دورية أكاديمية

Factors influencing cell fate in the infarct rim.

التفاصيل البيبلوغرافية
العنوان: Factors influencing cell fate in the infarct rim.
المؤلفون: Yao H; Department of Pediatrics, University of California, San Diego, La Jolla, California 92093-0735, USA., Shu Y, Wang J, Brinkman BC, Haddad GG
المصدر: Journal of neurochemistry [J Neurochem] 2007 Mar; Vol. 100 (5), pp. 1224-33. Date of Electronic Publication: 2007 Jan 08.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural
اللغة: English
بيانات الدورية: Publisher: Wiley on behalf of the International Society for Neurochemistry Country of Publication: England NLM ID: 2985190R Publication Model: Print-Electronic Cited Medium: Print ISSN: 0022-3042 (Print) Linking ISSN: 00223042 NLM ISO Abbreviation: J Neurochem Subsets: MEDLINE
أسماء مطبوعة: Publication: 2001- : Oxford, UK : Wiley on behalf of the International Society for Neurochemistry
Original Publication: New York : Raven Press
مواضيع طبية MeSH: Brain Infarction/*pathology, Animals ; Brain Infarction/metabolism ; Cations, Monovalent ; Cell Death ; Cell Hypoxia ; Culture Media ; Extracellular Fluid/metabolism ; Glucose/deficiency ; Glutamic Acid/metabolism ; Hippocampus/metabolism ; Hippocampus/pathology ; Hydrogen-Ion Concentration ; Ischemic Attack, Transient/metabolism ; Ischemic Attack, Transient/pathology ; Mice ; Organ Culture Techniques ; Oxygen/metabolism ; Potassium/metabolism ; Sodium/metabolism ; Temperature
مستخلص: In focal ischemia, the fate of penumbral cells is closely linked to the infarcted tissue. Because of the release of cytosolic material from damaged cells, the biochemical and ionic alterations within the core are dramatic. Hence, adjacent cells ( infarct rim) are generally exposed to these changes and may be deleteriously affected. To mimic such conditions in vitro, we have employed a slice culture system and used an ischemic solution (IS) that resembles the milieu in the territory of infarct rim. In contrast to normal artificial cerebral spinal fluid, IS is characterized by low O(2), glucose, pH; excitotoxic levels of glutamate; and ionic alterations. In organotypic hippocampal slice cultures, we examined cell injury/death using propidium iodide following exposure to IS. Our data show significant cell injury starting at approximately 8 h following IS exposure with cell injury spreading as a function of exposure duration. We further studied the effect of each component in the IS separately, i.e., acidosis, hypoxia, ionic shifts or glutamate exitotoxicity and were able to isolate the contribution of each of these effectors to the IS-induced cell death. Our results suggest that in IS, acidosis exacerbates the potential for injury while ionic shifts, especially those of K(+) and Na(+), alleviate the potential for cell death.
معلومات مُعتمدة: P01 HD 32573 United States HD NICHD NIH HHS; P30 NS047101 United States NS NINDS NIH HHS; R01 HL 66237 United States HL NHLBI NIH HHS
المشرفين على المادة: 0 (Cations, Monovalent)
0 (Culture Media)
3KX376GY7L (Glutamic Acid)
9NEZ333N27 (Sodium)
IY9XDZ35W2 (Glucose)
RWP5GA015D (Potassium)
S88TT14065 (Oxygen)
تواريخ الأحداث: Date Created: 20070116 Date Completed: 20070402 Latest Revision: 20141120
رمز التحديث: 20240628
DOI: 10.1111/j.1471-4159.2006.04299.x
PMID: 17217421
قاعدة البيانات: MEDLINE
الوصف
تدمد:0022-3042
DOI:10.1111/j.1471-4159.2006.04299.x