RESUMO
Traumatic lower urinary tract injuries are uncommon and mainly occur in patients with severe trauma and multiple abdominopelvic injuries. In the presence of other substantial injuries, bladder and urethral injuries may be overlooked and cause significant morbidity and mortality. Therefore, it is important that radiologists are familiar with mechanisms and injuries that are high risk for bladder and urethral trauma. We review the imaging findings associated with these injuries and the appropriate modalities and techniques to further evaluate the patient and accurately diagnose these injuries. Computed tomography cystography and conventional retrograde urethrography are effective tools in identifying injuries to the lower urinary tract and play a crucial role in patient care and prognosis.
Assuntos
Uretra/lesões , Bexiga Urinária/lesões , Ferimentos e Lesões/diagnóstico por imagem , Cistografia , Humanos , Tomografia Computadorizada por Raios X , Uretra/diagnóstico por imagem , Bexiga Urinária/diagnóstico por imagem , Ferimentos e Lesões/etiologia , Ferimentos e Lesões/terapiaRESUMO
Activation of Rac1 GTPase signaling is stimulated by phosphorylation and release of RhoGDI by the effector p21-activated kinase 1 (PAK1), but it is unclear what initiates this potential feed-forward mechanism for regulation of Rac activity. Phosphatidic acid (PA), which is produced from the lipid second messenger diacylglycerol (DAG) by the action of DAG kinases (DGKs), is known to activate PAK1. Here, we investigated whether PA produced by DGKzeta initiates RhoGDI release and Rac1 activation. In DGKzeta-deficient fibroblasts PAK1 phosphorylation and Rac1-RhoGDI dissociation were attenuated, leading to reduced Rac1 activation after platelet-derived growth factor stimulation. The cells were defective in Rac1-regulated behaviors, including lamellipodia formation, membrane ruffling, migration, and spreading. Wild-type DGKzeta, but not a kinase-dead mutant, or addition of exogenous PA rescued Rac activation. DGKzeta stably associated with PAK1 and RhoGDI, suggesting these proteins form a complex that functions as a Rac1-selective RhoGDI dissociation factor. These results define a pathway that links diacylglycerol, DGKzeta, and PA to the activation of Rac1: the PA generated by DGKzeta activates PAK1, which dissociates RhoGDI from Rac1 leading to changes in actin dynamics that facilitate the changes necessary for cell motility.