Genomes and Genes

Species

Babbette LaMarca

Summary

Publications

  1. Cunningham M, Vaka V, McMaster K, Ibrahim T, Cornelius D, Amaral L, et al. Renal natural killer cell activation and mitochondrial oxidative stress; new mechanisms in AT1-AA mediated hypertensive pregnancy. Pregnancy Hypertens. 2019;15:72-77 pubmed publisher
    ..05). In conclusion, AT1-AA's increased MAP, NK cells, and mtROS which were attenuated by AT1-AA inhibition, thus highlighting new mechanisms of AT1-AA and the importance of drug therapy targeted to AT1-AAs in hypertensive pregnancies. ..
  2. Harmon A, Ibrahim T, Cornelius D, Amaral L, Cunningham M, Wallace K, et al. Placental CD4+ T cells isolated from preeclamptic women cause preeclampsia-like symptoms in pregnant nude-athymic rats. Pregnancy Hypertens. 2019;15:7-11 pubmed publisher
    ..5 fold in rats with PE CD4+ T cells versus those receiving to NP CD4+ T cells. These data indicate an important role for placental PE CD4+ T cells to cause many characteristics of PE during pregnancy. ..
  3. Cornelius D, Amaral L, Harmon A, Wallace K, Thomas A, Campbell N, et al. An increased population of regulatory T cells improves the pathophysiology of placental ischemia in a rat model of preeclampsia. Am J Physiol Regul Integr Comp Physiol. 2015;309:R884-91 pubmed publisher
    ..50 ± 0.3 bpm with NP TRegs. This study demonstrates that NP TRegs can significantly improve inflammatory mediators, such as IL-17, TNF-α, and AT1-AA, which have been shown to increase blood pressure during pregnancy. ..
  4. Cornelius D, Castillo J, Porter J, Amaral L, Campbell N, Paige A, et al. Blockade of CD40 ligand for intercellular communication reduces hypertension, placental oxidative stress, and AT1-AA in response to adoptive transfer of CD4+ T lymphocytes from RUPP rats. Am J Physiol Regul Integr Comp Physiol. 2015;309:R1243-50 pubmed publisher
    ..05). AT1-AA was also normalized with inhibition of CD40L. These data suggest that placental ischemia-induced T-cell communication via the CD40L is one important mechanism leading to much of the pathophysiology of PE. ..
  5. Vaka V, McMaster K, Cunningham M, Ibrahim T, Hazlewood R, Usry N, et al. Role of Mitochondrial Dysfunction and Reactive Oxygen Species in Mediating Hypertension in the Reduced Uterine Perfusion Pressure Rat Model of Preeclampsia. Hypertension. 2018;: pubmed publisher
    ..Impaired mitochondrial function and vascular, placental, and renal mitochondrial ROS play an important role in hypertension and reduced fetal weight in response to placental ischemia during pregnancy. ..
  6. Cunningham M, Castillo J, Ibrahim T, Cornelius D, Campbell N, Amaral L, et al. AT1-AA (Angiotensin II Type 1 Receptor Agonistic Autoantibody) Blockade Prevents Preeclamptic Symptoms in Placental Ischemic Rats. Hypertension. 2018;71:886-893 pubmed publisher
    ..05) In conclusion, AT1-AA inhibition prevents the rise in maternal blood pressure and several pathophysiological factors associated with preeclampsia in RUPP rats and could be a potential therapy for preeclampsia. ..
  7. Amaral L, Cornelius D, Harmon A, Moseley J, Martin J, LaMarca B. 17-hydroxyprogesterone caproate significantly improves clinical characteristics of preeclampsia in the reduced uterine perfusion pressure rat model. Hypertension. 2015;65:225-31 pubmed publisher
    ..05). Our findings demonstrate that even though modest, lowering blood pressure with 17-OHPC could be a viable treatment option for suppressing inflammation, uterine artery vasoconstriction while improving litter size. ..
  8. Wallace K, Cornelius D, Scott J, Heath J, Moseley J, Chatman K, et al. CD4+ T cells are important mediators of oxidative stress that cause hypertension in response to placental ischemia. Hypertension. 2014;64:1151-8 pubmed publisher
    ..05). These data demonstrate an important role for CD4(+) T cells in mediating another factor, oxidative stress, to cause hypertension during preeclampsia. ..
  9. LaMarca B, Cornelius D, Harmon A, Amaral L, Cunningham M, Faulkner J, et al. Identifying immune mechanisms mediating the hypertension during preeclampsia. Am J Physiol Regul Integr Comp Physiol. 2016;311:R1-9 pubmed publisher
    ..Therefore, the purpose of this review is to highlight hypertensive mechanisms stimulated by inflammatory factors in response to placental ischemia, thereby elucidating a role. ..

