Редактирование: ABCC1 (раздел)

==Publications==

{{medline-entry
|title=Dual pathways mediate β-amyloid stimulated glutathione release from astrocytes.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/26200696
|abstract=Oxidative stress plays an important role in the progression of Alzheimer's disease (AD) and other neurodegenerative conditions. Glutathione (GSH), the major antioxidant in the central nervous system, is primarily synthesized and released by astrocytes. We determined if β-amyloid (Aβ42), crucially involved in Alzheimer's disease, affected GSH release. Monomeric Aβ (mAβ) stimulated GSH release from cultured cortical astrocytes more effectively than oligomeric Aβ (oAβ) or fibrillary Aβ (fAβ). Monomeric Aβ increased the expression of the transporter [[ABCC1]] (also referred to as MRP1) that is the main pathway for GSH release. GSH release from astrocytes, with or without mAβ stimulation, was reduced by pharmacological inhibition of [[ABCC1]]. Astrocytes robustly express connexin proteins, especially connexin43 (Cx43), and mAβ also stimulated Cx43 hemichannel-mediated glutamate and GSH release. Aβ-stimulation facilitated hemichannel opening in the presence of normal extracellular calcium by reducing astrocyte cholesterol level. Aβ treatment did not alter the intracellular concentration of reduced or oxidized glutathione. Using a mouse model of AD with early onset Aβ deposition (5xFAD), we found that cortical [[ABCC1]] was significantly increased in temporal register with the surge of Aβ levels in these mice. [[ABCC1]] levels remained elevated from 1.5 to 3.5 months of age in 5xFAD mice, before plunging to subcontrol levels when amyloid plaques appeared. Similarly, in cultured astrocytes, prolonged incubation with aggregated Aβ, but not mAβ, reduced induction of [[ABCC1]] expression. These results support the hypothesis that in the early stage of AD pathogenesis, less aggregated Aβ increases GSH release from astrocytes (via [[ABCC1]] transporters and Cx43 hemichannels) providing temporary protection from oxidative stress which promotes AD development.
|mesh-terms=* Aging
* Alzheimer Disease
* Amyloid beta-Peptides
* Animals
* Astrocytes
* Calcium
* Cells, Cultured
* Cerebral Cortex
* Cholesterol
* Connexin 43
* Disease Models, Animal
* Glutathione
* Mice, Inbred C57BL
* Mice, Transgenic
* Multidrug Resistance-Associated Proteins
* Oxidation-Reduction
* Plaque, Amyloid
|keywords=* ABCC1
* Alzheimer's disease
* cholesterol
* connexin hemichannel
* glutathione
* β-amyloid
|full-text-url=https://sci-hub.do/10.1002/glia.22886
}}
{{medline-entry
|title=Independent regulation of [[ABCB1]] and ABCC activities in thymocytes and bone marrow mononuclear cells during aging.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/17635801
|abstract=Aging modifies a number of functional and phenotypic parameters of cells from the immune system. In this study, the activities of two members of the superfamily of ATP-binding cassette (ABC) transport proteins, [[ABCB1]] and ABCC (measured by rhodamine 123 efflux and Fluo-3 efflux respectively), were compared in murine bone marrow cells and thymocytes of young (3-4 weeks old), adult (2-3 months old) and old (18 months old) mice. [[ABCB1]] activity was shown to be age regulated in murine bone marrow mononuclear cells and thymocytes. In the bone marrow, the increased amount of cells with [[ABCB1]] activity observed in old mice was restricted to the c-kit(-)Sca-1( ) and c-kit( )Sca-1( ) subpopulations. Only a small percentage of c-kit( ) cells in the thymus had [[ABCB1]] activity, and this subpopulation increased with age. In the thymus, old age augmented this activity in the CD4(-) CD8(-) double-negative cells and in the CD4( ) and CD8( ) single-positive populations. The activity of another ABC transporter, the ABCC-related activity, was also modified by age in the bone marrow. However, the age-related increase was observed in the subpopulations were [[ABCB1]] was not modified, namely the non-progenitor population (c-kit(-)Sca-1(-)cells) and c-kit( )Sca-1(-) cells. Nearly, all thymocytes expressed the [[ABCC1]] molecule in an active form and aging did not affect this pattern. This study demonstrates an independent upregulation of [[ABCB1]] and ABCC activities during the aging process. The increases were observed in different subsets of cells but followed a developmentally regulated pattern. The functions played by these transporters and alterations in aging are discussed.
|mesh-terms=* ATP Binding Cassette Transporter, Subfamily B
* ATP Binding Cassette Transporter, Subfamily B, Member 1
* ATP-Binding Cassette Transporters
* Aging
* Animals
* Bone Marrow Cells
* Cells, Cultured
* Hematopoietic Stem Cells
* Leukocytes, Mononuclear
* Male
* Mice
* Mice, Inbred C57BL
* Multidrug Resistance-Associated Proteins
* Thymus Gland

|full-text-url=https://sci-hub.do/10.1111/j.1365-3083.2007.01965.x
}}