scholarly journals Maternal Uterine Vascular Remodeling During Pregnancy

Physiology ◽  
2009 ◽  
Vol 24 (1) ◽  
pp. 58-71 ◽  
Author(s):  
George Osol ◽  
Maurizio Mandala
Keyword(s):  
Extracellular Matrix ◽  
Blood Flow ◽  
Vascular Remodeling ◽  
Normal Pregnancy ◽  
Uterine Blood Flow ◽  
Growth And Remodeling ◽  
Cellular Mechanisms ◽  
Cellular Processes ◽  
Uteroplacental Blood Flow ◽  
Uterine Circulation

Sufficient uteroplacental blood flow is essential for normal pregnancy outcome and is accomplished by the coordinated growth and remodeling of the entire uterine circulation, as well as the creation of a new fetal vascular organ: the placenta. The process of remodeling involves a number of cellular processes, including hyperplasia and hypertrophy, rearrangement of existing elements, and changes in extracellular matrix. In this review, we provide information on uterine blood flow increases during pregnancy, the influence of placentation type on the distribution of uterine vascular resistance, consideration of the patterns, nature, and extent of maternal uterine vascular remodeling during pregnancy, and what is known about the underlying cellular mechanisms.

scholarly journals Uteroplacental Circulation in Normal Pregnancy and Preeclampsia: Functional Adaptation and Maladaptation

2021 ◽  
Vol 22 (16) ◽  
pp. 8622
Author(s):  
Xiangqun Hu ◽  
Lubo Zhang
Keyword(s):  
Blood Flow ◽  
Hormonal Regulation ◽  
Vascular Function ◽  
Vascular Dysfunction ◽  
Well Being ◽  
Normal Pregnancy ◽  
Functional Adaptation ◽  
Vasoactive Factors ◽  
Uteroplacental Blood Flow ◽  
Underlying Mechanisms

Uteroplacental blood flow increases as pregnancy advances. Adequate supply of nutrients and oxygen carried by uteroplacental blood flow is essential for the well-being of the mother and growth/development of the fetus. The uteroplacental hemodynamic change is accomplished primarily through uterine vascular adaptation, involving hormonal regulation of myogenic tone, vasoreactivity, release of vasoactive factors and others, in addition to the remodeling of spiral arteries. In preeclampsia, hormonal and angiogenic imbalance, proinflammatory cytokines and autoantibodies cause dysfunction of both endothelium and vascular smooth muscle cells of the uteroplacental vasculature. Consequently, the vascular dysfunction leads to increased vascular resistance and reduced blood flow in the uteroplacental circulation. In this article, the (mal)adaptation of uteroplacental vascular function in normal pregnancy and preeclampsia and underlying mechanisms are reviewed.

scholarly journals Expression Profiling of Glioblastoma Cell Lines Reveals Novel Extracellular Matrix-Receptor Genes Correlated With the Responsiveness of Glioma Patients to Ionizing Radiation

2021 ◽  
Vol 11 ◽  
Author(s):  
Rodolfo Bortolozo Serafim ◽  
Patrick da Silva ◽  
Cibele Cardoso ◽  
Luis Fernando Macedo Di Cristofaro ◽  
Renato Petitto Netto ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Cell Lines ◽  
The Cancer Genome Atlas ◽  
Surgical Removal ◽  
Cellular Mechanisms ◽  
Cellular Processes ◽  
Dna Damage Signaling ◽  
Cancer Genome Atlas ◽  
Almost All ◽  
Upregulated Genes

Glioblastoma (GBM) is the most lethal and frequent type of brain tumor, leading patients to death in approximately 14 months after diagnosis. GBM treatment consists in surgical removal followed by radio and chemotherapy. However, tumors commonly relapse and the treatment promotes only a slight increase in patient survival. Thus, uncovering the cellular mechanisms involved in GBM resistance is of utmost interest, and the use of cell lines has been shown to be an extremely important tool. In this work, the exploration of RNAseq data from different GBM cell lines revealed different expression signatures, distinctly correlated with the behavior of GBM cell lines regarding proliferation indexes and radio-resistance. U87MG and U138MG cells, which presented expressively reduced proliferation and increased radio-resistance, showed a particular expression signature encompassing enrichment in many extracellular matrix (ECM) and receptor genes. Contrasting, U251MG and T98G cells, that presented higher proliferation and sensibility to radiation, exhibited distinct signatures revealing consistent enrichments for DNA repair processes and although several genes from the ECM-receptor pathway showed up-regulation, enrichments for this pathway were not detected. The ECM-receptor is a master regulatory pathway that is known to impact several cellular processes including: survival, proliferation, migration, invasion, and DNA damage signaling and repair, corroborating the associations we found. Furthermore, searches to The Cancer Genome Atlas (TCGA) repository revealed prognostic correlations with glioma patients for the majority of genes highlighted in the signatures and led to the identification of 31 ECM-receptor genes individually correlated with radiation responsiveness. Interestingly, we observed an association between the number of upregulated genes and survivability greater than 5 years after diagnosis, where almost all the patients that presented 21 or more upregulated genes were deceased before 5 years. Altogether our findings suggest the clinical relevance of ECM-receptor genes signature found here for radiotherapy decision and as biomarkers of glioma prognosis.

