Up-regulation of adenosine receptors in the cochlea by cisplatin

Ford, Mary S.; Nie, Zhongzhen; Whitworth, Craig; Rybak, Leonard P.; Ramkumar, Vickram

doi:10.1016/s0378-5955(97)00103-2

Cited by 60 publications

(37 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition, challenge with various cytotoxic agents, including cisplatin and anthracyclines, increase A1AR expression and promoter activity through activation of NFκB (Nie et al, 1998). Induction of A1AR expression by cisplatin, possibly mediated via NFκB, also occurs in the chinchilla cochlea (Ford et al 1997) and in the rat kidney (Bhat et al 2001). In addition, NFkB has been implicated in the induction of A1AR in the cochlea in response to noise exposure (Ramkumar et al 2004), and in basal forebrain in response to sleep deprivation (Basheer et al 2001).…”

Section: Discussionmentioning

confidence: 99%

Expression of striatal adenosine and dopamine receptors in mice deficient in the p50 subunit of NF-κB

Xie¹,

Jhaveri²,

Ding³

et al. 2007

Life Sciences

Self Cite

View full text Add to dashboard Cite

The striatal dopamine D 2 receptor (D2R) and adenosine A2A receptor (A2AAR) exhibit mutually antagonistic effects through physical interactions and by differential modulation of post-receptor signaling pathways. The expression of the A2AAR and the D2R are differentially regulated by nuclear factor-κB (NFkB). In this report, we determined the role of NFkB in regulation of these receptors by comparing mice deficient in the NFκB p50 subunit (p50 KO) with genetically intact B6129PF2/J (F2) mice. Quantification of adenosine receptor (AR) subtypes in mouse striatum by real time PCR, immunocytochemistry and radioligand binding assays showed more A2AAR but less A1AR in p50 KO mice as compared with F2 mice. Striata from p50 KO mice also had less D2R mRNA and [ 3 H]-methylspiperone binding than did striata from F2 mice. G αolf and G αs proteins, which are transducers of A2AAR signals, were also present at a higher level in striata from the p50 KO versus F2 mice. In contrast, the G αi1 protein, which transduces signals from the A1AR and D2R, was significantly reduced in striata from p50 -/ mice. Behaviorally, p50 KO mice exhibited increased locomotor activity relative to that of F2 mice after caffeine ingestion. These data are consistent with a role for the NFkB in the regulation of A1AR, A2AAR, D2R and possibly their coupling G proteins in the striatum. Dysregulation of these receptors in the striata of p50 KO mice might sensitize these animals to locomotor stimulatory action of caffeine.

show abstract

Section: Discussionmentioning

confidence: 99%

Expression of striatal adenosine and dopamine receptors in mice deficient in the p50 subunit of NF-κB

Xie¹,

Jhaveri²,

Ding³

et al. 2007

Life Sciences

Self Cite

View full text Add to dashboard Cite

show abstract

“…Cisplatin exposure in vivo caused an increase in lipid peroxidation by-products and decreased levels of antioxidant enyzme activities in the cochlea which were normalized by antioxidants and free radical scavengers [Rybak et al, 1995. Ford et al [1997] found that there may be a dissociation between acute cisplatin ototoxicity as evidenced by endocochlear potentials and compound action potentials and lipid peroxidation which occurs after the acute functional damage. Our laboratory found that cisplatin exposure in vivo led to increased amounts of ROS and decreased levels of antioxidant enzyme activities [Kopke et al, 1997].…”

Section: Cisplatin-induced Apoptosismentioning

confidence: 96%

Mechanisms of Cell Death in the Injured Auditory System: Otoprotective Strategies

et al. 2002

View full text Add to dashboard Cite

Oxidative stress insults such as neurotrophin withdrawal, sound trauma, hypoxia/ischemia, ototoxic antibiotics, and chemotherapeutic agents have been shown to induce apoptosis of both auditory hair cells and neurons. In this paper, we review some components of the apoptotic pathways leading to the death of hair cells and auditory induced by growth factor withdrawal or cisplatin intoxication: (1) reactive oxygen species and free radicals are formed as by-products of several metabolic pathways and these molecules can themselves cause cell damage by reacting with cellular proteins; (2) activation of caspases, and (3) activation of calpain. These mechanisms have several different points at which inhibitors could be targeted to protect cells from programmed cell death, including the prevention of oxidative stress-induced apoptosis and the activation of caspases and calpains.

show abstract

“…4). Activation of the A1AR gene might account for cisplatin-induced up-regulation of the A1AR in rat cochlea (93) and testis (94), in renal proximal kidney cell in cultures (95) and in primary cultures of rat embryonic neurons (D.M. Hallam et al, unpublished).…”

Section: Oxidative Stress Regulates A1ar Expression Via Activation Ofmentioning

confidence: 99%

Adenosine, Oxidative Stress and Cytoprotection

Ramkumar

Hallam

Nie

2001

Japanese Journal of Pharmacology

Self Cite

View full text Add to dashboard Cite

ABSTRACT-Adenosine, a metabolite of ATP, serves a number of important physiological roles in the body. These actions contribute to sedation, bradycardia, vasorelaxation, inhibition of lipolysis and regulation of the immune system and are mediated, in part, through activation of three distinct adenosine receptor (AR) subtypes. To date, four receptor types have been cloned: A1, A2A, A2B and A3. It is becoming increasing clear that adenosine contributes significantly to cytoprotection, a function mediated principally by the A1AR and A3AR. In this review, we survey the literature on the role of adenosine and the mechanisms underlying cytoprotection and ischemic preconditioning, a process characterized by cytoprotection derived from repeated brief ischemic challenges. An important recent observation is that the expression of several AR subtypes could be regulated by oxidative stress to provide a greater cytoprotective role. Thus, like other proteins known to be regulated during ischemia, the A1AR and A3AR can be considered as being inducible receptors.

show abstract

Up-regulation of adenosine receptors in the cochlea by cisplatin

Cited by 60 publications

References 34 publications

Expression of striatal adenosine and dopamine receptors in mice deficient in the p50 subunit of NF-κB

Expression of striatal adenosine and dopamine receptors in mice deficient in the p50 subunit of NF-κB

Mechanisms of Cell Death in the Injured Auditory System: Otoprotective Strategies

Adenosine, Oxidative Stress and Cytoprotection

Contact Info

Product

Resources

About