Bone marrow support of the heart in pressure overload is lost with aging
Exogenous stem cell delivery is under investigation to prevent and treat cardiac dysfunction. It is less studied as to the extent endogenous bone marrow derived stem cells contribute to cardiac homeostais in response to stress and the affects of aging on this stress response. To determine the role o...
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| Veröffentlicht in: | PloS one 2010-12, Vol.5 (12), p.e15187-e15187 |
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| creator | Sopko, Nikolai A Turturice, Benjamin A Becker, Mitchell E Brown, Chase R Dong, Feng Popović, Zoran B Penn, Marc S |
| description | Exogenous stem cell delivery is under investigation to prevent and treat cardiac dysfunction. It is less studied as to the extent endogenous bone marrow derived stem cells contribute to cardiac homeostais in response to stress and the affects of aging on this stress response.
To determine the role of bone marrow (BM) derived stem cells on cardiac homeostasis in response to pressure overload (PO) and how this response is altered by aging.
Young (8 weeks) and old (>40 weeks) C57/b6 mice underwent homo- and heterochronic BM transplantation prior to transverse aortic constriction (TAC). We found that older BM is associated with decreased cardiac function following TAC. This decreased function is associated with decrease in BM cell engraftment, increased myocyte apoptosis, decreased myocyte hypertrophy, increased myocardial fibrosis and decreased cardiac function. Additionally, there is a decrease in activation of resident cells within the heart in response to PO in old mice. Interestingly, these effects are not due to alterations in vascular density or inflammation in response to PO or differences in ex vivo stem cell migration between young and old mice.
BM derived stem cells are activated in response to cardiac PO, and the recruitment of BM derived cells are involved in cardiac myocyte hypertrophy and maintenance of function in response to PO which is lost with aging. |
| doi_str_mv | 10.1371/journal.pone.0015187 |
| format | Article |
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To determine the role of bone marrow (BM) derived stem cells on cardiac homeostasis in response to pressure overload (PO) and how this response is altered by aging.
Young (8 weeks) and old (>40 weeks) C57/b6 mice underwent homo- and heterochronic BM transplantation prior to transverse aortic constriction (TAC). We found that older BM is associated with decreased cardiac function following TAC. This decreased function is associated with decrease in BM cell engraftment, increased myocyte apoptosis, decreased myocyte hypertrophy, increased myocardial fibrosis and decreased cardiac function. Additionally, there is a decrease in activation of resident cells within the heart in response to PO in old mice. Interestingly, these effects are not due to alterations in vascular density or inflammation in response to PO or differences in ex vivo stem cell migration between young and old mice.
BM derived stem cells are activated in response to cardiac PO, and the recruitment of BM derived cells are involved in cardiac myocyte hypertrophy and maintenance of function in response to PO which is lost with aging.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0015187</identifier><identifier>PMID: 21203577</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Age ; Aging ; Animals ; Aorta ; Aorta - pathology ; Apoptosis ; Atherosclerosis ; Autophagy ; Biology ; Biomechanics ; Bone marrow ; Bone Marrow - physiology ; Bone Marrow Cells - cytology ; Bone Marrow Transplantation ; Cell adhesion & migration ; Cell cycle ; Cell migration ; Cell Movement ; Cell Proliferation ; Cellular stress response ; Cytokines ; Echocardiography - methods ; Fibrosis ; Heart ; Heart - physiology ; Heart attacks ; Heart diseases ; Heart failure ; Homeostasis ; Hypertrophy ; Laboratories ; Male ; Medical research ; Medicine ; Mice ; Mice, Inbred C57BL ; Muscle Cells - cytology ; Myocytes, Cardiac - cytology ; Pressure ; Residential density ; Signal transduction ; Stem cell transplantation ; Stem cells ; Stem Cells - cytology ; Transplantation</subject><ispartof>PloS one, 2010-12, Vol.5 (12), p.e15187-e15187</ispartof><rights>COPYRIGHT 2010 Public Library of Science</rights><rights>2010 Sopko et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Sopko et al. 2010</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c691t-3b553e27314d13c915cf49f35114372a639c59e78890dda4c8a86533c7fea4023</citedby><cites>FETCH-LOGICAL-c691t-3b553e27314d13c915cf49f35114372a639c59e78890dda4c8a86533c7fea4023</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3006343/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3006343/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,724,777,781,861,882,2096,2915,23847,27905,27906,53772,53774,79349,79350</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21203577$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Prosper, Felipe</contributor><creatorcontrib>Sopko, Nikolai A</creatorcontrib><creatorcontrib>Turturice, Benjamin A</creatorcontrib><creatorcontrib>Becker, Mitchell E</creatorcontrib><creatorcontrib>Brown, Chase R</creatorcontrib><creatorcontrib>Dong, Feng</creatorcontrib><creatorcontrib>Popović, Zoran B</creatorcontrib><creatorcontrib>Penn, Marc S</creatorcontrib><title>Bone marrow support of the heart in pressure overload is lost with aging</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Exogenous stem cell delivery is under investigation to prevent and treat cardiac dysfunction. It is less studied as to the extent endogenous bone marrow derived stem cells contribute to cardiac homeostais in response to stress and the affects of aging on this stress response.
