Research paperInteraction of drugs with P-glycoprotein in brain capillaries
References (40)
- et al.
ATPase activity of partially purified P-glycoprotein from multidrug-resistant Chinese hamster ovary cells
Biochim Biophys Acta
(1992) - et al.
High levels of P-glycoprotein detected in isolated brain capillaries
Biochim Biophys Acta
(1993) - et al.
Functional involvement of P-glycoprotein in blood-brain barrier
J Biol Chem
(1992) - et al.
Disruption of the mouse mdrla P-glycoprotein gene leads to a deficiency in the blood-brain barrier and to increased sensitivity to drugs
Cell
(1994) - et al.
Restricted transport of cyclosporin A across the blood-brain barrier by a multidrug transporter, P-glycoprotein
Biochem Pharmacol
(1993) Cyclosporins as drug resistance modifiers
Biochem Pharmacol
(1992)- et al.
γ-Glutamyl-p-nitroanilide: a new convenient substrate for determination and study of l- and d-γ-glutamyltranspeptidase activities
Biochim Biophys Acta
(1963) A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding
Anal Biochem
(1976)- et al.
P-glycoprotein of blood barrier: Cross-reactivity of MAb C219 with a 190 kDa protein in bovine and rat isolated brain capillaries
Biochim Biophys Acta
(1995) - et al.
Photoaffinity probes for the α1-adrenergic receptor and the calcium channel bind to a common domain in P-glycoprotein
J Biol Chem
(1990)
Differential transport properties of two mdr gene products are distinguished by progesterone
J Biol Chem
Resistance modification by PSC-833, a novel non-immunosuppressive cyclosporin A
Eur J Cancer
Increased mdr-1/P-glycoprotein expression after treatment of human colon carcinoma cells with P-glycoprotein antagonists
J Biol Chem
Derivation and characterization of a mouse tumour cell line with acquired resistance to cyclosporin A
Eur J Cancer
Pharmacology of drugs that alter multidrug resistance in cancer
Pharmacol Rev
Biochemistry of multidrug resistance mediated by the multidrug transporter
Annu Rev Biochem
Cell surface P-glycoprotein associated with multidrug resistance in mammalian cell lines
Science
Amplification of P-glycoprotein genes in multi-drug-resistant mammalian cell lines
Nature
Multidrug-resistance gene (P-glycoprotein) is expressed by endothelial cells at blood-brain barrier sites
Immunohistochemical localization in normal tissues of different epitopes in the multidrug transport protein P170: Evidence for localization in brain capillaries and crossreactivity of one antibody with a muscle protein
J Histochem Cytochem
Cited by (90)
Tailoring of P-glycoprotein for effective transportation of actives across blood-brain-barrier
2021, Journal of Controlled ReleaseCitation Excerpt :The mechanism of interaction of stem cells (mesenchymal stem cells) with endothelial cells exists through crawling, spreading, and pseudopodia (para-cellular diapedesis). Another alternative mechanism includes TNFα-activated endothelial membranes and transcellular diapedesis by non-apoptotic membrane via pores and gaps in between the cells across BBB. [17,18, 25] There exists a continuous lipophilic physical boundary between the CNS and the peripheral circulation as well as vascular capacity known as the blood-brain-barrier that comprises the physical and chemical barrier for maintaining the neural environment and proper brain functions.
Pathophysiology of Kernicterus
2017, Fetal and Neonatal Physiology, 2-Volume SetEvidence for effects on thermoregulation after acute oral exposure to type I and type II pyrethroids in infant rats
2015, Neurotoxicology and TeratologyCitation Excerpt :CYPM is a mix of eight isomers greatly differing in acute toxicity in mammals (EFSA, 2011), whereas BIF consists of only a few highly toxic isomers (ECHA, 2011). Additionally, expression of multidrug-resistance protein P-glycoprotein, an efflux transporter localized on the apical membrane of brain capillary endothelial cells (Jette et al., 1995), reaches adult levels of expression at ~ 28 days of age (Matsuoka et al., 1999). Thus, the finding of a greater susceptibility in infants compared to adult rats after exposure to CYPM may be a consequence of maturing enzymes with age-related, differential detoxifying activity towards its isomers, which may in turn determine larger peak tissue concentrations of the most toxic CYPM isomers in the infant than in the adult nervous system, as proposed by Anand et al. (2006) and Cantalamessa (1993).
Blockade of endothelin B receptor improves the efficacy of levetiracetam in chronic epileptic rats
2015, SeizureCitation Excerpt :In the present study, both MDR1 and MDR3 expression was increased in the hippocampus of epileptic animals compared to controls. This discrepancy may be a consequence of the difference in species between humans and rodents, because MDR3 is the major form of PGP expression in the murine brain vessels [38]. Interestingly, the present data revealed that only MDR3 expression in the hippocampus of non-responders was higher than those of responders.
Cytotoxicity of the indole alkaloid reserpine from Rauwolfia serpentina against drug-resistant tumor cells
2015, PhytomedicineCitation Excerpt :These results are in accord to previous data reporting on the photoaffinity labeling of P-glycoprotein and its inhibition by reserpine (Qian and Beck 1990). The inhibition of P-glycoprotein's efflux function by reserpine was subsequently confirmed by other authors (Schlemmer and Sirotnak 1994; Bhat et al. 1995; Jetté et al. 1995; Sarver et al. 2002). In addition to these studies, we did not only confirm reserpine's inhibitory activity on P-glycoprotein's function, but we also suggested the amino acids responsible for reserpine's binding in the pharmacophore of P-glycopotein by molecular docking.
[<sup>11</sup>C]quinidine and [<sup>11</sup>C]laniquidar PET imaging in a chronic rodent epilepsy model: Impact of epilepsy and drug-responsiveness
2013, Nuclear Medicine and BiologyCitation Excerpt :However, this concern is also valid for several of the classic P-gp substrates and long-known competitive inhibitors such as quinidine. Quinidine proved to be among the most efficacious compounds for inhibiting photo-affinity labeling of P-gp [44,45] indicating that quinidine binds to P-gp with high affinity and thus, is rather categorized as a bulky substrate with long interaction times at the transporter molecule. Thus, PET data obtained with [11C]quinidine will probably also be affected by both, transport of the tracer by P-gp as well as direct binding to the transporter molecule.