Offspring of hypertensive placental ischemia rats have hypertension and mitochondrial dysfunction during pregnancy

Simple item page
dc.creatorPowell, Madison
dc.creatorCromartie, Whitney
dc.creatorSmith, Jonna
dc.creatorCunningham, Mark
dc.date.accessioned2022-05-13T16:07:27Z
dc.date.available2022-05-13T16:07:27Z
dc.date.issued2022
dc.descriptionResearch Appreciation Day Award Winner - 2022 Texas College of Osteopathic Medicine, 2022 TCOM Student Research Award - 1st Place
dc.description.abstractPurpose: Preeclampsia is a pregnancy complication commonly observed in the third trimester of pregnancy and is often characterized by hypertension, placental ischemia, and Intrauterine growth restriction (IUGR), also referred to as fetal growth restriction. The causes of IUGR vary but are associated with maternal hypertension and placenta abnormalities. Clinical studies show that IUGR daughters of women with preeclampsia have an increased risk of developing hypertensive pregnancies, such as preeclampsia. Common factors associated with the pathophysiology of preeclampsia are systemic and tissue mitochondrial dysfunction, endothelial cell dysfunction, inflammation, and oxidative stress. Previous studies from our laboratory show that pregnant IUGR rats, derived from our reduced uterine perfusion pressure preclinical rodent model of preeclampsia (RUPP), develop hypertension during their own pregnancies along with an increase in brain size and systemic oxidative stress. However, the role of end-organ mitochondrial dysfunction has not been explored and is the focus of this study. We hypothesize that brain, heart, and kidney mitochondrial dysfunction will be present in pregnant IUGR rats. Methods: To measure mitochondrial dysfunction in the brain, heart, and kidney tissue, we will perform western blots on manganese superoxide dismutase (MnSOD), a mitochondrial specific antioxidant, and mitochondrial electron transport chain (ETC) complexes I-V in both normal pregnant (CON) and IUGR pregnant rats. Results: MnSOD protein abundance was decreased in the brain of IUGR vs CON pregnant rats (88±3 vs 100±3 % IU/Protein/CON, p= 0.05). No differences were observed in the heart and kidney of IUGR and CON pregnant rats. Brain mitochondrial complexes II (144±14 vs 100±5 % IU/Protein/CON, p< 0.05), III (119±7 vs 100±2 % IU/Protein/CON, p= 0.06), and V (125±3 vs 100±4 % IU/Protein/CON, p< 0.01) were increased in IUGR vs CON pregnant rats, and no changes were observed in the heart. However, kidney mitochondrial complexes III (84±3 vs 100±0.3 % IU/Protein/CON, p< 0.05) and V (87±2 vs 100±1 % IU/Protein/CON, p< 0.05) were decreased in IUGR vs CON pregnant rats. Conclusions: Pregnant IUGR rats have hypertension and renal mitochondrial dysfunction. The decreased amount of brain specific mitochondrial antioxidants in IUGR pregnant rats may contribute to elevated systemic and local oxidative stress. The increase in ETC mitochondrial proteins in brain may be a compensatory mechanism to increase mitochondrial function in the swelling brain. Furthermore, the increase in ETC function in the brain may also increase mitochondrial reactive oxygen species levels, which may not be able to be quenched due to the decrease in brain mitochondrial antioxidants. Nevertheless, the increase in brain mitochondrial ETC proteins warrants further investigation. In conclusion, rather or not the increase in end-organ mitochondrial dysfunction is a cause or consequence of hypertension in pregnant IUGR rats is unknown? Future studies will be designed to address this question.
dc.description.sponsorshipAmerican Heart Association Career Development Award #18CDA34110264
dc.identifier.urihttps://hdl.handle.net/20.500.12503/31065
dc.language.isoen
dc.titleOffspring of hypertensive placental ischemia rats have hypertension and mitochondrial dysfunction during pregnancy
dc.typeposter
dc.type.materialtext

Files

Collections

Pediatrics & Women's Health