Mechanism of acetylcholine-induced calcium signaling during neuronal differentiation of P19 embryonal carcinoma cells in vitro

Resende, Rodrigo R.; Gomes, Kátia N.; Adhikari, Avishek; Britto, Luiz R.G.; Ulrich, Henning

doi:10.1016/j.ceca.2007.04.007

Cited by 44 publications

(50 citation statements)

References 61 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Bj-PRO-7a and muscarine-evoked [Ca 21 ] i transients were similar (Figs. 2A and 2B) and consistent with previous studies (32).…”

Section: Brief Reportsupporting

confidence: 93%

“…This hypothesis is supported by the observation that muscarinic M1-M3 receptors have their expression increased during neural differentiation of P19 cells (26,32,33), in agreement with the Bj-PRO-7a-evoked calcium response, while undifferentiated cells did not exhibit any response to such stimulus.…”

Section: Resultssupporting

confidence: 66%

“…Additionally, P19 embryonal carcinoma cells were used as a model for in vitro neural differentiation, which express mAChRs endogenously depending on their developmental stage. Differentiated P19 cells express functional M1, M2, M3, and M5 mAChRs, whereas no muscarinic-induced receptor activity could be observed in undifferentiated cells (32).…”

Section: Resultsmentioning

confidence: 87%

“…Considering the responses observed in CHO-M1 and neural-differentiated P19 cells expressing functional M1, M2, M3, and M5 receptors (32), it is suggested that changes in intracellular calcium concentrations promoted by Bj-PRO-7a resulted from the activation of M1 muscarinic receptor subtype coupled via a-subunits of the G q/11 family. This hypothesis is supported by the observation that muscarinic M1-M3 receptors have their expression increased during neural differentiation of P19 cells (26,32,33), in agreement with the Bj-PRO-7a-evoked calcium response, while undifferentiated cells did not exhibit any response to such stimulus.…”

Section: Resultsmentioning

confidence: 99%

See 3 more Smart Citations

The snake venom peptide Bj‐PRO‐7a is a M1 muscarinic acetylcholine receptor agonist

et al. 2010

Self Cite

View full text Add to dashboard Cite

Proline-rich peptides from Bothrops jararaca venom (Bj-PRO) were characterized based on the capability to inhibit the somatic angiotensin-converting enzyme. The pharmacological action of these peptides resulted in the development of Captopril, one of the best examples of a target-driven drug discovery for treatment of hypertension. However, biochemical and biological properties of Bj-PROs were not completely elucidated yet, and many recent studies have suggested that their activity relies on angiotensinconverting enzyme-independent mechanisms. Here, we show that Bj-PRO-7a (

show abstract

“…Bj-PRO-7a and muscarine-evoked [Ca 21 ] i transients were similar (Figs. 2A and 2B) and consistent with previous studies (32).…”

Section: Brief Reportsupporting

confidence: 93%

Section: Resultssupporting

confidence: 66%

Section: Resultsmentioning

confidence: 87%

Section: Resultsmentioning

confidence: 99%

See 2 more Smart Citations

The snake venom peptide Bj‐PRO‐7a is a M1 muscarinic acetylcholine receptor agonist

et al. 2010

Self Cite

View full text Add to dashboard Cite

show abstract

“…In several cell types, ACh has been shown to induce cell proliferation (47,57,58). More recently, a study by Diamandis et al (48) reported that ACh can potently promote proliferation in neuronal stem cells.…”

Section: Discussionmentioning

confidence: 99%

CD38/cADPR/Ca2+ Pathway Promotes Cell Proliferation and Delays Nerve Growth Factor-induced Differentiation in PC12 Cells

