2.50
Hdl Handle:
http://hdl.handle.net/10755/165504
Category:
Abstract
Type:
Presentation
Title:
GENE EXPRESSION CHANGES IN AGED VASCULAR ENDOTHELIAL CELLS
Author(s):
Cabrera, Rosaria; Merkle, Carrie J.; Montgomery, David W.
Author Details:
Rosaria Cabrera, BS, Physiological Sciences, Tucson, Arizona, USA; Carrie J. Merkle, PhD, RN, FAAN; David W. Montgomery, PhD
Abstract:
Death from breast cancer is due to metastatic disease. The mechanisms of metastasis are largely unknown, though the endothelium is involved. Our goal was to determine if there are age-related changes in gene expression in human microvascular endothelial cells (HMVECs) that might facilitate breast cancer metastasis. The aims were to: Aim 1: Age HMVECs in-vitro to form groups identified by population doubling (PD) number, Aim 2: Identify morphological differences in HMVEC age groups, Aim 3: Identify age-related changes in expression of angiogenesis, extracellular matrix/adhesion molecule, and stress/toxicity pathway genes. Our previous work has shown that breast cancer cell addition to in-vitro aged, but not young, bovine pulmonary artery endothelial cells causes persistent gaps to form between neighboring endothelial cells and facilitates breast cancer cell transmigration of endothelial cells. These observations warrant additional study because: 1. endothelial transmigration occurs in metastasis, and 2. breast cancer metastasis causes death. Aim 1: HMVECs from the lung of a three year-old female were obtained at PD 20 and serially aged. Aim 2: HMVECs of specific PDs were examined by microscopy. Cell size and density were determined. VE-cadherin, an endothelial adhesion protein, was quantified. Aim 3: RNA from HMVECs at PD 24, 31 and 40 was isolated. Using SuperArray GEArrayTM Q series kits, cDNA probes were formed and added to membranes containing genes for angiogenesis, extracellular matrix/adhesion molecules, and stress/toxicity pathways. Images were captured digitally and analyzed. Aim 2: Data were analyzed by ANOVA. Aim 3: Data were analyzed by the manufacturer’s protocol and definitions for gene expression, gene expression increases and gene expression decreases. Aim 1: HMVECs were successfully aged to PD 43. Aim 2: As HMVECs age (increase in PD), cell area increases and cell density decreases. Higher PD HMVECs have less VE-cadherin. Aim 3: Expression of over seventy genes was identified. Expression decreased in two genes (caveolin and a catenin-related protein) and increased in seven genes (specific integrins, plasminogen activator inhibitor and a laminin). These changes may facilitate metastasis, a hypothesis being tested in rodents. Since vascular aging increases with high blood pressure, high lipids, and stress hormones, it is possible that interventions to reduce cardiovascular disease may prevent metastasis.
Repository Posting Date:
27-Oct-2011
Date of Publication:
27-Oct-2011
Conference Date:
2005
Conference Name:
30th Annual Oncology Nursing Society Congress
Conference Host:
Oncology Nursing Society
Conference Location:
Orlando, Florida, USA
Sponsors:
Funding Sources: The University of Arizona Honors College and NIH P20-NR07794
Note:
This is an abstract-only submission. If the author has submitted a full-text item based on this abstract, you may find it by browsing the Virginia Henderson Global Nursing e-Repository by author. If author contact information is available in this abstract, please feel free to contact him or her with your queries regarding this submission. Alternatively, please contact the conference host, journal, or publisher (according to the circumstance) for further details regarding this item. If a citation is listed in this record, the item has been published and is available via open-access avenues or a journal/database subscription. Contact your library for assistance in obtaining the as-published article.

Full metadata record

DC FieldValue Language
dc.type.categoryAbstracten_US
dc.typePresentationen_GB
dc.titleGENE EXPRESSION CHANGES IN AGED VASCULAR ENDOTHELIAL CELLSen_GB
dc.contributor.authorCabrera, Rosariaen_US
dc.contributor.authorMerkle, Carrie J.en_US
dc.contributor.authorMontgomery, David W.en_US
dc.author.detailsRosaria Cabrera, BS, Physiological Sciences, Tucson, Arizona, USA; Carrie J. Merkle, PhD, RN, FAAN; David W. Montgomery, PhDen_US
dc.identifier.urihttp://hdl.handle.net/10755/165504-
dc.description.abstractDeath from breast cancer is due to metastatic disease. The mechanisms of metastasis are largely unknown, though the endothelium is involved. Our goal was to determine if there are age-related changes in gene expression in human microvascular endothelial cells (HMVECs) that might facilitate breast cancer metastasis. The aims were to: Aim 1: Age HMVECs in-vitro to form groups identified by population doubling (PD) number, Aim 2: Identify morphological differences in HMVEC age groups, Aim 3: Identify age-related changes in expression of angiogenesis, extracellular matrix/adhesion molecule, and stress/toxicity pathway genes. Our previous work has shown that breast cancer cell addition to in-vitro aged, but not young, bovine pulmonary artery endothelial cells causes persistent gaps to form between neighboring endothelial cells and facilitates breast cancer cell transmigration of endothelial cells. These observations warrant additional study because: 1. endothelial transmigration occurs in metastasis, and 2. breast cancer metastasis causes death. Aim 1: HMVECs from the lung of a three year-old female were obtained at PD 20 and serially aged. Aim 2: HMVECs of specific PDs were examined by microscopy. Cell size and density were determined. VE-cadherin, an endothelial adhesion protein, was quantified. Aim 3: RNA from HMVECs at PD 24, 31 and 40 was isolated. Using SuperArray GEArrayTM Q series kits, cDNA probes were formed and added to membranes containing genes for angiogenesis, extracellular matrix/adhesion molecules, and stress/toxicity pathways. Images were captured digitally and analyzed. Aim 2: Data were analyzed by ANOVA. Aim 3: Data were analyzed by the manufacturer’s protocol and definitions for gene expression, gene expression increases and gene expression decreases. Aim 1: HMVECs were successfully aged to PD 43. Aim 2: As HMVECs age (increase in PD), cell area increases and cell density decreases. Higher PD HMVECs have less VE-cadherin. Aim 3: Expression of over seventy genes was identified. Expression decreased in two genes (caveolin and a catenin-related protein) and increased in seven genes (specific integrins, plasminogen activator inhibitor and a laminin). These changes may facilitate metastasis, a hypothesis being tested in rodents. Since vascular aging increases with high blood pressure, high lipids, and stress hormones, it is possible that interventions to reduce cardiovascular disease may prevent metastasis.en_GB
dc.date.available2011-10-27T12:19:49Z-
dc.date.issued2011-10-27en_GB
dc.date.accessioned2011-10-27T12:19:49Z-
dc.conference.date2005en_US
dc.conference.name30th Annual Oncology Nursing Society Congressen_US
dc.conference.hostOncology Nursing Societyen_US
dc.conference.locationOrlando, Florida, USAen_US
dc.description.sponsorshipFunding Sources: The University of Arizona Honors College and NIH P20-NR07794-
dc.description.noteThis is an abstract-only submission. If the author has submitted a full-text item based on this abstract, you may find it by browsing the Virginia Henderson Global Nursing e-Repository by author. If author contact information is available in this abstract, please feel free to contact him or her with your queries regarding this submission. Alternatively, please contact the conference host, journal, or publisher (according to the circumstance) for further details regarding this item. If a citation is listed in this record, the item has been published and is available via open-access avenues or a journal/database subscription. Contact your library for assistance in obtaining the as-published article.-
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