Calcium signaling in vertebrate embryonic patterning and morphogenesis

Slusarski, Diane C.; Pelegri, Francisco

doi:10.1016/j.ydbio.2007.04.043

Cited by 143 publications

(116 citation statements)

References 173 publications

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“…In addition to the canonical Wnt pathway, two non-canonical Wnt pathways exist: the planar cell polarity (PCP) pathway (Fanto and McNeill, 2004) and the calcium pathway (Slusarski and Pelegri, 2007). Especially, ROCK has been shown to mediate the PCP pathway (Marlow et al, 2002).…”

Section: Consequently Sh-sy5y Cells May Fulfill the Definitions Of Nmentioning

confidence: 99%

ROCK2 regulates bFGF-induced proliferation of SH-SY5Y cells through GSK-3β and β-catenin pathway

Boku¹,

Nakagawa²,

Toda³

et al. 2013

Brain Research

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Increased neurogenesis by promoting proliferation of neural precursor cells in the adult dentate gyrus might be beneficial for the treatment of psychiatric disorders. Results demonstrate that bFGF is necessary for the proliferation of neural precursor cells and that the glycogen synthase kinase-3β (GSK-3β) and β-catenin pathway plays a role in it. However, the detailed mechanism of proliferation of neural precursor cells remains unclear. To elucidate that mechanism, we investigated the role of Rho-associated coiled-coil kinase (ROCK) in bFGF-induced proliferation using SH-SY5Y cells as a model of neural precursor-like cells. Y27632, a specific inhibitor of ROCK, decreased bFGF-induced proliferation. Lithium (Li), an inhibitor of GSK-3β, recovered Y27632-decreased proliferation and quercetin (Que), an inhibitor of β-catenin pathway, reversed the recovery effect of Li. Both nuclear β-catenin and cyclin D1 expression were altered by bFGF, Y27632, Li, and Que in parallel with the case of proliferation. Furthermore, bFGF inactivated GSK-3β through increasing the phosphorylation of Ser 9 on GSK-3β, which is reversed by Y27632 through increased phosphorylation of Tyr 216 on GSK-3β. ROCK has two subtypes: ROCK1 and ROCK2. Investigation with siRNA for ROCKs showed that ROCK2 is involved in bFGF-induced proliferation, but not ROCK1. These results suggest that ROCK2 might mediate bFGF-induced proliferation of SH-SY5Y cells through GSK-3β and β-catenin pathway. Further investigation of detailed mechanisms regulating the ROCK2/GSK-3β/β-catenin pathway might engender the development of new therapeutic targets of psychiatric disorders.

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Section: Consequently Sh-sy5y Cells May Fulfill the Definitions Of Nmentioning

confidence: 99%

ROCK2 regulates bFGF-induced proliferation of SH-SY5Y cells through GSK-3β and β-catenin pathway

Boku¹,

Nakagawa²,

Toda³

et al. 2013

Brain Research

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“…67 WNT/CA 2+ PATHWAY The Wnt/Ca 2+ pathway may function as a critical modulator of both canonical and Wnt/JNK/PCP pathways. 1 Wnt/Fz (specifically Wnt-5a, Wnt-11) 68,69 activates phospholipase C via the trimeric G protein, resulting in the generation of diacylglycerol and inositol triphosphate. The latter increases intracellular Ca 2+ levels and Ca 2+ fluxes.…”

Section: Canonical Wnt Pathwaymentioning

confidence: 99%

Potential cross-talk between (pro)renin receptors and Wnt/frizzled receptors in cardiovascular and renal disorders

Balakumar

Jagadeesh

2011

Hypertens Res

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The renin-angiotensin system and Wnt/frizzled receptor signaling pathways are important in the development of essential organs, and their aberrant activation results in cardiovascular and renal pathologies. The (pro)renin receptor ((P)RR)-bound (pro)renin is enzymatically active generating angiotensin-II and activating mitogen-activated protein kinases, leading to cell proliferation and to upregulation of profibrotic genes expression, resulting in end-organ damage. The (P)RR does more than bind to (pro)renin, because it is functionally linked to the vacuolar-H + -ATPase (v-H + -ATPase) that regulates pH of cellular and intracellular vesicles, and to Wnt signaling. This signaling pathway is essential for cell survival, embryonic development and has had a role in various disease states as evidenced by mutation or genetic ablation of the (P)RR gene. This suggests two types of functions of (P)RRs, first one as a receptor for (pro)renin and second one as an accessory subunit of the v-H + -ATPase and a cofactor of the Wnt/Fz receptor complex. This review will discuss both of these functions of (P)RRs thereby giving new perspectives as to the roles of (P)RRs in cardiovascular and renal pathologies.

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“…Ion channels, integrin signaling, and the primary cilia have all been implicated in transducing the external biophysical environment of chondrocytes into electrical and/or chemical intracellular signaling (7)(8)(9). Specifically, intracellular Ca 2+ signaling has emerged as a common regulatory mechanism for controlling gene and protein expression (10)(11)(12).…”

mentioning

confidence: 99%

TRPV4-mediated mechanotransduction regulates the metabolic response of chondrocytes to dynamic loading

O’Conor

Leddy

Benefield

et al. 2014

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

384

448

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Mechanical loading of joints plays a critical role in maintaining the health and function of articular cartilage. The mechanism(s) of chondrocyte mechanotransduction are not fully understood, but could provide important insights into new physical or pharmacologic therapies for joint diseases. Transient receptor potential vanilloid 4 (TRPV4), a Ca 2+ -permeable osmomechano-TRP channel, is highly expressed in articular chondrocytes, and loss of TRPV4 function is associated with joint arthropathy and osteoarthritis. The goal of this study was to examine the hypothesis that TRPV4 transduces dynamic compressive loading in articular chondrocytes. We first confirmed the presence of physically induced, TRPV4-dependent intracellular Ca 2+ signaling in agarose-embedded chondrocytes, and then used this model system to study the role of TRPV4 in regulating the response of chondrocytes to dynamic compression. Inhibition of TRPV4 during dynamic loading prevented acute, mechanically mediated regulation of proanabolic and anticatabolic genes, and furthermore, blocked the loadinginduced enhancement of matrix accumulation and mechanical properties. Furthermore, chemical activation of TRPV4 by the agonist GSK1016790A in the absence of mechanical loading similarly enhanced anabolic and suppressed catabolic gene expression, and potently increased matrix biosynthesis and construct mechanical properties. These findings support the hypothesis that TRPV4-mediated Ca 2+ signaling plays a central role in the transduction of mechanical signals to support cartilage extracellular matrix maintenance and joint health. Moreover, these insights raise the possibility of therapeutically targeting TRPV4-mediated mechanotransduction for the treatment of diseases such as osteoarthritis, as well as to enhance matrix formation and functional properties of tissue-engineered cartilage as an alternative to bioreactor-based mechanical stimulation. mechanobiology | ion channel | calcium signaling | TGF-beta | tissue engineering

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Calcium signaling in vertebrate embryonic patterning and morphogenesis

Cited by 143 publications

References 173 publications

ROCK2 regulates bFGF-induced proliferation of SH-SY5Y cells through GSK-3β and β-catenin pathway

ROCK2 regulates bFGF-induced proliferation of SH-SY5Y cells through GSK-3β and β-catenin pathway

Potential cross-talk between (pro)renin receptors and Wnt/frizzled receptors in cardiovascular and renal disorders

TRPV4-mediated mechanotransduction regulates the metabolic response of chondrocytes to dynamic loading

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