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. Author manuscript; available in PMC: 2014 May 15.
Published in final edited form as: Birth Defects Res A Clin Mol Teratol. 2013 May 30;97(6):373–385. doi: 10.1002/bdra.23149

Figure 4.

Figure 4

Systemic loss of Periostin does not affect the presence of saccular lung myofibroblasts or ultimate alveolar development. Representative H/E stained lung sections from Periostin null (A–C) and age-matched littermate control (D–F) pups raised in room-air through P4, P7, and P28. G,H: Quantification of alveolar development by MLI (G) and nodal density (H). Immunostaining for αSMA in P4 Periostin null (I) and control (J) lungs. Note similar expression pattern within septal tips and around blood vessels (v). K: Whole lung αSMA levels at P4 were quantified by means of densitometry of immunoblots relative to α-Tubulin loading control. N = 3 to 7 mice per group; Scale bars = 50 μ; no significant differences when analyzed by Student's t test (p > 0.05 vs. control at equivalent postnatal ages).