Activation of the CRF<sub>1</sub> receptor causes ERK1/2 mediated increase in GRK3 expression in CATH.a cells

Salim, Samina; Hite, Brian; Eikenburg, Douglas C.

doi:10.1016/j.febslet.2007.06.006

Cited by 14 publications

(20 citation statements)

References 29 publications

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“…Our observation that an index of oxidative stress, protein carbonylation, was increased in the LC only in LH rats may help explain this difference. We and others have investigated the regulation of cellular GRK3 levels[14, 40, 41]. Activation of CRF 1 receptors leads to increased expression of GRK3 in cultured CATH.a neuronal cells, a mouse LC tumor cell line[14].…”

Section: Discussionmentioning

confidence: 99%

“…We and others have investigated the regulation of cellular GRK3 levels[14, 40, 41]. Activation of CRF 1 receptors leads to increased expression of GRK3 in cultured CATH.a neuronal cells, a mouse LC tumor cell line[14]. In addition, increased intracellular calcium, as might be expected during excessive activation of neurons and oxidative stress, is associated with increased degradation of GRK3 in neurons[42].…”

Section: Discussionmentioning

confidence: 99%

“…Research in our laboratory for several years has focused on regulation of cellular signaling in response to the stress hormones/neurotransmitters epinephrine (EPI) and corticotropin-releasing hormone by GRK3 [12–14]. GRK3 preferentially causes agonist-dependent phosphorylation of α 2 -AR and CRF 1 receptors, thereby regulating the desensitization and down-regulation of these receptors (CRF 1 )[13, 15, 16].…”

Section: Introductionmentioning

confidence: 99%

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Differential effects of inescapable stress on locus coeruleus GRK3, alpha2-adrenoceptor and CRF1 receptor levels in learned helpless and non-helpless rats: A potential link to stress resilience

Taneja¹,

Salim²,

Saha³

et al. 2011

Behavioural Brain Research

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Exposure of rats to unpredictable, inescapable stress results in two distinct behaviors during subsequent escape testing. One behavior, suggestive of lack of stress resilience, is prolonged escape latency compared to non-stressed rats and is labeled learned helplessness (LH). The other behavior suggestive of stress resilience is normal escape latency and is labeled non-helpless (NH). This study examines the effects of unpredictable, inescapable tail-shock stress (TSS) on alpha2-adrenoceptor (α2-AR) and corticotropin-releasing factor 1 receptor (CRF1) regulation as well as protein levels of G protein-coupled receptor kinase 3 (GRK3), GRK2, tyrosine hydroxylase (TH) plus carbonylated protein levels in locus coeruleus (LC), amygdala (AMG), cortex (COR) and striatum (STR). In NH rats, α2-AR and CRF1 receptors were significantly down-regulated in LC after TSS. No changes in these receptor levels were observed in the LC of LH rats. GRK3, which phosphorylates receptors and thereby contributes to α2-AR and CRF1 receptor down-regulation, was reduced in the LC of LH but not NH rats. GRK2 levels were unchanged. In AMG, GRK3 but not GRK2 levels were reduced in LH but not NH rats, and receptor regulation was impaired in LH rats. In STR, no changes in GRK3 or GRK2 levels were observed. Finally, protein carbonylation, an index of oxidative stress, was increased in the LC and AMG of LH but not NH rats. We suggest that reduced stress resilience after TSS may be related to oxidative stress, depletion of GRK3 and impaired regulation of α2-AR and CRF1 receptor in LC.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Differential effects of inescapable stress on locus coeruleus GRK3, alpha2-adrenoceptor and CRF1 receptor levels in learned helpless and non-helpless rats: A potential link to stress resilience

Taneja¹,

Salim²,

Saha³

et al. 2011

Behavioural Brain Research

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“…Very little is known, however, regarding cellular and molecular factors governing the CRF 1 or CRF 2 receptor's preference for a specific upstream regulator of ERK‐MAPK signal transduction. Interestingly, CRF 1 receptor ERK‐MAPK signaling can activate Sp‐1 and Ap‐2 transcription, thereby upregulating expression of GRK3, which mediates homologous desensitization of CRF 1 receptors 48 . This process may be impaired in anxiety and depressive disorders.…”

