Efficient postendocytic membrane traffic in polarized epithelial cells is thought to be regulated in part by the actin cytoskeleton. RhoA modulates assemblies of actin in the cell, and it has been shown to regulate pinocytosis and phagocytosis; however, its effects on postendocytic traffic are largely unexplored. To this end, we expressed wild-type RhoA (RhoAWT), dominant active RhoA (RhoAV14), and dominant inactive RhoA (RhoAN19) in Madin-Darby canine kidney (MDCK) cells expressing the polymeric immunoglobulin receptor. RhoAV14 expression stimulated the rate of apical and basolateral endocytosis, whereas RhoAN19 expression decreased the rate from both membrane domains. Polarized basolateral recycling of transferrin was disrupted in RhoAV14-expressing cells as a result of increased ligand release at the apical pole of the cell. Degradation of basolaterally internalized epidermal growth factor was slowed in RhoAV14-expressing cells. Although apical recycling of immunoglobulin A (IgA) was largely unaffected in cells expressing RhoAV14, transcytosis of basolaterally internalized IgA was severely impaired. Morphological and biochemical analyses demonstrated that a large proportion of IgA internalized from the basolateral pole of RhoAV14-expressing cells remained within basolateral early endosomes and was slow to exit these compartments. RhoAN19 and RhoAWT expression had little effect on these postendocytic pathways. These results indicate that in polarized MDCK cells activated RhoA may modulate endocytosis from both membrane domains and postendocytic traffic at the basolateral pole of the cell.
A 34-year-old African-American male without medical history presented to the Emergency Department (ED) with a 2-month history of a lesion on his nose. The patient stated it began gradually and had increased in size, despite treatment with over-the-counter steroid cream. He denied any history of trauma or other skin lesions. The patient did report a history of intermittent chest pain with deep inspiration and a mild nonproductive cough with occasional dyspnea. He denied tobacco use, took no medications, and had no known drug allergies.Vital signs were within normal limits. Physical examination was remarkable only for a firm, 2 ϫ 3 cm multinodular lesion on the left alar rim and nasal bridge, with overlying shiny violacious skin (Figures 1, 2). There was no ulceration, drainage, or tenderness. In addition, there were multiple non-tender, enlarged cervical lymph nodes bilaterally, the largest measuring 2 ϫ 4 cm. The remainder of the head and neck examination was normal. The lungs were clear to auscultation and the heart was regular in rate and rhythm, without murmurs, rub, or gallop.In view of the patient's history of cough, intermittent dyspnea, chest pain, and the suspicious skin lesion, a chest X-ray was ordered. The chest X-ray suggested hilar adenopathy, which was then confirmed by chest computed tomography (CT) scan. Blood and urine tests were unremarkable. The patient was admitted with a presumptive diagnosis of sarcoidosis, and fine needle aspiration of the cervical lymph nodes revealed histology consistent with non-caseating granulomas. The patient's skin lesion was also biopsied, demonstrating the same histologic findings. The lesion was diagnosed as lupus pernio secondary to sarcoidosis.
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