Dexamethasone preventing contractile and cytoskeletal protein changes in the rabbit basilar artery after subarachnoid hemorrhage
| Autor: | Christine Sercombe, Philippe Gomis, Yves Roger Tran-Dinh, Richard Sercombe |
|---|---|
| Rok vydání: | 2005 |
| Předmět: |
Pathology
medicine.medical_specialty Subarachnoid hemorrhage Anti-Inflammatory Agents Muscle Proteins Inflammation Vimentin Collagen Type I Dexamethasone medicine.artery medicine Extracellular Basilar artery Animals Microscopy Confocal biology business.industry Gene Expression Profiling Anatomy Subarachnoid Hemorrhage medicine.disease Immunohistochemistry Disease Models Animal Basilar Artery Systemic administration biology.protein Rabbits medicine.symptom business Type I collagen medicine.drug |
| Zdroj: | Journal of Neurosurgery. 102:715-720 |
| ISSN: | 0022-3085 |
| DOI: | 10.3171/jns.2005.102.4.0715 |
| Popis: | Object. The aim of this project was to study the perturbations of four smooth-muscle proteins and an extracellular protein, type I collagen, after subarachnoid hemorrhage (SAH) and to examine the possible preventive effects of dexamethasone. Methods. Using a one-hemorrhage rabbit model, the authors first examined the effects of SAH on the expression of α-actin, h-caldesmon, vimentin, smoothelin-B, and type I collagen; second, they studied whether post-SAH systemic administration of dexamethasone (three daily injections) corrected the induced alterations. Measurements were obtained at Day 7 post-SAH. The proteins were studied by performing immunohistochemical staining and using a laserscanning confocal microscope. Compared with control (sham-injured) arteries, the density of the media of arteries subjected to SAH was reduced for α-actin (−11%, p = 0.01) and h-caldesmon (−15%, p = 0.06) but increased for vimentin (+15%, p = 0.04) and smoothelin-B (+53%, p = 0.04). Among animals in which SAH was induced, arteries in those treated with dexamethasone demonstrated higher values of density for α-actin (+13%, p = 0.05) and h-caldesmon (+20%, p = 0.01), lower values for vimentin (−55%, p = 0.05), and nonsignificantly different values for smoothelin-B. The density of type I collagen in the adventitia decreased significantly after SAH (−45%, p = 0.01), but dexamethasone treatment had no effect on this decrease. Conclusions. The SAH-induced alterations in the density of three of four smooth-muscle proteins were prevented by dexamethasone treatment; two of these proteins—α-actin and h-caldesmon—are directly related to contraction. This drug may potentially be useful to prevent certain morphological and functional changes in cerebral arteries after SAH. |
| Databáze: | OpenAIRE |
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