Supplementary Materials

The PDF file includes:

  • Materials and Methods
  • Fig. S1. Normoxic hypercapnia alters gene expression in mouse lung.
  • Fig. S2. Quantification of Mef2D-positive cell in mouse ASM cells.
  • Fig. S3. High CO2 causes caspase-dependent cleavage of Mef2D protein, resulting in down-regulation of miR-133a, but does not induce apoptosis in mouse ASM cells.
  • Fig. S4. Acute hypercapnia causes ASM relaxation due to hypercapnia-associated acidosis.
  • Fig. S5. Central respiratory resistance in WT and Caspase-7–null mice.
  • Fig. S6. RhoA protein abundance and Mlc phosphorylation in mouse primary alveolar type II cells.
  • Fig. S7. Quantification of cleaved Mef2D in ASM cells from Caspase-7–null mice.
  • Fig. S8. Schematic of nonapoptotic role of Caspase-7 in ASM contractility during hypercapnia.
  • Fig. S9. Same signaling pathways activated in mouse ASM cells when exposed to similar pCO2 values to the COPD patients.
  • Legends for tables S1 and S2
  • References (42, 43)

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Other Supplementary Material for this manuscript includes the following:

  • Table S1. Processed data from mRNA and miR microarray analysis of lungs isolated from C57BL/6J mice exposed to normoxic hypercapnia or room air for 3 or 7 days (Excel file).
  • Table S2. Primary data (Excel file).