The bronchopulmonary dysplasia (BPD) is a respiratory disease of the premature child which lead to a reduction of gas exchange surface and to a prolonged respiratory failure. This disease has morphologic and functional consequences at adulthood and is today considered to be an early determinant of respiratory diseases at adulthood. The physiopathology of BPD is not well known. Several mechanisms could be involved especially a reparation failure favored by an increase of cellular senescence which is a permanent stop of cellular proliferation. The transcription factor 16 Ink4a, considered as a marker of aging, is one of the essential markers of senescence. Its increase during prematurity was shown at the blood cells of the cordon, but its involvement in BPD and its evolution in child are not yet studied.
Study Type
INTERVENTIONAL
Allocation
NON_RANDOMIZED
Purpose
BASIC_SCIENCE
Masking
NONE
Enrollment
80
For the arms "Term newborns (≥37GA)" and "Premature newborns" the only intervention is a blood punction on the cordon. For the arms "Child between 7 and 15 years old" with or without BPD the only intervention is a blood punction on peripheral blood.
Centre Hospitalier Intercommunal de Créteil
Créteil, France
p16 expression
p16 expression measured by qPCR in newborns cord blood cells and in circulating leukocytes of children aged from 7 to 15
Time frame: Day 1
Telomeres length
Telomeres length of circulating leukocytes
Time frame: Day 1
Genetic expression of p21, p53, H2Ax
Genetic expression of p21, p53, H2Ax of circulating leukocytes
Time frame: Day 1
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