Gene expression profiling of first trimester placentas from pregnancies at high risk of developing preeclampsia
Anderson, Ulrik Dolberg LU ; Thilaganathan, Baskaran ; Gram, Magnus LU
; Åkerström, Bo
LU
and Hansson, Stefan
LU
(2013)
European Congress of the International Society for the Study of Hypertension in Pregnancy
In Pregnancy Hypertension
3(2).
p.69-69
- Abstract
INTRODUCTION: Preeclampsia (PE) is an important cause of fetal and maternal morbidity and mortality. It is considered a two-stage disease, the first stage characterized by a defect placentation and the second stage by maternal manifestations. Details of the patho-physiology behind the transition from stage one to stage two remain unclear.
OBJECTIVE: Was to study first trimester placental gene expression in patients identified as high risk for PE by either Doppler ultrasound or the biochemical markers cell free fetal hemoglobin (HbF) and alpha-1-microglobulin (A1M).
METHODS: Placental samples were obtained from seven women at highrisk of PE as determined by Doppler ultrasound of the uterine arteries and eight women with... (More)
INTRODUCTION: Preeclampsia (PE) is an important cause of fetal and maternal morbidity and mortality. It is considered a two-stage disease, the first stage characterized by a defect placentation and the second stage by maternal manifestations. Details of the patho-physiology behind the transition from stage one to stage two remain unclear.
OBJECTIVE: Was to study first trimester placental gene expression in patients identified as high risk for PE by either Doppler ultrasound or the biochemical markers cell free fetal hemoglobin (HbF) and alpha-1-microglobulin (A1M).
METHODS: Placental samples were obtained from seven women at highrisk of PE as determined by Doppler ultrasound of the uterine arteries and eight women with normal uterine artery resistance who for other reasons terminated their pregnancies surgically. Maternal serum samples were analyzed for HbF and A1M. The patients were risk stratified according to two risk classifications: (I) High vs. low uterine artery resistance and (II) High HbF and A1M vs. low HbF and A1M. Total RNA from the placentas was used for whole genome microarray. The results were analyzed by bioinformatics and genes of interest confirmed with qPCR.
RESULTS: A total of 453 and 332 significantly altered genes were identified in the two study groups. Bioinformatics revealed 12 genes of interest in study group I and 7 genes of interest in study group II.
CONCLUSIONS: Genes related to vascular tonus regulation and inflammatory response were identified in study group I suggesting that a lack of tonus regulation and increased inflammation might contribute to the high uterine artery resistance seen in this group. Genes related to regulation of hematopoiesis was found in group II suggesting dysfunctional hematopoiesis as a factor explaining the high levels of cell-free HbF seen.
(Less)
- author
- Anderson, Ulrik Dolberg
LU
; Thilaganathan, Baskaran
; Gram, Magnus
LU
; Åkerström, Bo
LU
and Hansson, Stefan
LU
- organization
- publishing date
- 2013-04
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Journal Article
- in
- Pregnancy Hypertension
- volume
- 3
- issue
- 2
- article number
- PP006
- pages
- 69 - 69
- publisher
- Elsevier
- conference name
- European Congress of the International Society for the Study of Hypertension in Pregnancy
- conference location
- Tromsö, Norway
- conference dates
- 2013-06-12 - 2013-06-14
- external identifiers
-
- pmid:26105862
- ISSN
- 2210-7789
- DOI
- 10.1016/j.preghy.2013.04.034
- language
- English
- LU publication?
- yes
- id
- 7220578e-4fdf-4886-b53e-74adccbc84e7
- date added to LUP
- 2018-04-25 16:16:24
- date last changed
- 2021-04-29 02:35:54
@misc{7220578e-4fdf-4886-b53e-74adccbc84e7,
abstract = {{<p>INTRODUCTION: Preeclampsia (PE) is an important cause of fetal and maternal morbidity and mortality. It is considered a two-stage disease, the first stage characterized by a defect placentation and the second stage by maternal manifestations. Details of the patho-physiology behind the transition from stage one to stage two remain unclear.</p><p>OBJECTIVE: Was to study first trimester placental gene expression in patients identified as high risk for PE by either Doppler ultrasound or the biochemical markers cell free fetal hemoglobin (HbF) and alpha-1-microglobulin (A1M).</p><p>METHODS: Placental samples were obtained from seven women at highrisk of PE as determined by Doppler ultrasound of the uterine arteries and eight women with normal uterine artery resistance who for other reasons terminated their pregnancies surgically. Maternal serum samples were analyzed for HbF and A1M. The patients were risk stratified according to two risk classifications: (I) High vs. low uterine artery resistance and (II) High HbF and A1M vs. low HbF and A1M. Total RNA from the placentas was used for whole genome microarray. The results were analyzed by bioinformatics and genes of interest confirmed with qPCR.</p><p>RESULTS: A total of 453 and 332 significantly altered genes were identified in the two study groups. Bioinformatics revealed 12 genes of interest in study group I and 7 genes of interest in study group II.</p><p>CONCLUSIONS: Genes related to vascular tonus regulation and inflammatory response were identified in study group I suggesting that a lack of tonus regulation and increased inflammation might contribute to the high uterine artery resistance seen in this group. Genes related to regulation of hematopoiesis was found in group II suggesting dysfunctional hematopoiesis as a factor explaining the high levels of cell-free HbF seen.</p>}},
author = {{Anderson, Ulrik Dolberg and Thilaganathan, Baskaran and Gram, Magnus and Åkerström, Bo and Hansson, Stefan}},
issn = {{2210-7789}},
keywords = {{Journal Article}},
language = {{eng}},
note = {{Conference Abstract}},
number = {{2}},
pages = {{69--69}},
publisher = {{Elsevier}},
series = {{Pregnancy Hypertension}},
title = {{Gene expression profiling of first trimester placentas from pregnancies at high risk of developing preeclampsia}},
url = {{http://dx.doi.org/10.1016/j.preghy.2013.04.034}},
doi = {{10.1016/j.preghy.2013.04.034}},
volume = {{3}},
year = {{2013}},
}