Endothelial Colony-Forming Cells Dysfunctions Are Associated with Arterial Hypertension in a Rat Model of Intrauterine Growth Restriction.
Stephanie SimonciniHanna CoppolaAngela RoccaIsaline BachmannEstelle GuillotLeila ZippoFrançoise Dignat-GeorgeFlorence SabatierRomain BedelAnne WilsonNathalie Rosenblatt-VelinJean-Baptiste ArmengaudSteeve MenétreyAnne-Christine PeyterUmberto SimeoniCatherine YzydorczykPublished in: International journal of molecular sciences (2021)
Infants born after intrauterine growth restriction (IUGR) are at risk of developing arterial hypertension at adulthood. The endothelium plays a major role in the pathogenesis of hypertension. Endothelial colony-forming cells (ECFCs), critical circulating components of the endothelium, are involved in vasculo-and angiogenesis and in endothelium repair. We previously described impaired functionality of ECFCs in cord blood of low-birth-weight newborns. However, whether early ECFC alterations persist thereafter and could be associated with hypertension in individuals born after IUGR remains unknown. A rat model of IUGR was induced by a maternal low-protein diet during gestation versus a control (CTRL) diet. In six-month-old offspring, only IUGR males have increased systolic blood pressure (tail-cuff plethysmography) and microvascular rarefaction (immunofluorescence). ECFCs isolated from bone marrow of IUGR versus CTRL males displayed a decreased proportion of CD31+ versus CD146+ staining on CD45- cells, CD34 expression (flow cytometry, immunofluorescence), reduced proliferation (BrdU incorporation), and an impaired capacity to form capillary-like structures (Matrigel test), associated with an impaired angiogenic profile (immunofluorescence). These dysfunctions were associated with oxidative stress (increased superoxide anion levels (fluorescent dye), decreased superoxide dismutase protein expression, increased DNA damage (immunofluorescence), and stress-induced premature senescence (SIPS; increased beta-galactosidase activity, increased p16INK4a, and decreased sirtuin-1 protein expression). This study demonstrated an impaired functionality of ECFCs at adulthood associated with arterial hypertension in individuals born after IUGR.
Keyphrases
- arterial hypertension
- low birth weight
- blood pressure
- induced apoptosis
- dna damage
- oxidative stress
- preterm infants
- stress induced
- gestational age
- cord blood
- endothelial cells
- cell cycle arrest
- bone marrow
- human milk
- flow cytometry
- preterm birth
- nitric oxide
- signaling pathway
- poor prognosis
- nk cells
- birth weight
- depressive symptoms
- hydrogen peroxide
- pregnant women
- physical activity
- type diabetes
- metabolic syndrome
- hypertensive patients
- skeletal muscle
- dna repair
- atrial fibrillation
- vascular endothelial growth factor
- mass spectrometry
- ischemia reperfusion injury
- living cells
- heat shock protein
- pregnancy outcomes