RESUMO
Objective:To construct the rat models of orthotopic bladder cancer induced by N-methyl-nitrosourea (MNU),and to evaluate the value of magnetic resonance imaging (MRI)in the noninvasive diagnosis of the bladder cancer model.Methods:Sixty femail SD rats were divided into experiment group (n=45)and control group (n=15).The rats experiment group were induced with MNU (2 mg per rat)by intravesical administration every other week,for 4 times.Meantime,the rats in control group were treated with normal saline (0.2 mL per rat)by intravesical administration.At the end of the 14th week,all rats were examined by MRI and the pathological changes of bladder tissue were detected.Results:In experiment group,43 rats were alived and 2 rats were died at the end of the 14th week;the survial rate was 95.6% and the death rate was 4.4%;the abnormal signals were found in each of 43 rats by MRI which manifested as bladder tumor, and the same results were identified by pathology;the tumor formation rate was 100%.In control group,14 rats were alived and 1 rat was died at the end of the 14th week;the survival rate was 93.3%,and the death rate was 6.7%;there was no abnormal signal in the MRI examination and no bladder cancer in the pathological examination;the tumor formation rate was 0.The tumor formation rates of bladder cancer of the rats in two groups had significant difference (P 0.05).Conclusion:The method to establish the rat models of orthotopic bladder cancer induced by MNU is simple and reliable;the results of MRI are consistent with the pathological results and MRI examination is a reliable diagnostic method concerning this model.
RESUMO
Integrin αIIbß3 is critical for platelet-mediated blood clotting. Tetraspanins are well-established regulators of integrins and genetic loss of tetraspanin CD151 or TSSC6 in mice leads to increased bleeding due to inadequate integrin αIIbß3 outside-in signaling. Conversely, mild but enhanced integrin αIIbß3 activation and hyperaggregation is observed in CD9 and CD63 null mice respectively. CD82 is reportedly expressed in platelets; however its function is unknown. Using genetically engineered CD82 null mice, we investigated the role of the tetraspanin CD82 in platelet activation. Loss of CD82 resulted in reduced bleed times in vivo. CD82 was present on the surface of both human and mouse platelets, and its levels did not change upon platelet activation or degranulation. No differences in platelet activation, degranulation, or aggregation in response to ADP or collagen were detected in CD82 null mice. However, the kinetics of clot retraction was enhanced, which was intrinsic to the CD82-null platelets. Integrin αIIbß3 surface expression was elevated on the platelets from CD82 null mice and they displayed enhanced adhesion and tyrosine kinase signaling on fibrinogen. This is the first report on CD82 function in platelets; which we found intrinsically modulates clot retraction, integrin αIIbß3 expression, cell adhesion, and tyrosine signaling.
