Abstract

The effects of mild endurance exercise training on the small airways in mdxmice are unknown. We compared epithelial thickness and turnover, apoptosis,and stress marker expression in small airways of mdx mice and wild-type (WT)controls, at rest and during exercise training. Mdx and WT mice wererandomly assigned to sedentary (mdx-S, n=17; WT-S, n=19) or trained (mdx-EX, n=14; WT-EX, n=16) groups. Low-intensity endurance training (runningon a wheel) was done 5 d/wk for 6 wk at progressively increasing speed (rpmfrom 16 to 24) and time (15 min to 1 h). Lungs were processed for lightmicroscopy and periodic acid Schiff (PAS) staining. Hsp60 and PCNA werequantified by immunohistochemistry. Apoptosis was assessed by TUNEL.Bronchial epithelial thickness decreased over time in WT mice irrespective oftraining (linear regression for time trends: WT-S: R2=0.43, r= -0.65; WT-EX:R2=0.68, r= -0.82, p<0.0005 for both); conversely, no significant changeoccurred in mdx mice. The number of PAS+ goblet cells was much lower inthe bronchiolar epithelium of mdx compared to WT mice in all conditions. At30 days, PCNA positivity was higher in EX than S animals in both groups;however, at 45 days it sharply decreased in mdx-S and -EX, but not in WTmice. The percentage of TUNEL+ cells was higher in mdx-EX than WT-EXmice at 45 days. In mdx mice, expression of Hsp60 progressively decreased(p<0.01), and was inversely related to the percentage of TUNEL+ cells(R2=0.44, r=-0.66, p=0.01). In conclusion, bronchiolar epithelium in mdx miceis poor of goblet cells, and progressively deteriorates over time possiblybecause of loss of stress-related protective mechanism. Mild training did notcause any additional damage.
Lingua originaleEnglish
Numero di pagine1
Stato di pubblicazionePublished - 2015

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