OBJECTIVE：To study the effcet of Nitric oxide (No) on transcriptional expression of c-fos and c-jun oncogene of cultured rabbit arterial smooth muscle cells (ASMC),and its mechanism.METHODS:(1)To culture rabbit ASMC from explants;(2) To determine if NO,FeSO4,and methylene blue have toxic effect on ASMC by cell counting;(3)RNA isolation from ASMC by Guanidinium Thiocyanate-phenol-chloroform method;(4)RNA-DNA blot hybridization.RESULTS:Under the condition of no toxic effects,NO inhibited the expression of c-fos and c-jun oncogene of ASMC apparently,FeSO4 and methylene blue antagonized the inhibition effcet.CONCLUSION:NO inhibited the expression of c-fos and c-jun oncogene of ASMC through cGMP.This may be related to the important mechanism that NO inhibits the proliferation of ASMC.

Uncovering the risk factors of pulmonary hypertension and its mechanisms is crucial for the prevention and treatment of the disease.In the current study,we showed that experimental periodontitis,which was established by ligation of molars followed by orally smearing subgingival plaques from patients with periodontitis,exacerbated hypoxia-induced pulmonary hypertension in mice.Mechanistically,periodontitis dysregulated the pulmonary microbiota by promoting ectopic colonization and enrichment of oral bacteria in the lungs,contributing to pulmonary infiltration of interferon gamma positive(IFNγ+)T cells and aggravating the progression of pulmonary hypertension.In addition,we identified Prevotella zoogleoformans as the critical periodontitis-associated bacterium driving the exacerbation of pulmonary hypertension by periodontitis,and the exacerbation was potently ameliorated by both cervical lymph node excision and IFNγ neutralizing antibodies.Our study suggests a proof of concept that the combined prevention and treatment of periodontitis and pulmonary hypertension are necessary.