Stem Cells and Calcium Signaling

Tonelli, Fernanda Maria Policarpo; Santos, Anderson K.; Gomes, Dawidson Assis; Silva, Saulo L. da; Gomes, Kátia N.; Ladeira, Luiz Orlando; Resende, Rodrigo R.

doi:10.1007/978-94-007-2888-2_40

Cited by 120 publications

(105 citation statements)

References 123 publications

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“…These results indicate that both nAChR subtypes are likely involved in SCO generation and that there is a differential modulation of nAChRs on the frequency and amplitude of SCO. The differential modulation of nAChR subtypes on the frequency and amplitude of [Ca 2ϩ ] i oscillations supported the notion that the frequency and amplitude of [Ca 2ϩ ] i oscillations encode different information contained in the Ca 2ϩ signal (2,29). Albeit the different effects of DH␤E on the frequency and amplitude of SCO, DH␤E pretreatment prevented the nicotinic increment of frequency and the amplitude of [Ca 2ϩ ] i oscillations, suggesting that ␣ 4 ␤ 2 -nAChRs play a critical role in both SCO and NCO.…”

Section: Discussionsupporting

confidence: 57%

Nicotinic modulation of Ca²⁺ oscillations in rat cortical neurons in vitro

Wang

Guo

et al. 2016

American Journal of Physiology-Cell Physiology

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roles of nicotine on Ca 2ϩ oscillations [intracellular Ca 2ϩ ([Ca 2ϩ ]i) oscillation] in rat primary cultured cortical neurons were studied. The spontaneous [Ca 2ϩ ]i oscillations (SCO) were recorded in a portion of the neurons (65%) cultured for 7-10 days in vitro. Application of nicotine enhanced [Ca 2ϩ ]i oscillation frequency and amplitude, which were reduced by the selective ␣4␤2-nicotinic acetylcholine receptors (nAChRs) antagonist dihydro-␤-erythroidine (DH␤E) hydrobromide, and the selective ␣7-nAChRs antagonist methyllycaconitine citrate (MLA, 20 nM). DH␤E reduced SCO frequency and prevented the nicotinic increase in the frequency. DH␤E somewhat enhanced SCO amplitude and prevented nicotinic increase in the amplitude. MLA (20 nM) itself reduced SCO frequency without affecting the amplitude but blocked nicotinic increase in [Ca 2ϩ ]i oscillation frequency and amplitude. Furthermore, coadministration of both ␣ 4␤2-and ␣7-nAChRs antagonists completely prevented nicotinic increment in [Ca 2ϩ ]i oscillation frequency and amplitude. Thus, our results indicate that both ␣ 4␤2-and ␣7-nAChRs mediated nicotine-induced [Ca 2ϩ ]i oscillations, and two nAChR subtypes differentially regulated SCO. intracellular calcium ion concentration oscillations; nicotine; ␣4␤2-nicotinic acetylcholine receptors; ␣7-nicotinic acetylcholine receptors; calcium NICOTINIC ACETYLCHOLINE RECEPTORS (nAChRs) mediate the excitability of neuronal circuits related to the memory, motivation, and mood (15, 16), are reduced in neurodegenerative and neuropsychiatric disorders such as schizophrenia and Alzheimer's disease (6,22,24), and have been proposed as potential therapeutic targets for these diseases (13,28).At least four different nAChR subtypes, non-␣ 7 (␣ 2 , ␣ 3 ␤ 4 , ␣ 4 ␤ 2 )-and ␣ 7 -nAChRs, are expressed in the cortex. The most commonly expressed nAChR subtype is the ␣ 4 ␤ 2 -receptor (90%), which is characterized by its high affinity for acetylcholine (ACh) and nicotinic agonists (10,30 ] i oscillations are implicated in the regulation of neural plasticity (3, 26), which may be related to the increased efficiency and specificity of gene expression. Studies show both oscillation amplitude and frequency are critical for the regulation of gene expression and transcription (14,25).Although it has been reported that activation of nAChRs induces [Ca 2ϩ ] i oscillations, which is mediated by Ca 2ϩ influx and melatonin release from pinealocytes (17), the effect of nicotine on [Ca 2ϩ ] i oscillations in cortical neurons has not been reported. In this study, we investigated the nicotinic modulation of [Ca 2ϩ ] i oscillations in rat cortical neurons in primary culture and found that nicotinic enhancement of the oscillatory Ca 2ϩ signals is mediated through both ␣ 4 ␤ 2 -and ␣ 7 -nAChRs. MATERIALS AND METHODS Cortical neuronal cultures.Primary cultures of cortical neurons were prepared from 17-to 18-day-old Sprague-Dawley rat embryos as described previously (14a). All cell culture reagents were purchased from Invitrog...

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Section: Discussionsupporting

confidence: 57%

Nicotinic modulation of Ca²⁺ oscillations in rat cortical neurons in vitro

Wang

Guo

et al. 2016

American Journal of Physiology-Cell Physiology

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“…Hence, we wondered whether ion channels could be involved in transducing matrix mechanical cues to intracellular signaling pathways linked to lineage specification. In particular, we focused here on cationic stretch-activated channels (SACs) because they are known to detect mechanical forces with high sensitivity and broad dynamic range and because they are permeable to Ca 2+ , an important second messenger implicated in cell fate (14,15). We examined the role of SACs in neural stem cells, for which mechanical cues influence specification along the neuronal-glial lineage (8,16,17).…”

mentioning

confidence: 99%

Stretch-activated ion channel Piezo1 directs lineage choice in human neural stem cells