Yue

Wei

Lam

et al. 2009

Journal of Biological Chemistry

View full text Add to dashboard Cite

Intracellular Ca2؉ mobilization plays an important role in a wide variety of cellular processes, and multiple second messengers are responsible for mediating intracellular Ca 2؉ changes. Here we explored the role of one endogenous Ca 2؉ -mobilizing nucleotide, cyclic adenosine diphosphoribose (cADPR), in the proliferation and differentiation of neurosecretory PC12 cells. We found that cADPR induced Ca 2؉ release in PC12 cells and that CD38 is the main ADP-ribosyl cyclase responsible for the acetylcholine (ACh)-induced cADPR production in PC12 cells. In addition, the CD38/cADPR signaling pathway is shown to be required for the ACh-induced Ca 2؉ increase and cell proliferation. Inhibition of the pathway, on the other hand, accelerated nerve growth factor (NGF)-induced neuronal differentiation in PC12 cells. Conversely, overexpression of CD38 increased cell proliferation but delayed NGF-induced differentiation. Our data indicate that cADPR plays a dichotomic role in regulating proliferation and neuronal differentiation of PC12 cells. Mobilization of intracellular Ca2ϩ stores is involved in diverse cell functions, including fertilization, cell proliferation, and differentiation (1-4). At least three endogenous Ca 2ϩ -mobilizing messengers have been identified, including inositol trisphosphate (IP 3 ), 3 nicotinic adenine acid dinucleotide phosphate (NAADP), and cyclic adenosine diphosphoribose (cADPR). Similar to IP 3 , cADPR can mobilize calcium release in a wide variety of cell types and species, from protozoa to animals. The cADPR-mediated Ca 2ϩ signaling has been indicated in a variety of cellular processes (5-7), from abscisic acid signaling and regulation of the circadian clock in plants, to mediating long-term synaptic depression in hippocampus.Ample evidence shows that the ryanodine receptors are the main intracellular targets for cADPR (1,2,8). Ryanodine receptors (RyRs) are intracellular Ca 2ϩ channels widely expressed in various cells and tissues, including muscles and neurons. It is the major cellular mediator of Ca 2ϩ -induced Ca 2ϩ release (CICR) in cells. There are three isoforms of ryanodine receptors: RyR1, RyR2, and RyR3, all of which have been implicated in the cADPR signaling (1, 2, 8). However, evidence regarding cADPR acting directly on the receptors is lacking (9). It has been suggested that accessory proteins, such as calmodulin and FK506-binding protein (FKBP), may be involved instead (10 -15).cADPR is formed from nicotinamide adenine dinucleotide (NAD) by ADP-ribosyl cyclases. Six ADP-ribosyl cyclases have been identified so far: Aplysia ADP-ribosyl cyclase, three sea urchin homologues (16,17), and two mammalian homologues, CD38 and CD157 (18). CD38 is a membrane-bound protein and the main mammalian ADP-ribosyl cyclase. As a novel multifunctional enzyme, CD38 catalyzes the synthesis and hydrolysis of both cADPR and NAADP, two structurally and functionally distinct Ca 2ϩ messengers. Virtually all mammalian tissues ever examined have been shown to express CD38. CD38 knockout mice exhibit mult...

show abstract

Neural Differentiation of P19 Carcinoma Cells and Primary Neurospheres: Cell Morphology, Proliferation, Viability, and Functionality

Negraes

Schwindt

Trujillo

et al. 2012

CP Stem Cell Biology

Self Cite

View full text Add to dashboard Cite

This unit describes the culture and induction of in vitro models of neural differentiation and strategies to evaluate the participation of extrinsic and intrinsic factors in modulation of this process. Protocols focus on large‐scale expansion of pluripotent P19 murine embryonic carcinoma cells and their induction to neural differentiation in the presence of retinoic acid, closely resembling conditions of early neuroectodermal differentiation. Procedures are also described for obtaining rat neural precursor cells (NPCs) or neurospheres and for differentiating them in the absence of growth factors. Experimental strategies are reported using P19 cells and NPCs as in vitro models for studying the actions of extrinsic and intrinsic factors on morphology, proliferation, viability, neural phenotype determination, and progress of differentiation, as well as the functionality of ion channels and metabotropic receptors in inducing calcium fluxes at different developmental stages. The methods described here may be useful for optimizing in vitro protocols for stem cell differentiation into defined neural populations, as well as for studying mechanisms that underlie neurogenesis and gliogenesis. Curr. Protoc. Stem Cell Biol. 20:2D.9.1‐2D.9.22. © 2012 by John Wiley & Sons, Inc.

show abstract

Mechanism of acetylcholine-induced calcium signaling during neuronal differentiation of P19 embryonal carcinoma cells in vitro

Cited by 44 publications

References 61 publications

The snake venom peptide Bj‐PRO‐7a is a M1 muscarinic acetylcholine receptor agonist

The snake venom peptide Bj‐PRO‐7a is a M1 muscarinic acetylcholine receptor agonist

CD38/cADPR/Ca2+ Pathway Promotes Cell Proliferation and Delays Nerve Growth Factor-induced Differentiation in PC12 Cells

Neural Differentiation of P19 Carcinoma Cells and Primary Neurospheres: Cell Morphology, Proliferation, Viability, and Functionality

Contact Info

Product

Resources

About