preeclampsia is a pregnancy-specific hypertensive disorder characterized by proteinuria and/or multisystem involvement. Disease-specific therapy has yet to be developed due to the lack of understanding of underlying mechanism(s). We postulate that accelerated ageing in general, and particularly cellular senescence, play a role in its pathophysiology. We compared women with preeclampsia vs. normotensive pregnancies with respect to epigenetic markers of ageing and markers of senescence in tissues/organs affected by preeclampsia (blood, urine, adipose tissue, and kidney). We demonstrate that preeclamptic compared to normotensive pregnant women: (i) undergo accelerated epigenetic ageing during pregnancy, as demonstrated by an "epigenetic clock"; (ii) exhibit higher levels/expression of senescence-associated secretory phenotype factors in blood and adipose tissue; (iii) display increased expression of p16 in adipose tissue and renal sections, and (iv) demonstrate decreased levels of urinary α-Klotho (an anti-ageing protein) at the time of delivery. Finally, we provide data indicating that pre-treatment with dasatinib, a senolytic agent, rescues the angiogenic potential of mesenchymal stem cells (MSC) obtained from preeclamptic pregnancies, and promotes angiogenesis, even under pro-inflammatory conditions. Taken together, our results identify senescence as one of the mechanisms underpinning the pathophysiology of preeclampsia. Therapeutic strategies that target senescent cells may offer novel mechanism-based treatments for preeclampsia. This work was supported by NIH grants, R01 HL136348, R37 AG013925, P01 AG062413, R01 DK11916, generous gifts from the Connor Fund, Robert J. and Theresa W. Ryan and from The George G. Beasley family, the Noaber Foundation, and the Henry and Emma Meyer Professorship in Molecular Genetics.
ArticleNumber	103536
Author	Suvakov, Sonja Tchkonia, Tamara Zhu, Yi Tu, Haitao Kirkland, James L. Nath, Karl A. Grande, Joseph P. White, Wendy M. Garovic, Vesna D. Ghamrawi, Ranine Cubro, Hajrunisa Prata, Larissa G.P. Langhi Milic, Natasa M. Tobah, Yvonne S. Butler Milosavljevic, Aleksandar Cunningham, Julie M. Chebib, Fouad T.
Author_xml	– sequence: 1 givenname: Sonja orcidid: 0000-0002-3743-1213 surname: Suvakov fullname: Suvakov, Sonja email: Suvakov.sonja@mayo.edu organization: Division of Nephrology and Hypertension, Mayo Clinic, Rochester, MN, USA – sequence: 2 givenname: Ranine surname: Ghamrawi fullname: Ghamrawi, Ranine email: ghamrawi.ranine@mayo.edu organization: Division of Nephrology and Hypertension, Mayo Clinic, Rochester, MN, USA – sequence: 3 givenname: Hajrunisa surname: Cubro fullname: Cubro, Hajrunisa email: hajrunisa.cubro@louisville.edu organization: Division of Nephrology and Hypertension, Mayo Clinic, Rochester, MN, USA – sequence: 4 givenname: Haitao surname: Tu fullname: Tu, Haitao organization: Division of Nephrology and Hypertension, Mayo Clinic, Rochester, MN, USA – sequence: 5 givenname: Wendy M. surname: White fullname: White, Wendy M. email: White.Wendy@mayo.edu organization: Department of Obstetrics and Gynaecology, Mayo Clinic, Rochester, MN, USA – sequence: 6 givenname: Yvonne S. Butler surname: Tobah fullname: Tobah, Yvonne S. Butler email: ButlerTobah.Yvonne@mayo.edu organization: Department of Obstetrics and Gynaecology, Mayo Clinic, Rochester, MN, USA – sequence: 7 givenname: Natasa M. surname: Milic fullname: Milic, Natasa M. organization: Division of Nephrology and Hypertension, Mayo Clinic, Rochester, MN, USA – sequence: 8 givenname: Joseph P. surname: Grande fullname: Grande, Joseph P. email: grande@mayo.edu organization: Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA – sequence: 9 givenname: Julie M. surname: Cunningham fullname: Cunningham, Julie M. email: cunningham.julie@mayo.edu organization: Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA – sequence: 10 givenname: Fouad T. orcidid: 0000-0002-3949-5720 surname: Chebib fullname: Chebib, Fouad T. email: Chebib.Fouad@mayo.edu organization: Division of Nephrology and Hypertension, Mayo Clinic, Rochester, MN, USA – sequence: 11 givenname: Larissa G.P. Langhi surname: Prata fullname: Prata, Larissa G.P. Langhi email: langhi.larissa@mayo.edu organization: Robert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN, USA – sequence: 12 givenname: Yi surname: Zhu fullname: Zhu, Yi email: Zhu.Yi@mayo.edu organization: Robert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN, USA – sequence: 13 givenname: Tamara surname: Tchkonia fullname: Tchkonia, Tamara email: Tchkonia.Tamar@mayo.edu organization: Robert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN, USA – sequence: 14 givenname: James L. surname: Kirkland fullname: Kirkland, James L. email: Kirkland.James@mayo.edu organization: Robert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN, USA – sequence: 15 givenname: Karl A. surname: Nath fullname: Nath, Karl A. email: Nath.Karl@mayo.edu organization: Division of Nephrology and Hypertension, Mayo Clinic, Rochester, MN, USA – sequence: 16 givenname: Aleksandar surname: Milosavljevic fullname: Milosavljevic, Aleksandar email: amilosav@bcm.edu organization: Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX, USA – sequence: 17 givenname: Vesna D. orcidid: 0000-0001-6891-0578 surname: Garovic fullname: Garovic, Vesna D. email: garovic.vesna@mayo.edu organization: Division of Nephrology and Hypertension, Mayo Clinic, Rochester, MN, USA
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Keywords	senescence ageing preeclampsia epigenetic clock
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Snippet	Preeclampsia is a pregnancy-specific hypertensive disorder characterized by proteinuria and/or multisystem involvement. Disease-specific therapy has yet to be... AbstractBackgroundPreeclampsia is a pregnancy-specific hypertensive disorder characterized by proteinuria and/or multisystem involvement. Disease-specific... Background: Preeclampsia is a pregnancy-specific hypertensive disorder characterized by proteinuria and/or multisystem involvement. Disease-specific therapy...
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SubjectTerms	Adipose Tissue - metabolism Adult Advanced Basic Science ageing Biomarkers - metabolism Cells, Cultured Cellular Senescence Cyclin-Dependent Kinase Inhibitor p16 - metabolism Dasatinib - pharmacology Epigenesis, Genetic epigenetic clock Female Humans Internal Medicine Kidney - metabolism Klotho Proteins - metabolism Mesenchymal Stem Cells - drug effects Mesenchymal Stem Cells - metabolism Pre-Eclampsia - genetics Pre-Eclampsia - metabolism Pre-Eclampsia - pathology preeclampsia Pregnancy Protein Kinase Inhibitors - pharmacology Research Paper senescence
Title	Epigenetic and senescence markers indicate an accelerated ageing-like state in women with preeclamptic pregnancies
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