More Information

Publications19

  1. Cunningham M, Williams J, Amaral L, Usry N, Wallukat G, Dechend R, et al. Agonistic Autoantibodies to the Angiotensin II Type 1 Receptor Enhance Angiotensin II-Induced Renal Vascular Sensitivity and Reduce Renal Function During Pregnancy. Hypertension. 2016;68:1308-1313 pubmed
    ..These data indicate the importance of AT1-AAs to enhance ANG II-induced renal vasoconstriction and reduce renal function as mechanisms to cause hypertension as observed during preeclampsia. ..
  2. Faulkner J, Amaral L, Cornelius D, Cunningham M, Ibrahim T, Heep A, et al. Vitamin D supplementation reduces some AT1-AA-induced downstream targets implicated in preeclampsia including hypertension. Am J Physiol Regul Integr Comp Physiol. 2017;312:R125-R131 pubmed publisher
  3. LaMarca B, Amaral L, Harmon A, Cornelius D, Faulkner J, Cunningham M. Placental Ischemia and Resultant Phenotype in Animal Models of Preeclampsia. Curr Hypertens Rep. 2016;18:38 pubmed publisher
    ..This review will highlight various animal models and the major findings indicating the importance of placental ischemia to lead to the pathophysiology observed in preeclamptic patients. ..
  4. Harmon A, Cornelius D, Amaral L, Faulkner J, Cunningham M, Wallace K, et al. The role of inflammation in the pathology of preeclampsia. Clin Sci (Lond). 2016;130:409-19 pubmed publisher
  5. Faulkner J, Cornelius D, Amaral L, Harmon A, Cunningham M, Darby M, et al. Vitamin D supplementation improves pathophysiology in a rat model of preeclampsia. Am J Physiol Regul Integr Comp Physiol. 2016;310:R346-54 pubmed publisher
    ..7 ± 19.9 pg/ml in RUPP rats. VD treatment reduced CD4+ T cells, AT1-AA, ET-1, sFlt-1, and blood pressure in the RUPP rat model of PE and could be an avenue to improve treatment of hypertension in response to placental ischemia. ..
  6. Santiago Font J, Amaral L, Faulkner J, Ibrahim T, Vaka V, Cunningham M, et al. Serelaxin improves the pathophysiology of placental ischemia in the reduced uterine perfusion pressure rat model of preeclampsia. Am J Physiol Regul Integr Comp Physiol. 2016;311:R1158-R1163 pubmed publisher
  7. Cornelius D, Amaral L, Wallace K, Campbell N, Thomas A, Scott J, et al. Reduced uterine perfusion pressure T-helper 17 cells cause pathophysiology associated with preeclampsia during pregnancy. Am J Physiol Regul Integr Comp Physiol. 2016;311:R1192-R1199 pubmed publisher
  8. Faulkner J, Plenty N, Wallace K, Amaral L, Cunningham M, Murphy S, et al. Selective inhibition of 20-hydroxyeicosatetraenoic acid lowers blood pressure in a rat model of preeclampsia. Prostaglandins Other Lipid Mediat. 2018;134:108-113 pubmed publisher
    ..In conclusion, 20-HETE inhibition in RUPP rats reduces BP and fetal death, and is associated with an increase in EET/20-HETE ratio. ..
  9. Amaral L, Faulkner J, ElFarra J, Cornelius D, Cunningham M, Ibrahim T, et al. Continued Investigation Into 17-OHPC: Results From the Preclinical RUPP Rat Model of Preeclampsia. Hypertension. 2017;70:1250-1255 pubmed publisher
    ..2±11 in RUPP+17-OHPC, P<0.05. These data indicate that GD15 17-OHPC improves pathophysiology in RUPP rats, possibly via improving sFlt-1 reduced NO during pregnancy. ..
  10. Amaral L, Wallace K, Owens M, LaMarca B. Pathophysiology and Current Clinical Management of Preeclampsia. Curr Hypertens Rep. 2017;19:61 pubmed publisher
    ..This review will highlight factors implicated in the pathophysiology of preeclampsia and current treatments for the management of this disease. ..