TY - JOUR
T1 - Identifying immune mechanisms mediating the hypertension during preeclampsia
AU - LaMarca, Babbette
AU - Cornelius, Denise C.
AU - Harmon, Ashlyn C.
AU - Amaral, Lorena M.
AU - Cunningham, Mark W.
AU - Faulkner, Jessica L.
AU - Wallace, Kedra
N1 - Funding Information:
This work was supported by National Institutes of Health Grants HL105324, HL126301, HL124715, HL51971, HL78147, and HD067541.
Publisher Copyright:
© 2016 the American Physiological Society.
PY - 2016/7
Y1 - 2016/7
N2 - Preeclampsia (PE) is a pregnancy-associated disorder that affects 5–8% of pregnancies and is a major cause of maternal, fetal, and neonatal morbidity and mortality. Hallmark characteristics of PE are new onset hypertension after 20 wk gestation with or without proteinuria, chronic immune activation, fetal growth restriction, and maternal endothelial dysfunction. However, the pathophysiological mechanisms that lead to the development of PE are poorly understood. Recent data from studies of both clinical and animal models demonstrate an imbalance in the subpopulations of CD4+ T cells and a role for these cells as mediators of inflammation and hypertension during pregnancy. Specifically, it has been proposed that the imbalance between two CD4+ T cell subtypes, regulatory T cells (Tregs) and T-helper 17 cells (Th17s), is involved in the pathophysiology of PE. Studies from our laboratory highlighting how this imbalance contributes to vasoactive factors, endothelial dysfunction, and hypertension during pregnancy will be discussed in this review. Therefore, the purpose of this review is to highlight hypertensive mechanisms stimulated by inflammatory factors in response to placental ischemia, thereby elucidating a role.
AB - Preeclampsia (PE) is a pregnancy-associated disorder that affects 5–8% of pregnancies and is a major cause of maternal, fetal, and neonatal morbidity and mortality. Hallmark characteristics of PE are new onset hypertension after 20 wk gestation with or without proteinuria, chronic immune activation, fetal growth restriction, and maternal endothelial dysfunction. However, the pathophysiological mechanisms that lead to the development of PE are poorly understood. Recent data from studies of both clinical and animal models demonstrate an imbalance in the subpopulations of CD4+ T cells and a role for these cells as mediators of inflammation and hypertension during pregnancy. Specifically, it has been proposed that the imbalance between two CD4+ T cell subtypes, regulatory T cells (Tregs) and T-helper 17 cells (Th17s), is involved in the pathophysiology of PE. Studies from our laboratory highlighting how this imbalance contributes to vasoactive factors, endothelial dysfunction, and hypertension during pregnancy will be discussed in this review. Therefore, the purpose of this review is to highlight hypertensive mechanisms stimulated by inflammatory factors in response to placental ischemia, thereby elucidating a role.
KW - Cytokines
KW - Hypertension
KW - Inflammation
KW - Pregnancy
UR - http://www.scopus.com/inward/record.url?scp=84984650297&partnerID=8YFLogxK
U2 - 10.1152/ajpregu.00052.2016
DO - 10.1152/ajpregu.00052.2016
M3 - Review article
C2 - 27097659
AN - SCOPUS:84984650297
SN - 0363-6119
VL - 311
SP - R1-R9
JO - American Journal of Physiology - Regulatory Integrative and Comparative Physiology
JF - American Journal of Physiology - Regulatory Integrative and Comparative Physiology
IS - 1
ER -