ABSTRACT
A 35-years-old pregnant woman with Marfan's syndrome visited the emergent department. She had sudden severe back pain. She was at the 20th week of gestation. An emergent chest computed tomo-graphy scan showed Stanford type B acute aortic dissection. After admission, strict blood pressure control was started. According to aortic valve insufficiency and fluid retention with pregnancy, acute heart and respiratory failure was getting worse. It seemed risky for both mother and the fetus to continue pregnancy. After sincere and detailed discussion between the patient and our multidisciplinary medical team, the patient decided to continue pregnancy. An urgent Bentall operation was performed. A careful attention was paid for the fetus during and after the surgery. Strict blood pressure control was also continued. The mother and the 30-week-gestation newborn recovered uneventfully. During four years of follow-up, thoracic and thoraco-abdominal aortic replacement was performed. The patient survived all of these procedures without any complication.
Subject(s)
Aortic Aneurysm, Thoracic , Aortic Dissection , Marfan Syndrome , Adult , Aortic Dissection/diagnostic imaging , Aortic Dissection/etiology , Aortic Dissection/surgery , Aorta/surgery , Aortic Aneurysm, Thoracic/diagnostic imaging , Aortic Aneurysm, Thoracic/etiology , Aortic Aneurysm, Thoracic/surgery , Female , Humans , Infant, Newborn , Marfan Syndrome/complications , Marfan Syndrome/surgery , Pregnancy , Pregnant WomenABSTRACT
The present study investigated the function of caspase-4 in endoplasmic reticulum (ER) stress-induced apoptosis in human neuronal cell line SH-SY5Y. Tunicamycin, which is known to induce ER stress, activated both caspase-9 and caspase-4, and the activation of caspase-4 preceded that of caspase-9. The caspase-4 inhibitor LEVD-CHO suppressed both the apoptosis and caspase-9 activation. In addition, human recombinant active caspase-4 cleaved wild type and D330A mutant substituted Asp-330 for alanine of human recombinant procaspase-9, but did not cleave D315A mutant substituted Asp-315 for alanine. These results suggest that caspase-4 directly activates caspase-9 by the processing of procaspase-9 at Asp-315 in ER stress-induced neuronal apoptosis.
Subject(s)
Caspase 9/metabolism , Caspases, Initiator/metabolism , Endoplasmic Reticulum/physiology , Neurons/physiology , Stress, Physiological , Tunicamycin/pharmacology , Apoptosis/drug effects , Caspase Inhibitors , Cell Line , Endoplasmic Reticulum/drug effects , Enzyme Activation , Humans , Neurons/cytology , Neurons/enzymology , Recombinant Proteins/metabolismABSTRACT
The present study investigated the function of caspase-4 in endoplasmic reticulum (ER) stress-induced apoptosis in human neuronal cell line SH-SY5Y. Tunicamycin, which is known to induce ER stress, activated both caspase-9 and caspase-4, and the activation of caspase-4 preceded that of caspase-9. The caspase-4 inhibitor LEVD-CHO suppressed both the apoptosis and caspase-9 activation. In addition, human recombinant active caspase-4 cleaved wild type and D330A mutant substituted Asp-330 for alanine of human recombinant procaspase-9, but did not cleave D315A mutant substituted Asp-315 for alanine. These results suggest that caspase-4 directly activates caspase-9 by the processing of procaspase-9 at Asp-315 in ER stress-induced neuronal apoptosis.
