Activation of PKCalpha and pulmonary vascular remodelling in broilers

Objective: The present study was conducted to examine the presence of protein kinase C* (PKC*) in the pulmonary arterioles of broilers during the development of pulmonary hypertension and pulmonary vascular remodelling. Method: One hundred and sixty day-old Avian-2000 broilers were divided equally into a control group and a cold temperature group. All the birds were reared in normal temperatures up to day 14, with the lighting schedule at 24 h per day. Thereafter, birds in the cold temperature group were subjected to low temperature by lowering 1-2 °C per day to 12-14 °C, and then kept constant until day 49, while birds in the control group were still brooded at normal temperatures. All the birds were fed a diet of pellets throughout the study. Samples of blood were taken from the wing vein, and of heart and lung collected after the birds were killed with an overdose of sodium pentobarbitial, at days 24, 32, 39 and 45 of age, respectively. Right ventricle to total ventricle ratio (RV/TV) and packed cell volume (PCV) were measured. Vessel wall area to vessel total area ratio (WA/TA) and mean media thickness in pulmonary arterioles (mMTPA) was examined using computer-image analytic software. Expression of PKC in pulmonary muscular arterioles was assessed by immunohistochemistry and quantified by measuring optical density (OD) using computer-image analytic software. Results: The incidence of pulmonary hypertension syndrome (PHS) was 12.5% in birds exposed to cold, and 3.75% in the control group (P < 0.05). PCV in the cold temperature group was elevated after day 32 (P < 0.05), and RV/TV ratio increased on day 45 (P < 0.05). Both the WA/TA and mMTPA of birds subjected to cold were significantly elevated (P < 0.05). The OD values were not significantly increased before day 32 (P > 0.05), however, one week later (at day 39 of age), the difference between the two groups was significant (P < 0.05). The increased PKC* expression was positively correlated with the values of mMTPA and WA/TA. Conclusion: PKC* expression was up-regulated during the development of pulmonary hypertension. The activation of PKC* might be involved in the development of pulmonary vascular remodelling.