Section: Crf Receptor Signal Transduction Pathwaysmentioning

confidence: 99%

Role of CRF Receptor Signaling in Stress Vulnerability, Anxiety, and Depression

Hauger

Risbrough

Oakley

et al. 2009

Annals of the New York Academy of Sciences

190

176

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Markers of hyperactive central corticotropin releasing factor (CRF) systems and CRF-related single nucleotide polymorphisms (SNPs) have been identified in patients with anxiety and depressive disorders. Designing more effective antagonists may now be guided by data showing that small molecules bind to transmembrane domains. Specifically, CRF1 receptor antagonists have been developed as novel anxiolytic and antidepressant treatments. Because CRF1 receptors become rapidly desensitized by G protein-coupled receptor kinase (GRK) and β-arrestin mechanisms in the presence of high agonist concentrations, neuronal hypersecretion of synaptic CRF alone may be insufficient to account for excessive central CRF neurotransmission in stress-induced affective pathophysiology. In addition to desensitizing receptor function, GRK phosphorylation and β-arrestin binding can shift a G protein-coupled receptor (GPCR) to signal selectively via the extracellular signal-regulated kinase/mitogen-activated protein kinase (ERK-MAPK) or Akt pathways independent of G proteins. Also, Epac-dependent CRF1 receptor signaling via the ERK-MAPK pathway has been found to potentiate brain-derived neurotrophic factor (BDNF)-stimulated TrkB signaling. Thus, genetic or acquired abnormalities in GRK and β-arrestin function may be involved in the pathophysiology of stress-induced anxiety and depression.

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“…For example, CATH.a cells are derived from the mouse locus coeruleus brain region and are used in examining cellular pathways involved in the anxiety response (25). HepG2 is a human liver-derived cell line which is utilized for examining the insulin signaling pathway (19).…”

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Human kidney-2 cells harbor functional dopamine D1 receptors that require Giαfor Gq/11αsignaling

Pokkunuri

Chugh

Asghar

2013

American Journal of Physiology-Renal Physiology

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A recent study demonstrated that the dopamine D1 receptor (D1R) is nonfunctional in human kidney cells, HK2 cells, in terms of their inability to couple to G s protein in response to the D1R agonist fenoldopam. Since D1R also couples to G q protein, we tested whether D1R is functional in HK2 cells in terms of their ability to couple to G q and produce downstream signaling. For comparison, we also studied another receptor, angiotensin II type 1 receptor (AT1R) known to couple to G q. Protein kinase C (PKC) and 86rubidium transport activities were determined as surrogate downstream signaling markers. Fenoldopam and angiotensin II increased PKC activity, which decreased in the presence of respective receptor antagonists (SCH23390 for D1R; candesartan for AT1R), PKC (chelerythrine chloride) and G i protein (pertussis toxin) inhibitors and G q/11α siRNA. Furthermore, fenoldopam and angiotensin II increased 35S-GTPγS binding, an index of receptor-G protein coupling, which decreased with pertussis toxin and in G q/11α-depleted cells. Also, fenoldopam-mediated inhibition of 86rubidium transport (an index of Na-K-ATPase activity) was attenuated with SCH23390, chelerythrine chloride, pertussis toxin, and G q/11α siRNA. Moreover, fenoldopam caused a decrease in cytosolic and increase in membranous abundance of G q/11α. The immunoprecipitated levels of G q/11α in the membranes were greater in fenoldopam-treated cells, and G iα coimmunoprecipitated with G q/11α. Our results suggest that both D1R and AT1R are functional in HK2 cells, enabling G q-mediated downstream signaling in a G i dependent manner.

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Activation of the CRF₁ receptor causes ERK1/2 mediated increase in GRK3 expression in CATH.a cells

Cited by 14 publications

References 29 publications

Differential effects of inescapable stress on locus coeruleus GRK3, alpha2-adrenoceptor and CRF1 receptor levels in learned helpless and non-helpless rats: A potential link to stress resilience

Differential effects of inescapable stress on locus coeruleus GRK3, alpha2-adrenoceptor and CRF1 receptor levels in learned helpless and non-helpless rats: A potential link to stress resilience

Role of CRF Receptor Signaling in Stress Vulnerability, Anxiety, and Depression

Human kidney-2 cells harbor functional dopamine D1 receptors that require Giαfor Gq/11αsignaling

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Activation of the CRF1 receptor causes ERK1/2 mediated increase in GRK3 expression in CATH.a cells

Cited by 14 publications

References 29 publications

Differential effects of inescapable stress on locus coeruleus GRK3, alpha2-adrenoceptor and CRF1 receptor levels in learned helpless and non-helpless rats: A potential link to stress resilience

Differential effects of inescapable stress on locus coeruleus GRK3, alpha2-adrenoceptor and CRF1 receptor levels in learned helpless and non-helpless rats: A potential link to stress resilience

Role of CRF Receptor Signaling in Stress Vulnerability, Anxiety, and Depression

Human kidney-2 cells harbor functional dopamine D1 receptors that require Giαfor Gq/11αsignaling

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Activation of the CRF₁ receptor causes ERK1/2 mediated increase in GRK3 expression in CATH.a cells