Cellular and molecular biology
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Cell. Mol. Biol. (Noisy-le-grand) · Mar 2002
Hyperthermia assists survival of astrocytes from oxidative-mediated necrotic cell death.
In response to many stresses and pathologic states, including different models of nervous system injury, cells synthesize a variety of proteins, most notably the inducible 72 kDa heat shock protein 70 (Hsp70), which plays important roles in maintaining cellular integrity and viability. We report here that cultured astrocytes from rat diencephalon express high levels of Hsp70 upon exposure to elevated temperatures, and are less vulnerable to a subsequent oxidative stress. Complex oxidative stress was induced by exposure of astrocytes to an aqueous extract of tobacco smoke. ⋯ Thermal stress also protected astrocytes from necrotic cell death but without affecting glutathione or ATP levels. We propose that heat shock protects astrocytes from necrosis induced by oxidative stress, probably as a result of Hsp70 synthesis, through an antioxidant-ATP independent mechanism. As Hsp70 may transfer from glial to neuronal cells, its synthesis by astrocytes may represent an important survival mechanism by which astrocytes protect neurons against oxidative-mediated cell death.
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Cell. Mol. Biol. (Noisy-le-grand) · Feb 2002
Review Case ReportsMolecular, immunological, enzymatic and biochemical studies of coproporphyrinogen oxidase deficiency in a family with hereditary coproporphyria.
A 27-year-old woman who had recurrent pain in renal bed since 1998 with increasing character, was stationary admitted. The patient showed dark urine, complained of hair loss and took since 1994 a hormonal oral contraceptive. No photosensitivity was observed. ⋯ Molecular analysis revealed a hitherto unknown mutation with the transversion of a cytosine to thymine at nucleotide position 854 in exon 4 of the coproporphyrinogen oxidase gene. The gene defect was confirmed by DGGE in the mother and her three daughters. The investigation of the immunological nature of the defective coproporphyrinogen oxidase gene from the whole family revealed decreased concentrations of coproporphyrinogen oxidase protein in the patient, her mother and her two sisters.
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Cell. Mol. Biol. (Noisy-le-grand) · Jun 2000
Comparative StudyAlterations in the interaction between iron regulatory proteins and their iron responsive element in normal and Alzheimer's diseased brains.
Iron regulatory proteins (IRPs) are cytoplasmic mRNA binding proteins involved in intracellular regulation of iron homeostasis. IRPs regulate expression of ferritin and transferrin receptor at the mRNA level by interacting with a conserved RNA structure termed the iron-responsive element (IRE). This concordant regulation of transferrin receptors and ferritin is designed so a cell can obtain iron when it is needed, and sequester iron when it is in excess. ⋯ At the cellular level, the outcome of this alteration in the molecular regulatory mechanism would be increased iron accumulation without an increase in ferritin; identical to the observation we reported in AD brains. The appearance of the single IRE/IRP complex in Alzheimer's brain extracts is associated with relatively high endogenous ribonuclease activity. We propose that elevated RNase activity is one mechanism by which the iron regulatory system becomes dysfunctional.
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Cell. Mol. Biol. (Noisy-le-grand) · May 2000
Tin-mesoporphyrin, a potent heme oxygenase inhibitor, for treatment of intracerebral hemorrhage: in vivo and in vitro studies.
Spontaneous intracerebral hemorrhage (ICH) is the stroke subtype with highest mortality and morbidity. ICH can also occur following traumatic brain injury and thrombolysis for ischemic stroke and myocardial infarction. Development of ICH-induced hemispheric edema can elevate intracranial pressure and cause death. ⋯ In conclusion, SnMP reduced intracerebral mass in an ICH model by decreasing both hematoma and edema volumes SnMP's mechanism of action is presently unknown but may involve its potent inhibition of heme oxygenase activity. SnMP's effect appears unrelated to ferritin iron release, antioxidant activity or initial clot formation. Since SnMP treatment could be brain protective following ICH, further investigations into neurological and neuropathological outcomes and as well as into its mechanism of action are warranted.
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Cell. Mol. Biol. (Noisy-le-grand) · Dec 1998
Comparative StudyAge-related differences in calcium accumulation in human arteries.
To elucidate the accumulation of calcium in the human arteries, the calcium contents of the thoracic aorta, coronary, common carotid, basilar, internal thoracic, axillary, radial, femoral, popliteal, and dorsalis pedis arteries, were analyzed by inductively coupled plasma atomic emission spectrometry (ICP-AES). The calcium content began to increase in both the thoracic aorta and femoral artery around the age of 50 years (yrs), in the popliteal artery at the age of 60 yrs, in the coronary, basilar and dorsalis pedis arteries at the age of 70 yrs, and in the common carotid artery at the age of 80 yrs. In the same time, the calcium content did not increase significantly in the internal thoracic and radial arteries. ⋯ With regard to the femoral artery, the accumulation of calcium and phosphorus occurred only in the tunica media, only in the tunica intima, or in both the tunicae media and intima. Therefore, the manner of accumulation of calcium and phosphorus in the femoral-arterial wall was different from that in the aortic wall. Comparing the upper and lower limb arteries, the calcium content was found to be higher in the femoral, popliteal, and dorsalis pedis arteries of the lower limb than that of the axillary and radial arteries of the upper limb.