Uteroplacental blood flow at rest and during exercise in late-gestation conscious rats

1993 ◽  
Vol 74 (5) ◽  
pp. 2079-2085 ◽  
Author(s):  
R. T. Dowell ◽  
C. D. Kauer
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Treadmill Running ◽  
Female Rat ◽  
Uterine Blood Flow ◽  
Work Intensity ◽  
Flow Measurements ◽  
Placental Perfusion ◽  
Uteroplacental Blood Flow ◽  
Near Term

The present studies were conducted to achieve three specific aims. First, techniques and procedures were developed to allow tissue and organ blood flow measurements by radioactive microsphere methodology in the conscious female rat. Second, technical aspects of the methodology were evaluated with emphasis on potential uteroplacental shunting of microspheres in the late-gestational period. Third, the above techniques and procedures were utilized to assess uteroplacental blood flow at rest and during exercise in conscious pregnant rats during the late stages of gestation, i.e., days 15, 19, and 22 of pregnancy. Results established the validity of tracer blood flow technical assumptions, and no significant increase in arteriovenous shunting of 15-microns microspheres either as pregnancy progressed or during superimposed exercise in near-term pregnant animals was detected. During the stages of pregnancy studied, cardiac output was enhanced approximately 20% near term. Marked and progressive increases in uterine blood flow were noted both in milliliters per minute and as percentage of cardiac output. Preferential placental perfusion during late-stage gestation was indicated by increased tissue flow (7 +/- 1, 84 +/- 12, 232 +/- 32 ml.min-1 x 100 g-1), increased percent cardiac output (1.7 +/- 0.1, 5.1 +/- 0.7, 11.0 +/- 1.7% cardiac output), and increased percent uterine blood flow (10 +/- 1, 59 +/- 3, 87 +/- 2% uterine flow) at days 15, 19, and 22 of gestation, respectively. Progressive maternal body weight increase during gestation enhanced exercise work intensity, as shown by heart rate and cardiac output at the end of 30 min of treadmill running at 8.5 m/min, 0% incline.

Importance of Axial Stress in Arterial Growth and Remodeling

2008 ◽  
Author(s):  
J. D. Humphrey
Keyword(s):  
Blood Pressure ◽  
Extracellular Matrix ◽  
Blood Flow ◽  
Shear Stress ◽  
Arterial Wall ◽  
Axial Stress ◽  
Matrix Proteins ◽  
Growth And Remodeling ◽  
Cyclic Stretching ◽  
Wall Shear

Since the mid-1970s, we have continued to understand better the fundamental importance of mechanotransduction in vascular biology. For example, beginning with Rosen and colleagues in 1974, we discovered that endothelial cells alter their production of vasoactive molecules in response to changes in flow-induced wall shear stress; beginning with Glagov and colleagues in 1976, we discovered that vascular smooth muscle cells alter their production of extracellular matrix proteins in response to changes in cyclic stretching comparable to that induced by pulsatile pressures [1]. Indeed, such findings are not surprising given the well know arterial adaptations that occur in response to sustained changes in blood flow or pressure. The caliber of an artery tends to increase (or decrease) in response to sustained increases (decreases) in blood flow and the thickness of the arterial wall tends to increase (or decrease) in response to sustained increases (decreases) in blood pressure. In both cases, it appears that the associated wall shear or intramural circumferential stresses are returned toward normal following the change in hemodynamics.

Abstract P214: Mechanotransduction And Uterine Blood Flow In Preeclampsia- The Role Of Piezo 1 Ion Channels.

