Signal Transduction Pathways Associated with &amp;alpha;&lt;sub&gt;1&lt;/sub&gt;-Adrenoceptor Subtypes in Cells and Tissues Including Human Prostate

Marshall, Ian; Burt, Richard P.; Chapple, Christopher R.

doi:10.1159/000052317

Cited by 26 publications

(18 citation statements)

References 17 publications

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“…As α1-ARs act via PLC-catalyzed production of two second-messengers, IP 3 and DAG (12), two mechanisms are probably involved in Ca 2+ entry in response to the stimulation of these receptors by agonists. The first is related to the IP 3 -evoked depletion of intracellular Ca 2+ stores and the subsequent activation of plasmalemmal SOCs, also thought to belong to the TRP-channel family (15).…”

Section: Discussionmentioning

confidence: 99%

“…Its stimulation leads principally to the activation of phospholipase C (PLC), ultimately resulting in an increase in intracellular free Ca 2+ via inositol triphosphate (IP 3 ) and diacylglycerol (DAG) production (12,13). Recent studies in vascular smooth muscles have shown that α1-ARs may also activate Ca 2+ -permeable nonselective cationic channels (14) and that TRPC6 -a member of the transient receptor potential (TRP) channel family originally found in Drosophila and then discovered in most mammalian tissues (15) -may be an essential component of these channels (16).…”

Section: Introductionmentioning

confidence: 99%

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α1-adrenergic receptors activate Ca2+-permeable cationic channels in prostate cancer epithelial cells

Thebault¹,

Roudbaraki²,

Sydorenko³

et al. 2003

J. Clin. Invest.

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. Y. Shuba's present address is: Bogomoletz Institute of Physiology, Kiev, Ukraine. Conflict of interest:The authors have declared that no conflict of interest exists. Nonstandard abbreviations used: α1-adrenergic receptor (α1-AR); human prostate cancer epithelial cell (hPCE cell); phospholipase C (PLC); inositol triphosphate (IP3); diacylglycerol (DAG); transient receptor potential (TRP); α1A subtype of α1-AR (α1A-AR); lymph node carcinoma of the prostate cells (LNCaP cells); intracellular Ca 2+ concentration ([Ca 2+ ]i); phenylephrine (Phe); intracellular Ca 2+ oscillations (osc); 2-aminophenyl borate (2-APB); store-operated Ca 2+ -channel (SOC); 1-oleoyl-2-acetyl-snglycerol (OAG); 1,2-dioctanoyl-sn-glycerol (DOG); extracellular Ca 2+ concentration ([Ca 2+ ]out); Phe-activated current (IPhe); current reversal potential (Erev).

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

α1-adrenergic receptors activate Ca2+-permeable cationic channels in prostate cancer epithelial cells

Thebault¹,

Roudbaraki²,

Sydorenko³

et al. 2003

J. Clin. Invest.

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“…For instance, stimulation of two receptors on prostate cancer epithelial cells, 1-adrenoceptor ( 1-AR) and metabotropic purinergic receptor (P2Y-R), produce divergent effects on cell proliferation: 1-AR stimulation enhances proliferation (Thebault, et al, 2006), and stimulation of P2Y-R results in growth arrest (Vanoverberghe, et al, 2003). These divergent effects on proliferation are surprising, given that both receptors act via a common phospholipase C (PLC)-catalyzed inositol phospholipid breakdown signalling pathway that results in the derivation of two second messengers important for Ca 2+ signalling (Marshall, et al, 1999, von Kugelgen, et al, 2000, IP 3 and diacylglycerol (DAG). Our recent work with primary human prostate cancer epithelial cells brought some insight into these puzzling observations (Thebault, et al, 2006).…”

Section: Specificity Of Ca 2+ Signalsmentioning

confidence: 99%

Calcium signalling and cancer cell growth

Capiod

Shuba

Skryma

et al. 2007

Subcellular Biochemistry

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Abstract:Cancer is caused by defects in the mechanisms underlying cell proliferation and cell death. Calcium ions are central to both phenomena, serving as major signalling agents with spatial localization, magnitude and temporal characteristics of calcium signals ultimately determining cell's fate. There are four primary compartments: extracellular space, cytoplasm, endoplasmic reticulum and mitochondria that participate in the cellular Ca 2+ circulation. They are separated by own membranes incorporating divers Ca 2+ -handling proteins whose concerted action provides for Ca 2+ signals with the spatial and temporal characteristics necessary to account for specific cellular response. The transformation of a normal cell into a cancer cell is associated with a major re-arrangement of Ca 2+ pumps, Na/Ca exchangers and Ca 2+ channels, which leads to the enhanced proliferation and impaired ability to die. In the present chapter we examine what changes in Ca 2+ signalling and the mechanisms that support it underlie the passage from normal to pathological cell growth and death control. Understanding this changes and identifying molecular players involved provides new prospects for cancers treatment

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“…Such divergent effects of two receptors on cell proliferation are surprising, because both a 1 -AR and P2Y-R are known to be coupled to the common phospholipase C (PLC)-catalyzed inositol phospholipids breakdown signaling pathway, via which a 1 agonists and extracellular ATP are capable of inducing apparently similar increases in intracellular free Ca 2+ ([Ca 2+ ] i ; refs. 12,13). The opposite end effects on cell proliferation can only be explained if the ACE controlled by each receptor uses different but still undetermined Ca 2+ -permeable membrane channels ultimately destined to target various intracellular effectors.…”

Section: Introductionmentioning

confidence: 99%

Differential Role of Transient Receptor Potential Channels in Ca2+ Entry and Proliferation of Prostate Cancer Epithelial Cells

et al. 2006

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One major clinical problem with prostate cancer is the cells' ability to survive and proliferate upon androgen withdrawal. Because Ca 2+ is central to growth control, understanding the mechanisms of Ca 2+ homeostasis involved in prostate cancer cell proliferation is imperative for new therapeutic strategies. Here, we show that agonist-mediated stimulation of A 1 -adrenergic receptors (A 1 -AR) promotes proliferation of the primary human prostate cancer epithelial (hPCE) cells by inducing store-independent Ca 2+ entry and subsequent activation of nuclear factor of activated T cells (NFAT) transcription factor. Such an agonist-induced Ca 2+ entry (ACE) relied mostly on transient receptor potential canonical 6 (TRPC6) channels, whose silencing by antisense hybrid depletion decreased both hPCE cell proliferation and ACE. In contrast, ACE and related growth arrest associated with purinergic receptors (P2Y-R) stimulation involved neither TRPC6 nor NFAT. Our findings show that A 1 -AR signaling requires the coupled activation of TRPC6 channels and NFAT to promote proliferation of hPCE cells and thereby suggest TRPC6 as a novel potential therapeutic target.

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Signal Transduction Pathways Associated with α<sub>1</sub>-Adrenoceptor Subtypes in Cells and Tissues Including Human Prostate

Cited by 26 publications

References 17 publications

α1-adrenergic receptors activate Ca2+-permeable cationic channels in prostate cancer epithelial cells

α1-adrenergic receptors activate Ca2+-permeable cationic channels in prostate cancer epithelial cells

Calcium signalling and cancer cell growth

Differential Role of Transient Receptor Potential Channels in Ca2+ Entry and Proliferation of Prostate Cancer Epithelial Cells

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