Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 2 de 2
Filter
Add more filters










Database
Language
Publication year range
1.
BMC Nephrol ; 13: 161, 2012 Dec 02.
Article in English | MEDLINE | ID: mdl-23199021

ABSTRACT

BACKGROUND: Complement activation products are present in atherosclerotic plaques. Recently, binding of complement to elastin and collagen in the aortic wall has been demonstrated, suggesting a role of complement in the development aortic stiffness and atherosclerosis. The definitive role of complement in atherosclerosis and arteriosclerosis, however, remains unclear. CASE PRESENTATION: We here describe a patient with hereditary complete deficiency of complement C4 suffering from Henoch-Schoenlein purpura and on renal replacement therapy for twenty-eight years. The patient had the full range of risk factors for vascular damage such as hypertension, volume overload, hyperphosphatemia and hyperparathyroidism. Despite that, his carotid artery intima media thickness was below the normal range and his pulse wave velocity was normal. In contrast, the patient's coronary and peripheral muscular arteries were heavily calcified. CONCLUSION: This case supports the hypothesis that complement plays an important role in the development of stiffness of elastic arteries. We speculate that inability to activate complement by the classical or lectin pathways protected the patient from atherosclerosis, arteriosclerosis, stiffening and calcification of the aorta and carotid arteries. Inhibition of complement activation may be a potential target for prophylactic and therapeutic interventions.


Subject(s)
Atherosclerosis/diagnosis , Atherosclerosis/physiopathology , Complement C4/deficiency , Renal Replacement Therapy/adverse effects , Vascular Stiffness/genetics , Atherosclerosis/genetics , Complement C4/genetics , Complement Pathway, Classical/genetics , Complement Pathway, Mannose-Binding Lectin/genetics , Elasticity/physiology , Humans , Male , Middle Aged , Renal Replacement Therapy/trends , Time Factors
2.
J Cereb Blood Flow Metab ; 22(8): 951-8, 2002 Aug.
Article in English | MEDLINE | ID: mdl-12172380

ABSTRACT

Apoptosis plays an essential role in the cascade of CNS cell degeneration after traumatic brain injury. However, the underlying mechanisms are poorly understood. The authors examined the temporal profile and cell subtype distribution of the proapoptotic protein Bid from 6 hours to 7 days after cortical impact injury in the rat. Increased protein levels of tBid were seen in the cortex ipsilateral to the injury site from 6 hours to 3 days after trauma. Immunohistologic examinations revealed expression of tBid in neurons, astrocytes, and oligodendrocytes from 6 hours to 3 days after impact injury, and concurrent assessment of DNA damage using TUNEL identified tBid-immunopositive cells with apoptoticlike morphology in the traumatized cortex. Moreover, Bid cleavage and activation of caspase-8 and caspase-9 occurred at similar time points and in similar brain regions (i.e., cortical layers 2 to 5) after impact injury. In contrast, there was no evidence of caspase-8 or caspase-9 processing or Bid cleavage in the ipsilateral hippocampus, contralateral cortex, and hippocampus up to 7 days after the injury. The results provide the first evidence of Bid cleavage in the traumatized cortex after experimental traumatic brain injury in vivo, and demonstrate that tBid is expressed in neurons and glial cells. Further, findings indicate that cleavage of Bid may be associated with the activation of the initiator caspase-8 and caspase-9. Finally, these data support the hypothesis that cleavage of Bid contributes to the apoptotic degeneration of different CNS cells in the injured cortex.


Subject(s)
Apoptosis , Brain Injuries/metabolism , Carrier Proteins/metabolism , Cerebral Cortex/metabolism , Hippocampus/metabolism , Neuroglia/metabolism , Neurons/metabolism , Animals , BH3 Interacting Domain Death Agonist Protein , Blotting, Western , Brain Injuries/pathology , Caspase 8 , Caspase 9 , Caspases/metabolism , Cerebral Cortex/pathology , Hippocampus/pathology , Immunohistochemistry , In Situ Nick-End Labeling , Male , Neuroglia/pathology , Neurons/pathology , Rats , Rats, Sprague-Dawley , Time Factors
SELECTION OF CITATIONS
SEARCH DETAIL
...