4 results on '"Maide Ozen"'
Search Results
2. Placental malperfusion in response to intrauterine inflammation and its connection to fetal sequelae.
- Author
-
Solange N Eloundou, JiYeon Lee, Dan Wu, Jun Lei, Mia C Feller, Maide Ozen, Yan Zhu, Misun Hwang, Bei Jia, Han Xie, Julia L Clemens, Michael W McLane, Samar AlSaggaf, Nita Nair, Marsha Wills-Karp, Xiaobin Wang, Ernest M Graham, Ahmet Baschat, and Irina Burd
- Subjects
Medicine ,Science - Abstract
Exposure to intrauterine inflammation (IUI) is associated with short- and long-term adverse perinatal outcomes. However, little data exist on utilizing placenta to prognosticate fetal injury in this scenario. Our study aimed to utilize imaging modalities to evaluate mechanisms contributing to placental injury following IUI exposure and correlated it to concomitant fetal brain injury. CD1 pregnant dams underwent laparotomies and received intrauterine injections of either lipopolysaccharide (LPS; a model of IUI) or phosphate-buffered saline (PBS). In utero ultrasound Doppler velocimetry of uterine and umbilical arteries and magnetic resonance imaging (MRI) of placental volumes with confirmatory immunohistochemical (vimentin) and histochemistry (fibrin) analyses were performed. ELISA for thrombosis markers, fibrinogen and fibrin was performed to analyze thrombi in placenta. Fetal brain immunohistochemistry was performed to detect microglial activation (ionized calcium-binding adaptor molecule 1, Iba1). On ultrasound, LPS group demonstrated elevated resistance indices, pulsatility indices and a greater occurrence of absent end-diastolic flow in the umbilical and uterine arteries. In the fetus, there was an increased cardiac Tei indices in the LPS group. MRI revealed decreased volume of placenta in the LPS group associated with placental thinning and placental endothelial damage on immunohistochemistry. Decreased fibrinogen content and more thrombi staining in placenta exposed to maternal LPS indicated the hypercoagulability. Furthermore, the expression of Iba1was significantly associated with placental thickness (r = -0.7890, Pearson correlation coefficient). Our data indicate that IUI can trigger events leading to maternal placental malperfusion and fetal vessel resistance, as well as predispose the developing fetus to cardiac dysfunction and brain damage. Furthermore, our data suggest that prenatal ultrasound can be a real-time clinical tool for assessing fetal risk for adverse neurologic outcomes following the potential IUI exposure.
- Published
- 2019
- Full Text
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3. Inflammation-induced alterations in maternal-fetal Heme Oxygenase (HO) are associated with sustained innate immune cell dysregulation in mouse offspring
- Author
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Ronald J. Wong, Maide Ozen, David K. Stevenson, Lauren L. Jantzie, Flora Kalish, Hui Zhao, and Yang Yang
- Subjects
Lipopolysaccharides ,Male ,Embryology ,Myeloid ,Neutrophils ,Physiology ,Placenta ,Maternal Health ,Systemic inflammation ,Monocytes ,Mice ,White Blood Cells ,Pregnancy ,Animal Cells ,Immune Physiology ,Medicine and Health Sciences ,Immune Response ,Mice, Knockout ,Multidisciplinary ,Obstetrics and Gynecology ,medicine.anatomical_structure ,Liver ,Medicine ,Female ,medicine.symptom ,Cellular Types ,Anatomy ,Research Article ,medicine.medical_specialty ,Genotype ,Offspring ,Immune Cells ,Science ,Immunology ,Inflammation ,Spleen ,Biology ,Fetus ,Signs and Symptoms ,Internal medicine ,medicine ,Animals ,Fetuses ,Innate immune system ,Blood Cells ,Reproductive System ,Biology and Life Sciences ,Dendritic Cells ,Cell Biology ,Immunity, Innate ,Heme oxygenase ,Endocrinology ,Women's Health ,Clinical Medicine ,Heme Oxygenase-1 ,Developmental Biology - Abstract
Heme oxygenase-1 (HO-1) is an evolutionarily conserved stress response enzyme and important in pregnancy maintenance, fetal and neonatal outcomes, and a variety of pathologic conditions. Here, we investigated the effects of an exposure to systemic inflammation late in gestation [embryonic day (E)15.5] on wild-type (Wt) and HO-1 heterozygous (Het, HO-1+/-) mothers, fetuses, and offspring. We show that alterations in fetal liver and spleen HO homeostasis during inflammation late in gestation can lead to a sustained dysregulation of innate immune cell populations and intracellular myeloid HO-1 expression in the spleen through young adolescence [postnatal day 25] in mice.
