ABSTRACT
<p><b>OBJECTIVE</b>To explore the effect of hypoxia on the fibrosis of corpus cavernosum smooth muscle cells (CCSMC) in SD rats.</p><p><b>METHODS</b>CCSMCs were cultured in vitro, identified by immunohistochemistry, and then exposed to hypoxia at the concentration of 1% O2 for 12, 24, 48 and 72 hours. Those exposed to normal oxygen concentration for the corresponding lengths of time were used as the control. The relative expressions of TGF-131, type I collagen and type DI collagen were determined by RT-PCR.</p><p><b>RESULTS</b>The in vitro cultured CCSMCs grew well, and the anti-a-smooth muscle actin monoclonal antibodies were positive on immunohistochemical staining. The relative expression levels of TGF-beta1, type I collagen and type mI collagen were positively correlated with the time of hypoxia interference within 48 hours, and did not increase further with prolonged exposure.</p><p><b>CONCLUSION</b>When exposed to hypoxia, the relative expressions of TGF-beta1, type I collagen and type mI collagen in the CCSMCs of SD rats increased with the length of time, and reached the peak at 48 hours. Hypoxia can cause fibrosis of CCSMCs in SD rats.</p>
Subject(s)
Animals , Male , Rats , Cell Hypoxia , Cells, Cultured , Collagen Type I , Metabolism , Extracellular Matrix , Fibrosis , Muscle, Smooth , Cell Biology , Pathology , Oxygen , Metabolism , Penis , Metabolism , Pathology , Rats, Sprague-Dawley , Transforming Growth Factor beta1 , MetabolismABSTRACT
<p><b>OBJECTIVE</b>To explore the relationship between hypoxia and the apoptosis of corpus cavernosum smooth muscle cells (CCSMC) in SD rats.</p><p><b>METHODS</b>CCSMCs were cultured in vitro and identified by immunohistochemistry, and then underwent hypoxia interference at the concentration of 1% O2 for 12, 24, 48 and 72 hours, with normal oxygen concentration as the control. Flow cytometry was used to determine the cycles and apoptosis of the cells.</p><p><b>RESULTS</b>The cultured CCSMCs grew well, positive for anti-smooth muscle alpha-actin monoclonal antibody immunohistochemical staining. Flow cytometry showed that the number of CCSMCs in G0/G1 was gradually increased within 48 hours and then decreased, just opposite to the proportion of the S phase cells. But no regular change was found in the proportion of the cells in the G2/M phase.</p><p><b>CONCLUSION</b>Hypoxia promotes the apoptosis of CCSMCs in a time-dependent manner, to the maximum at 48 hours, and then cell lysis may occur, but with no further apoptosis.</p>