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1.
Fig. 3.

Fig. 3. From: Prolonged mechanical ventilation with air induces apoptosis and causes failure of alveolar septation and angiogenesis in lungs of newborn mice.

Immunoblots of lung tissue from 6-day-old mice showing a significant increase in active caspase-3 protein relative to β-actin protein in lung after MV with air for 24 h with air at either 60 or 180 bpm compared with unventilated controls. *Significant difference compared with Control group, P < 0.05. Values are means and SD.

Lucia M. Mokres, et al. Am J Physiol Lung Cell Mol Physiol. 2010 January;298(1):L23-L35.
2.
Fig. 4.

Fig. 4. From: Prolonged mechanical ventilation with air induces apoptosis and causes failure of alveolar septation and angiogenesis in lungs of newborn mice.

Immunoblots for VEGF-A (A) and its receptors, VEGF-R1 (B) and VEGF-R2 (C), proteins relative to β-actin protein in lung, showing that MV with air for 24 h at 60 or 180 bpm yielded no significant change in either VEGF-A or VEGF-R1 protein, whereas MV with air at either respiratory rate caused a >50% reduction in lung content of VEGF-R2 protein. *Significant difference compared with Control group, P < 0.05. Values are means and SD. n = 4–5 per group.

Lucia M. Mokres, et al. Am J Physiol Lung Cell Mol Physiol. 2010 January;298(1):L23-L35.
3.
Fig. 9.

Fig. 9. From: Prolonged mechanical ventilation with air induces apoptosis and causes failure of alveolar septation and angiogenesis in lungs of newborn mice.

Working model of how positive-pressure MV with air might impact lung growth in newborn mice. MV (prolonged cyclic stretch) of the lung during postnatal development activates TGFβ, which induces endothelial and epithelial cell apoptosis and impairs VEGF signaling (reduced expression of VEGF-R2). TGFβ also increases production and dispersion of elastin from lung myofibroblasts. These changes can result in defective alveolar and lung capillary formation, regarded as hallmarks of the pathology seen in chronic lung disease (“the new bronchopulmonary dysplasia”).

Lucia M. Mokres, et al. Am J Physiol Lung Cell Mol Physiol. 2010 January;298(1):L23-L35.
4.
Fig. 5.

Fig. 5. From: Prolonged mechanical ventilation with air induces apoptosis and causes failure of alveolar septation and angiogenesis in lungs of newborn mice.

MV with air for 24 h reduces lung abundance of VEGF-R2 protein. A: immunohistochemistry (IHC) staining of zinc-fixed lung tissue section showing reduced VEGF-R2 protein (arrows, brown stain) in distal lung after MV with air for 24 h compared with the unventilated control lung. B: summary data (means and SD) show a ∼50% decrease in VEGF-R2 stain area relative to tissue area, measured by quantitative image analysis of 20 randomly selected fields (×400) in 2 tissue slides per animal. *Significant difference compared with Control group, P < 0.05. n = 4 per group.

Lucia M. Mokres, et al. Am J Physiol Lung Cell Mol Physiol. 2010 January;298(1):L23-L35.
5.
Fig. 2.

Fig. 2. From: Prolonged mechanical ventilation with air induces apoptosis and causes failure of alveolar septation and angiogenesis in lungs of newborn mice.

MV with air induces lung cell apoptosis. A: lung sections from 6-day-old mice showing TdT-mediated dUTP nick end labeling (TUNEL)-positive cells (arrows), indicative of apoptosis. Staining was present in both endothelial and epithelial cells. ×400 magnification. B: MV for 24 h with air caused a ∼5-fold increase in lung cell apoptosis compared with unventilated controls, as assessed by percentage of cells that were TUNEL-positive in 10 random fields of view. C: there was no significant change in lung cell proliferation as assessed by percentage of cells that stained positive for PCNA (lung sections not shown). *Significant difference compared with Control group, P < 0.05. Values are means and SD. n = 5–8 per group.

Lucia M. Mokres, et al. Am J Physiol Lung Cell Mol Physiol. 2010 January;298(1):L23-L35.
6.
Fig. 7.

Fig. 7. From: Prolonged mechanical ventilation with air induces apoptosis and causes failure of alveolar septation and angiogenesis in lungs of newborn mice.