Hypertension ◽  
2020 ◽  
Vol 76 (Suppl_1) ◽  
Author(s):  
Olufunke O Arishe ◽  
Vanessa Dela Justina ◽  
Fernanda B Priviero ◽  
Clinton R Webb
Keyword(s):  
Blood Flow ◽  
Vascular Remodeling ◽  
Vascular Reactivity ◽  
Small Diameter ◽  
Subsequent Development ◽  
Normal Pregnancy ◽  
Arterial Blood Flow ◽  
Pregnant Rats ◽  
Arterial Blood

Background: There is a large increase in uterine arterial blood flow during normal pregnancy. Structural and cellular adjustments occur in the uterine vasculature during pregnancy to accommodate this increased blood flow through a process is known as ‘vascular remodeling’. The etiology of preeclampsia involves aberrant placentation and vascular remodeling leading to reduced uteroplacental perfusion. However, the underlying source of the deficient vascular remodeling and the subsequent development of preeclampsia remains to be fully understood. Piezo 1 channels have been shown to be highly expressed in vascular smooth muscle cells of small-diameter arteries and play a role in the structural remodeling of the arteries. Studies have also shown that Piezo 1 is present in uterine arteries and it’s not exclusive to the endothelial cells. Hypothesis: This study tests the hypothesis that reduced Piezo 1 activity contributes to decreased uterine vascular relaxation in hypertensive pregnant rats. Methods: Hypertension was induced by treating the pregnant rats with synthetic CpG ODN (ODN 2395) via three intraperitoneal injections (100μg/rats) while the normotensive controls were treated with saline (vehicle) on the 14 th , 17th and 18 th days of pregnancy. Mean arterial pressure (MAP) was measured. In vitro vascular reactivity of uterine arterial (UA) ring segments were evaluated using isometric wire myograph system. Rings were pre-contracted with 3μM phenylephrine (PE), concentration responses of to Yoda1; a pharmacological agonist of Piezo 1 channel were compared. Statistical analysis was performed using nonlinear regression and Students’ t-test. Results: Our results show that MAP was greater in rats treated with ODN2395 vs untreated rats (112 ± 1 vs 90 ± 1 p =0.0004). Concentration-dependent relaxation responses to Yoda1 were greater in UAs of untreated rats compared to those treated with ODN2395 (EC50 0.06571 ± 0.09781 vs. 0.5774 ± 0.1187 p =0.0018). Conclusion: These results suggest that the reduced vasodilation in pregnancy-associated hypertension may be due to a reduced Piezo 1 channel activity.

scholarly journals Estrogen Receptors and Estrogen-Induced Uterine Vasodilation in Pregnancy

2020 ◽  
Vol 21 (12) ◽  
pp. 4349 ◽  
Author(s):  
Jin Bai ◽  
Qian-Rong Qi ◽  
Yan Li ◽  
Robert Day ◽  
Josh Makhoul ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Uterine Artery ◽  
Normal Pregnancy ◽  
Uterine Blood Flow ◽  
Growth And Survival ◽  
Respiratory Gases ◽  
G Protein Coupled ◽  
In Pregnancy

Normal pregnancy is associated with dramatic increases in uterine blood flow to facilitate the bidirectional maternal–fetal exchanges of respiratory gases and to provide sole nutrient support for fetal growth and survival. The mechanism(s) underlying pregnancy-associated uterine vasodilation remain incompletely understood, but this is associated with elevated estrogens, which stimulate specific estrogen receptor (ER)-dependent vasodilator production in the uterine artery (UA). The classical ERs (ERα and ERβ) and the plasma-bound G protein-coupled ER (GPR30/GPER) are expressed in UA endothelial cells and smooth muscle cells, mediating the vasodilatory effects of estrogens through genomic and/or nongenomic pathways that are likely epigenetically modified. The activation of these three ERs by estrogens enhances the endothelial production of nitric oxide (NO), which has been shown to play a key role in uterine vasodilation during pregnancy. However, the local blockade of NO biosynthesis only partially attenuates estrogen-induced and pregnancy-associated uterine vasodilation, suggesting that mechanisms other than NO exist to mediate uterine vasodilation. In this review, we summarize the literature on the role of NO in ER-mediated mechanisms controlling estrogen-induced and pregnancy-associated uterine vasodilation and our recent work on a “new” UA vasodilator hydrogen sulfide (H2S) that has dramatically changed our view of how estrogens regulate uterine vasodilation in pregnancy.

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