To determine the role of bone marrow (BM) derived stem cells on cardiac homeostasis in response to pressure overload (PO) and how this response is altered by aging.
Young (8 weeks) and old (>40 weeks) C57/b6 mice underwent homo- and heterochronic BM transplantation prior to transverse aortic constriction (TAC). We found that older BM is associated with decreased cardiac function following TAC. This decreased function is associated with decrease in BM cell engraftment, increased myocyte apoptosis, decreased myocyte hypertrophy, increased myocardial fibrosis and decreased cardiac function. Additionally, there is a decrease in activation of resident cells within the heart in response to PO in old mice. Interestingly, these effects are not due to alterations in vascular density or inflammation in response to PO or differences in ex vivo stem cell migration between young and old mice.
BM derived stem cells are activated in response to cardiac PO, and the recruitment of BM derived cells are involved in cardiac myocyte hypertrophy and maintenance of function in response to PO which is lost with aging.</description><subject>Age</subject><subject>Aging</subject><subject>Animals</subject><subject>Aorta</subject><subject>Aorta - pathology</subject><subject>Apoptosis</subject><subject>Atherosclerosis</subject><subject>Autophagy</subject><subject>Biology</subject><subject>Biomechanics</subject><subject>Bone marrow</subject><subject>Bone Marrow - physiology</subject><subject>Bone Marrow Cells - cytology</subject><subject>Bone Marrow Transplantation</subject><subject>Cell adhesion & migration</subject><subject>Cell cycle</subject><subject>Cell migration</subject><subject>Cell Movement</subject><subject>Cell Proliferation</subject><subject>Cellular stress response</subject><subject>Cytokines</subject><subject>Echocardiography - methods</subject><subject>Fibrosis</subject><subject>Heart</subject><subject>Heart - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sopko, Nikolai A</au><au>Turturice, Benjamin A</au><au>Becker, Mitchell E</au><au>Brown, Chase R</au><au>Dong, Feng</au><au>Popović, Zoran B</au><au>Penn, Marc S</au><au>Prosper, Felipe</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Bone marrow support of the heart in pressure overload is lost with aging</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2010-12-21</date><risdate>2010</risdate><volume>5</volume><issue>12</issue><spage>e15187</spage><epage>e15187</epage><pages>e15187-e15187</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Exogenous stem cell delivery is under investigation to prevent and treat cardiac dysfunction. It is less studied as to the extent endogenous bone marrow derived stem cells contribute to cardiac homeostais in response to stress and the affects of aging on this stress response.
To determine the role of bone marrow (BM) derived stem cells on cardiac homeostasis in response to pressure overload (PO) and how this response is altered by aging.
Young (8 weeks) and old (>40 weeks) C57/b6 mice underwent homo- and heterochronic BM transplantation prior to transverse aortic constriction (TAC). We found that older BM is associated with decreased cardiac function following TAC. This decreased function is associated with decrease in BM cell engraftment, increased myocyte apoptosis, decreased myocyte hypertrophy, increased myocardial fibrosis and decreased cardiac function. Additionally, there is a decrease in activation of resident cells within the heart in response to PO in old mice. Interestingly, these effects are not due to alterations in vascular density or inflammation in response to PO or differences in ex vivo stem cell migration between young and old mice.
BM derived stem cells are activated in response to cardiac PO, and the recruitment of BM derived cells are involved in cardiac myocyte hypertrophy and maintenance of function in response to PO which is lost with aging.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>21203577</pmid><doi>10.1371/journal.pone.0015187</doi><tpages>e15187</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Age Aging Animals Aorta Aorta - pathology Apoptosis Atherosclerosis Autophagy Biology Biomechanics Bone marrow Bone Marrow - physiology Bone Marrow Cells - cytology Bone Marrow Transplantation Cell adhesion & migration Cell cycle Cell migration Cell Movement Cell Proliferation Cellular stress response Cytokines Echocardiography - methods Fibrosis Heart Heart - physiology Heart attacks Heart diseases Heart failure Homeostasis Hypertrophy Laboratories Male Medical research Medicine Mice Mice, Inbred C57BL Muscle Cells - cytology Myocytes, Cardiac - cytology Pressure Residential density Signal transduction Stem cell transplantation Stem cells Stem Cells - cytology Transplantation |
| title | Bone marrow support of the heart in pressure overload is lost with aging |
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