MV with air for 24 h increases transforming growth factor-β (TGFβ) activation in lung. A: IHC staining of paraformaldehyde (PFA)-fixed lung sections showing increased nuclear staining for phosphorylated Smad2 (pSmad2; arrows, brown stain), a marker of TGFβ activation, after MV with air for 24 h (bottom) compared with unventilated controls (top). Quantitative image analysis was performed on 10 random fields (×400) in 2 randomly selected tissue slides per animal. B: summary data (means and SD) showing a >4-fold increase in pSmad2 protein expression after MV with air for 24 h compared with controls. *Significant difference compared with Control group, P < 0.05. n = 4 per group.

Lucia M. Mokres, et al. Am J Physiol Lung Cell Mol Physiol. 2010 January;298(1):L23-L35.
7.
Fig. 6.

Fig. 6. From: Prolonged mechanical ventilation with air induces apoptosis and causes failure of alveolar septation and angiogenesis in lungs of newborn mice.

MV with air for 24 h reduces lung endothelial cell number. A: IHC staining of zinc-fixed lung sections showing reduced CD31 protein (arrows, brown stain) in distal lung after MV with air for 24 h. B: summary data (means and SD) show a ∼50% decrease in CD31 stain area relative to tissue area, measured by quantitative analysis of 20 random fields (×400) in 2 randomly selected tissue slides per animal. n = 4 per group. C: immunoblots for CD31 protein relative to β-actin in lung, showing that MV for 24 h caused a ∼20% reduction of CD31 protein compared with unventilated controls. *Significant difference compared with Control group, P < 0.05.

Lucia M. Mokres, et al. Am J Physiol Lung Cell Mol Physiol. 2010 January;298(1):L23-L35.
8.
Fig. 1.

Fig. 1. From: Prolonged mechanical ventilation with air induces apoptosis and causes failure of alveolar septation and angiogenesis in lungs of newborn mice.

Mechanical ventilation (MV) with air inhibits alveolar septation. A: lung sections from 6-day-old mice showing increased alveolar size and reduced septation after MV with air for 24 h at either 60 or 180 breaths/min (bpm) compared with the unventilated control lung. Hematoxylin and eosin stain, ×200 magnification. Lung volumes (means ± SD) were not significantly different between the groups. B: summary data for alveolar size and number, assessed by quantitative image analysis of 12 random fields (×200) in 3–4 lung sections per animal. Alveolar area was ∼3-fold greater, and radial alveolar count was 40–50% less after MV at either 60 or 180 bpm compared with unventilated controls. *Significant difference compared with Control group, P < 0.05. Values are means and SD. n = 4–5 per group.

Lucia M. Mokres, et al. Am J Physiol Lung Cell Mol Physiol. 2010 January;298(1):L23-L35.
9.
Fig. 8.

Fig. 8. From: Prolonged mechanical ventilation with air induces apoptosis and causes failure of alveolar septation and angiogenesis in lungs of newborn mice.

MV with air for 24 h increases and redistributes lung elastin. A: immunoblots for tropoelastin protein relative to β-actin in lung showing a ∼2-fold increase after MV for 24 h at 60 or 180 bpm compared with the unventilated Control group. B: Hart's stained lung sections showing increased elastin (arrows) after MV for 24 h at 60 or 180 bpm and a shift in the distribution of elastic fibers from septal tips (Control lung) to alveolar walls (MV lungs). Wide arrows denote elastin in vessel wall, and narrow arrows point to elastin at septal tips (Control lung) or lining distal air spaces (MV lungs). ×400 magnification. C: quantitative image analysis of Hart's stained lung sections showing a ∼50% increase of cross-linked elastic fibers expressed as a percentage of lung tissue area after MV for 24 h compared with unventilated control lungs. D: elastin surface area relative to epithelial surface area shows a ∼25% increase after MV for 24 h at 60 or 180 bpm compared with unventilated control lungs. *Significant difference compared with Control group, P < 0.05. n = 4–6 per group. Values are means and SD.

Lucia M. Mokres, et al. Am J Physiol Lung Cell Mol Physiol. 2010 January;298(1):L23-L35.

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