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Biology subjects

Adnot, S.

Publications and source records attributed to Adnot, S..

3 recordsLinked to original sources

Induction of telomerase in p21-positive cells counteracts capillaries rarefaction in aging mice lung

Telomerase is required for long-term cell proliferation and linked to stem cells. This is evident in the lung where short telomeres are associated with lung dysfunction. We constructed a mouse model in which the telomerase (Tert) is expressed from the p21Cdkn1a promoter. We found that this peculiar Tert expression curb age-related emphysema and pulmonary perivascular fibrosis in old mice. In old mice lungs, such Tert expression preferentially occurs in endothelial cells where it reduces the number of senescent endothelial cells. Remarkably, we report that Tert counteracts the age-related decline in capillary density. This was associated with an increased number of Cd34+ cells identified as a subclass of capillary cells with proliferative capacity. Expression of catalytically inactive Tert neither prevents the decline of capillary density in old mice nor protects against age-related emphysema and fibrosis. These findings reveal that telomerase decreases age-decline of pulmonary functions by sustaining microvasculature regeneration and outgrowth.

molecular biology↗

Evaluation of lung VEGF-A transduction during hyperoxia-induced injury in rats

BackgroundSince Vascular Endothelial Growth Factor (VEGF) is a main factor for endothelial survival, we evaluated whether VEGF transduction could ameliorate hyperoxia induced injury, which is associated with predominant endothelial injury.\n\nMethods and ResultsTransduction (induced 48 hours before hyperoxic exposure) using adenoviral vector (Ad.) for VEGF (1010 viral particles [VP]) increased moderately survival under hyperoxia (fraction of inspired oxygen [FIO2] >95%) as compared with Ad.Null (1010 VP) transduction, whereas VEGF transduction with a lower dose (5.109 VP) had no effect. After 48 hours of hyperoxia, Ad.VEGF transduction increased lung VEGF concentration, prevented the diffuse loss of capillary bed and induced patchy areas of endothelial cell proliferation (CD31 immunostaining) with interstitial inflammatory cell recruitment as compared to Ad. Null transduction. Hyperoxia was associated with diffuse apoptosis that was inhibited only in patchy areas of endothelial proliferation under VEGF transduction. Hyperoxia-induced alveolar inflammation was similar with Ad.Null and Ad.VEGF. Under normoxia, the high dose of VEGF transduction induced diffuse alveolar inflammation whereas the low dose did not suggesting a pro-inflammatory effect of VEGF that may have participated to increased survival under hyperoxia.\n\nConclusionsWe demonstrate that lung VEGF-A transduction despite inhibition of the loss of capillary bed has a marginal effect of on animal survival during hyperoxia-induced injury.

pathology↗

Single-Dose Monocrotaline Pyrrole Injection as a Model of Pulmonary Endothelial Injury In Mice

Monocrotaline (MCT) is a plant substance that induces severe pulmonary hypertension in several animals except for mice. The aim of our study was to state whether monocrotaline pyrrole (MCTp), the main monocrotaline metabolite, could induce significant injury in mouse lung when given intravenously. MCTp caused moderate pulmonary inflammation, remodelling of small distal vessels (percentage of muscularized arteries: 33,5 vs 20,6%, p[≤]0,0006) and a right ventricular dysfunction (RVSP 27,8mmHg vs 16,4mmHg, p[≤]0,0001; Fulton index 0,35 vs 0,26, p[≤]0,0007). These vascular effects were associated with a decrease in eNOS protein expression in lung tissues and resolved after 45 days. In conclusion, we developed a model of endothelial dysfunction and transient pulmonary hypertension in mice.

physiology↗