Sood Laboratory
Location
Translational & Biomedical Resource Center
4th Floor
General Interests
Blood coagulation, Uterine and placental hemostasis, Thrombophilia and pregnancy complications, Placental abruption, Birth timing and biomarkers of preterm birth, Coagulation-inflammation crosstalk, Extraembryonic tissue development, Maternal-placental-fetal health
View Rashmi Sood Bio
Research Areas
Regulation of uterine and placental hemostasis
Hemostasis is the process by which our body prevents blood loss upon injury by forming blood clots. This process of blood clot formation must be kept in check to keep our blood vessels open and allow free blood flow. Pathological blood clot formation which restricts blood flow is called thrombosis. While injury that requires hemostasis can be physical, it can also be caused by normal biological processes, such as placentation. The placenta is a highly vascularized organ. Humans form a hemochorial placenta where specialized cells of fetal origin, called trophoblast cells, derive their nutrition by directly bathing in maternal blood. This process involves break down of maternal blood vessel walls, making the placenta prone to hemorrhage. The tendency to hemorrhage continues as the placenta develops and it peaks at parturition when the placenta separates from the uterus. Maintaining hemostasis and preventing thrombosis is, therefore, critical for preventing obstetric hemorrhage while maintaining vascular patency required for optimal placental function. A tendency towards excessive thrombosis is associated with pregnancy complications, such as fetal growth restriction, placental abruption, preeclampsia and preterm birth. Given the high incidence of these pregnancy complications and their severe consequences on maternal and fetal health, it is necessary to identify (1) key factors that regulate placental and uterine hemostasis, and (2) the sequelae of pathological thrombosis. To address this gap in knowledge, we generate and utilize murine models of maternal and fetal thrombophilia to examine the role of thrombotic processes in uteroplacental disease.
Research Articles
Absence of platelet thrombin receptor PAR4 prevents thrombotic and stroke-like phenotypes of thrombomodulin deficient mice
Human pregnancy and gestational syndromes
Prediction and prevention of gestational syndromes such as preeclampsia and spontaneous preterm delivery are a crucial challenge facing modern obstetrics. The placenta plays a key role in these complications. In the United States, about 1 in 10 babies are born before 37 weeks of gestation. It is a leading cause of neonatal death and the second leading cause of death below 5 years of age. Preterm babies that survive the neonatal period are predisposed to long-term health complications. Preeclampsia is another complex gestational syndrome that roughly affects 5 to 7% of all pregnancies. It is most typically characterized by maternal hypertension and proteinuria. Preeclampsia is frequently associated with fetal growth restriction and often requires premature delivery, putting neonates at risk of immediate and long-term adverse health consequences. It can progress into its potentially fatal form eclampsia and endanger the lives of the mother and fetus. There is a paucity of tools to monitor healthy progression of pregnancies and predict the risk of these major gestational syndromes. Our laboratory utilizes a sensitive bioassay to identify changes in maternal plasma associated with normal progression of pregnancy and abnormalities that are predictive of preterm birth and preeclampsia. In recent work conducted through funding from Advancing a Healthier Wisconsin Endowment, we find that features identified by this assay allow correct classification of preterm birth cases and normal term controls with 90% accuracy 8 weeks prior to preterm delivery. Our goal is to identify features that can be developed into useful biomarkers for prediction and early diagnosis.
Current Members
Recent Publications
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(Castillo MM, Yang Q, Sigala AS, McKinney DT, Zhan M, Chen KL, Jarzembowski JA, Sood R.) Sci Adv. 2020 Nov;6(45) PMID: 33158859 PMCID: PMC7673707 SCOPUS ID: 2-s2.0-85095802928 11/08/2020
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(Castillo MM, Yang Q, Zhan M, Pan AY, Lawlor MW, Mast AE, Sood R.) Blood Adv. 2019 Feb 12;3(3):489-498 PMID: 30755437 PMCID: PMC6373739 SCOPUS ID: 2-s2.0-85061474836 02/14/2019
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(Kanaji S, Orje JN, Kanaji T, Kamikubo Y, Morodomi Y, Chen Y, Zarpellon A, Eberhardt J, Forli S, Fahs SA, Sood R, Haberichter SL, Montgomery RR, Ruggeri ZM.) Blood Adv. 2018 Oct 09;2(19):2522-2532 PMID: 30287479 PMCID: PMC6177644 SCOPUS ID: 2-s2.0-85069786057 10/06/2018
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(van Mens TE, Liang HH, Basu S, Hernandez I, Zogg M, May J, Zhan M, Yang Q, Foeckler J, Kalloway S, Sood R, Karlson CS, Weiler H.) Blood Adv. 2017 Jun 27;1(15):1148-1158 PMID: 28920104 PMCID: PMC5600150 09/19/2017
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(Castillo MM, Yang Q, Sigala AS, McKinney DT, Zhan M, Chen KL, Jarzembowski JA, Sood R.) BioRxiv. https://doi.org/10.1101/2020.02.05.935940 02/05/2020
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(Castillo MM, Yang Q, Sood R.) Blood. 134 (Supplement_1): 2382; https://doi.org/10.1182/blood-2019-131453 11/13/2019
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(Castillo M, Ott E, Wujek R, Qiuli L, Schmainda K, Cohen S, Sood R.) Blood. 134 (Supplement_1): 3626; https://doi.org/10.1182/blood-2019-131811 11/13/2019
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(Castillo M, Yang Q, McKinney D, Shi Q, Sood R.) Blood. 134 (Supplement_1): 1057; https://doi.org/10.1182/blood-2019-123290 11/13/2019
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(Storage M, Yang Q, Zhan M, Sood R.) Res Pract Thromb Haemost. 1 (S1): 87; OC 02.5; https://doi.org/10.1002/rth2.12012 06/23/2017
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(Storage M, Yang Q, Zhan M, Sood R.) Res Pract Thromb Haemost. 1 (S1): 86; OC 02.1; https://doi.org/10.1002/rth2.12012 06/23/2017
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(Chun CZ, Sood R, Ramchandran R.) In: North P., Sander T. (eds) Vascular Tumors and Developmental Malformations.. Molecular and Translational Medicine. Springer, New York, NY. https://doi.org/10.1007/978-1-4939-3240-5_3 01/01/2016
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(Storage MM, An J, Liang H, Yang Q, Zogg M, Zhan M, Weiler H, Sood R.) Blood. 126 (23): 425; https://doi.org/10.1182/blood.V126.23.425.425 12/03/2015