Loss of smooth muscle myosin heavy chain results in the bladder and stomach developing lesion during foetal development in mice.

Smooth muscle myosin heavy chain (SM-MHC) is exclusively expresses in smooth muscle, which takes part in smooth muscle cell contraction. Here, we used an insertional mutation mouse whose heavy polypeptide 11 ( Myh11 ) gene has been disrupted and no SM-MHC protein has been detected. Compared to the wild-type and SM-MHC ^+/- mice, the SM-MHC ^-/- neonates had large round bellies, thin-walled giant bladders, and large stomachs with huge gas bubbles. Most of it died within 10 h and the rest within 20 h after birth. Further analysis of the developing foetuses from 16.5 days postcoitum (dpc) stage to newborn showed no significant ( P <0.05) difference in the ratio of Mendelian inheritance and average body weight among SM-MHC ^+/+ , SM-MHC ^+/- and SM-MHC ^-/- mice, whereas the abnormal exterior appearance was observed in each SM-MHC ^-/- bladders from 16.5 dpc. Histological analysis showed no difference in stomach tissues but evidently thin-walled smooth muscle layer and a giant cavity in bladders of SM-MHC ^-/- foetuses at various stages from 15.5 dpc to newborn. The results indicated that the defect of SM-MHC lead to the bladder developing lesions initially at 15.5 dpc stage in mouse and also implied that the SM-MHC loss might result in the gas bubbles in stomach. The study should facilitate further detailed analyses of the potential role of SM-MHC in bladder and stomach development.