Effect of intermittent hypoxia on RhoA/ROCK pathway in lung and on the muscularization in pulmonary vascular in rat model
10.11958/j.issn.0253-9896.2015.02.001
- VernacularTitle:间歇低氧对大鼠肺组织RhoA/ROCK通路及肺血管新生肌化的影响
- Author:
Xiaokun YANG
;
Mengli GAO
;
Yameng LIU
;
Caili LI
;
Jie CAO
;
Jing FENG
- Publication Type:Journal Article
- Keywords:
anoxia;
hypertension,pulmonary;
proliferating cell nuclear antigen;
actins;
intermittent hypoxia;
pulmonary hypertension;
RhoA/ROCK
- From:
Tianjin Medical Journal
2015;(2):113-116
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the effect of intermittent hypoxia (IH) on RhoA/ROCK pathway in lung and on the muscularization in pulmonary vascular in rat model. Methods Wistar rats (n=40) were randomly divided into two groups:the normal oxygen control group (n=20) and the IH group ( n=20). For 4 weeks, rats in control group and IH group were ex?posed to intermittent normal oxygen (21%O2) or IH (5%-21%O2) respectively. Then, mRNA transcription and protein trans?lation levels of RhoA/ROCK were examined by Real-time PCR and Western blot. Expression of proliferation cell nuclear an?tigen (PCNA) andα-smooth muscle actin (SM-α-actin ) of lung and pulmonary artery were detected by immunohistochemis?try. Results RhoA mRNA transcription level(0.463 ± 0.067 vs 0.182 ± 0.040), ROCK mRNA transcription level(0.384 ± 0.062 vs 0.192 ± 0.052), RhoA protein expression level(0.827 ± 0.065 vs 0.424 ± 0.075)and ROCK protein expression level (0.488±0.088 vs 0.336±0.102)were higher in IH group than those in control group(P<0.05);Levels of PCNA in lung tissue [(54.67±1.80)%vs (9.14±0.91)%], PCNA in pulmonary artery [(49.40±1.21)%vs (8.38±1.13)%], SM-α-actin in lung tis?sue [(42.66±1.63)%vs (35.44±1.41)%] and SM-α-actin in pulmonary artery [(62.62±2.53)%vs (45.54±2.58)%] were also higher in IH group than those in control group(P<0.05). Conclusion Rho/ROCK pathway may play an important role in developing pulmonary hypertension (PH) associated with IH;and IH can promote the muscularization in pulmonary vascular to accelerate PH.