Pathak¹,

Nourse

Tran³

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

487

509

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Neural stem cells are multipotent cells with the ability to differentiate into neurons, astrocytes, and oligodendrocytes. Lineage specification is strongly sensitive to the mechanical properties of the cellular environment. However, molecular pathways transducing matrix mechanical cues to intracellular signaling pathways linked to lineage specification remain unclear. We found that the mechanically gated ion channel Piezo1 is expressed by brainderived human neural stem/progenitor cells and is responsible for a mechanically induced ionic current. Piezo1 activity triggered by traction forces elicited influx of Ca 2+ , a known modulator of differentiation, in a substrate-stiffness-dependent manner. Inhibition of channel activity by the pharmacological inhibitor GsMTx-4 or by siRNA-mediated Piezo1 knockdown suppressed neurogenesis and enhanced astrogenesis. Piezo1 knockdown also reduced the nuclear localization of the mechanoreactive transcriptional coactivator Yes-associated protein. We propose that the mechanically gated ion channel Piezo1 is an important determinant of mechanosensitive lineage choice in neural stem cells and may play similar roles in other multipotent stem cells. (5) and that the mechanical properties of the culturing environment before transplantation can influence the outcome of in vivo stem cell transplants (6). Hence, a molecular and mechanistic understanding of how stem cells process mechanical cues and how this processing results in downstream signaling events and ultimately in fate decisions is needed for greater control over the fate of transplanted cells.Studies in mesenchymal and neural stem cells have revealed the involvement of focal adhesion zones and cytoskeletal proteins, such as integrins, nonmuscle myosin II (7), Rho GTPases (8-10), and vinculin (11), that participate in the generation of cellular traction forces. Recent work also has identified the nucleoskeletal protein lamin-A (12) and the transcriptional coactivators Yap (Yesassociated protein) and Taz (transcriptional coactivator with PDZbinding motif) (13) in mechanotransduction in mesenchymal stem cells. However, the mechanisms by which mechanical cues detected by cellular traction forces are transduced to downstream intracellular pathways of differentiation remain unclear.Ion channels are involved, directly or indirectly, in the transduction of all forms of physical stimuli-including sound, light, temperature, mechanical force, and even gravity-into intracellular signaling pathways. Hence, we wondered whether ion channels could be involved in transducing matrix mechanical cues to intracellular signaling pathways linked to lineage specification. In particular, we focused here on cationic stretch-activated channels (SACs) because they are known to detect mechanical forces with high sensitivity and broad dynamic range and because they are permeable to Ca 2+ , an important second messenger implicated in cell fate (14,15). We examined the role of SACs in neural stem cells, for which mechanical cues influence specification alo...

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“…Cells of cardiac and vascular tissues, for example, withstand more stress, and their Ca 2+ buffering ability is higher than other cells [28,29]. There are many studies in various matured cells on the patterns of the Ca 2+ oscillations regulated by signaling proteomes [30].…”

Section: Mesenchymal Stem Cells React Differently To Stress Pathologymentioning

confidence: 99%

“…Though low Ca 2+ levels are favorable for all cells in general, higher Ca 2+ levels beyond the threshold are detrimental to MSCs. In general, the physiological role of the Ca 2+ homeostasis largely regulates differentiation, proliferation and cell survival at the site of repair [30]. Studies have revealed the Ca 2+ handling properties of the precursors are similar to the adult differentiated cells as observed in the neuronal precursors compared with differentiated neuronal cells.…”

Section: Mesenchymal Stem Cells React Differently To Stress Pathologymentioning

confidence: 99%

Mesenchymal Stem Cells: A Future Option for Intervening Disease Management

Chandramoorthy¹,

Radhakrishnan²,

Gurusamy³

2017

Mesenchymal Stem Cells - Isolation, Characterization and Applications

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Regeneration, revitalizing and reversal (RRR) are the primordial functions of the stem cells in the field of regenerative medicine. Though there are several cases of successful stem cell transplantation the reversal of metabolic diseases and the acquired secondary complications like chronic renal failure, neuropathy, stroke or vascular diseases are not well studied. The transplanted cells in many cases failed to home or graft in the host with no reason to attribute for such failures. Therefore, it becomes necessary to address these secondary complications with cellular therapy. The oxidative stress of the cells and tissues are attributed to the hostile microenvironment, not suitable for the survival of newly recruited cells. From our few animal studies and published literatures sources elsewhere, we foresee a huge potential for using mesenchymal stem cells (MSCs) to initially combat the secondary cardiovascular and neuronal complications in the management of the metabolic diseases. However, not all the stem cells have been tested in these lines, and further we do not know, whether all the progenitor cells from various sources and origin will behave like MSCs, which needs to be studied extensively.

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Stem Cells and Calcium Signaling

Cited by 120 publications

References 123 publications

Nicotinic modulation of Ca²⁺ oscillations in rat cortical neurons in vitro

Nicotinic modulation of Ca²⁺ oscillations in rat cortical neurons in vitro

Stretch-activated ion channel Piezo1 directs lineage choice in human neural stem cells

Mesenchymal Stem Cells: A Future Option for Intervening Disease Management

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Stem Cells and Calcium Signaling

Cited by 120 publications

References 123 publications

Nicotinic modulation of Ca2+ oscillations in rat cortical neurons in vitro

Nicotinic modulation of Ca2+ oscillations in rat cortical neurons in vitro

Stretch-activated ion channel Piezo1 directs lineage choice in human neural stem cells

Mesenchymal Stem Cells: A Future Option for Intervening Disease Management

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Product

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Nicotinic modulation of Ca²⁺ oscillations in rat cortical neurons in vitro

Nicotinic modulation of Ca²⁺ oscillations in rat cortical neurons in vitro