- Published
- 2021
4. Placental malperfusion in response to intrauterine inflammation and its connection to fetal sequelae
- Author
-
Xiaobin Wang, Jun Lei, Julia L. Clemens, Han Xie, Marsha Wills-Karp, Solange N. Eloundou, Samar Al-Saggaf, Nita Nair, Bei Jia, Ahmet A. Baschat, Irina Burd, Ji Yeon Lee, Dan Wu, Ernest M. Graham, Yan Zhu, Michael W. McLane, Misun Hwang, Maide Ozen, and Mia C. Feller
- Subjects
0301 basic medicine ,Lipopolysaccharides ,Pathology ,Embryology ,Placenta Diseases ,Placenta ,Glycobiology ,Fibrinogen ,Pathology and Laboratory Medicine ,Biochemistry ,Umbilical Arteries ,Diagnostic Radiology ,Mice ,0302 clinical medicine ,Pregnancy ,Medicine and Health Sciences ,Brain Damage ,Immune Response ,030219 obstetrics & reproductive medicine ,Multidisciplinary ,biology ,Radiology and Imaging ,Arteries ,Thrombosis ,Magnetic Resonance Imaging ,3. Good health ,Fetal Diseases ,medicine.anatomical_structure ,Neurology ,In utero ,Medicine ,Female ,medicine.symptom ,Anatomy ,medicine.drug ,Research Article ,medicine.medical_specialty ,Imaging Techniques ,Science ,Immunology ,Brain damage ,Research and Analysis Methods ,Fibrin ,03 medical and health sciences ,Signs and Symptoms ,Diagnostic Medicine ,medicine ,Animals ,Vimentin ,Glycoproteins ,Inflammation ,Fetus ,Fetuses ,business.industry ,Reproductive System ,Biology and Life Sciences ,Proteins ,medicine.disease ,Cytoskeletal Proteins ,030104 developmental biology ,Brain Injuries ,biology.protein ,Cardiovascular Anatomy ,Blood Vessels ,business ,Developmental Biology - Abstract
Exposure to intrauterine inflammation (IUI) is associated with short- and long-term adverse perinatal outcomes. However, little data exist on utilizing placenta to prognosticate fetal injury in this scenario. Our study aimed to utilize imaging modalities to evaluate mechanisms contributing to placental injury following IUI exposure and correlated it to concomitant fetal brain injury. CD1 pregnant dams underwent laparotomies and received intrauterine injections of either lipopolysaccharide (LPS; a model of IUI) or phosphate-buffered saline (PBS). In utero ultrasound Doppler velocimetry of uterine and umbilical arteries and magnetic resonance imaging (MRI) of placental volumes with confirmatory immunohistochemical (vimentin) and histochemistry (fibrin) analyses were performed. ELISA for thrombosis markers, fibrinogen and fibrin was performed to analyze thrombi in placenta. Fetal brain immunohistochemistry was performed to detect microglial activation (ionized calcium-binding adaptor molecule 1, Iba1). On ultrasound, LPS group demonstrated elevated resistance indices, pulsatility indices and a greater occurrence of absent end-diastolic flow in the umbilical and uterine arteries. In the fetus, there was an increased cardiac Tei indices in the LPS group. MRI revealed decreased volume of placenta in the LPS group associated with placental thinning and placental endothelial damage on immunohistochemistry. Decreased fibrinogen content and more thrombi staining in placenta exposed to maternal LPS indicated the hypercoagulability. Furthermore, the expression of Iba1was significantly associated with placental thickness (r = -0.7890, Pearson correlation coefficient). Our data indicate that IUI can trigger events leading to maternal placental malperfusion and fetal vessel resistance, as well as predispose the developing fetus to cardiac dysfunction and brain damage. Furthermore, our data suggest that prenatal ultrasound can be a real-time clinical tool for assessing fetal risk for adverse neurologic outcomes following the potential IUI exposure.
- Published
- 2018
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