Canonical Transient Receptor Potential 1 Plays a Role in Basic Fibroblast Growth Factor (bFGF)/FGF Receptor-1-Induced Ca<sup>2</sup>+ Entry and Embryonic Rat Neural Stem Cell Proliferation

Fiorio, Alessandra; Maric, Dragan; Brazer, So-ching W.; Giacobini, Paolo; Liu, Xibao; Chang, Yoong Hee; Ambudkar, Indu S.; Barker, Jeffery L.

doi:10.1523/jneurosci.0951-04.2005

Cited by 144 publications

(101 citation statements)

References 46 publications

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“…In particular, TRPV1 and TRPV4 are gated by AA metabolites, and TRPV3 and TRPC4 are gated directly by AA itself (56)(57)(58)(59). Finally, some members of the TRP family of channels are involved in growth factorinduced calcium entry with a consequent role in cell cycle progression (60,61).…”

Section: Discussionmentioning

confidence: 99%

Arachidonic Acid–Induced Ca2+ Entry Is Involved in Early Steps of Tumor Angiogenesis

Fiorio

Grange

Antoniotti

et al. 2008

Molecular Cancer Research

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Growth factor -induced intracellular calcium signals in endothelial cells regulate cytosolic and nuclear events involved in the angiogenic process. Among the intracellular messengers released after proangiogenic stimulation, arachidonic acid (AA) plays a key role and its effects are strictly related to calcium homeostasis and cell proliferation. Here, we studied AA-induced intracellular calcium signals in endothelial cells derived from human breast carcinomas (B-TEC). AA promotes B-TEC proliferation and organization of vessel-like structures in vitro. The effect is directly mediated by the fatty acid without a significant contribution of its metabolites. AA induces Ca 2+ i signals in the entire capillary-like structure during the early phases of tubulogenesis in vitro. No such responses are detectable in B-TECs organized in more structured tubules. In B-TECs growing in monolayer, AA induces two different signals: a Ca 2+ i increase due to Ca 2+ entry and an inhibition of store-dependent Ca 2+ entry induced by thapsigargin or ATP. An inhibitor of Ca 2+ entry and angiogenesis, carboxyamidotriazole, significantly and specifically decreases AA-induced B-TEC tubulogenesis, as well as AA-induced Ca 2+ signals in B-TECs. We conclude that (a) AA-activated Ca 2+ entry is associated with the progression through the early phases of angiogenesis, mainly involving proliferation and tubulogenesis, and it is down-regulated during the reorganization of tumor-derived endothelial cells in capillary-like structures; and (b) inhibition of AA-induced Ca 2+ entry may contribute to the antiangiogenic action of carboxyamidotriazole. (Mol Cancer Res 2008;6(4):535 -45)

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Section: Discussionmentioning

confidence: 99%

Arachidonic Acid–Induced Ca2+ Entry Is Involved in Early Steps of Tumor Angiogenesis

Fiorio

Grange

Antoniotti

et al. 2008

Molecular Cancer Research

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“…This indicates that NF-B-induced TRPC1 expression is critical for cell proliferation/survival. TRPC1 and other members of its family, involved in SOCE, have been associated with cell proliferation and the level of expression of different TRP proteins has been linked with the proliferative capacity of different cell lineages (Pla et al, 2005). SOCE is implicated in activating signaling cascades, influencing cell division and promoting cell proliferation (Berridge et al, 2000;Golovina et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

“…In recent years, 28 mammalian members of the TRP superfamily have been identified, which are activated by diverse stimuli including heat, pressure, activation of G protein-coupled receptors, and intracellular store depletion (Moran et al, 2004). TRP channels are involved in a multitude of physiological events, which include secretion, pain transduction, osmoregulation, mechanosensitivity, cell growth, and differentiation (Moran et al, 2004;Pla et al, 2005).Growth and differentiation of keratinocytes is exquisitely determined by the [Ca 2ϩ ] i in the medium and the cytosol as well. However, the mechanism of this Ca 2ϩ -dependent regulation is not elaborately investigated.…”

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confidence: 99%

Up-Regulation of Transient Receptor Potential Canonical 1 (TRPC1) following Sarco(endo)plasmic Reticulum Ca²⁺ATPase 2 Gene Silencing Promotes Cell Survival: A Potential Role for TRPC1 in Darier's Disease

Pani

Cornatzer²,

Cornatzer

et al. 2006

MBoC

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The mechanism(s) involved in regulation of store operated calcium entry in Darier's disease (DD) is not known. We investigated the distribution and function of transient receptor potential canonical (TRPC) in epidermal skin cells. DD patients demonstrated up-regulation of TRPC1, but not TRPC3, in the squamous layers. Ca 2؉ influx was significantly higher in keratinocytes obtained from DD patients and showed enhanced proliferation compared with normal keratinocytes. Similar up-regulation of TRPC1 was also detected in epidermal layers of SERCA2 ؉/؊ mice. HaCaT cells expressed TRPC1 in the plasma membrane. Expression of sarco(endo)plasmic reticulum Ca 2؉ ATPase (SERCA)2 small interfering RNA (siRNA) in HaCaT cells increased TRPC1 levels and thapsigargin-stimulated Ca 2؉ influx, which was blocked by store-operated calcium entry inhibitors. Thapsigargin-stimulated intracellular Ca 2؉ release was decreased in DD cells. DD keratinocytes exhibited increased cell survival upon thapsigargin treatment. Alternatively, overexpression of TRPC1 or SERCA2-siRNA in HaCaT cells demonstrated resistance to thapsigargin-induced apoptosis. These effects were dependent on external Ca 2؉ and activation of nuclear factor-B. Isotretinoin reduced Ca 2؉ entry in HaCaT cells and decreased survival of HaCaT and DD keratinocytes. These findings put forward a novel consequence of compromised SERCA2 function in DD wherein up-regulation of TRPC1 augments cell proliferation and restrict apoptosis. We suggest that the anti-apoptotic effect of TRPC1 could potentially contribute to abnormal keratosis in DD. INTRODUCTIONDarier's disease (DD) is an autosomal dominant inherited skin disease, which is characterized by the loss of adhesion between epidermal cells and abnormal keratinization (Burge and Wilkinson 1992). Typical histological findings include focal areas of separation between suprabasal epidermal cells, unusual dyskeratosis with round dyskeratotic keratinocytes (Munro, 1992). Mutations in the sarco(endo)plasmic reticulum Ca 2ϩ ATPase (SERCA) isoform 2b (SERCA2b) gene leads to a loss of function, and these mutations have been shown to cause DD (Sakuntabhai et al., 1999). Most physiological systems are able to compensate for the loss of function of SERCA2b, possibly because of expression of other SERCA isoforms within those tissues (Dhitavat et al., 2003;Tavadia et al., 2004). However, of the multiple isoforms of SERCA1, -2, or -3, only SERCA2b is expressed in keratinocytes (Lytton and MacLennan, 1988;Ruiz-Perez et al., 1999). The mutated SERCA2 fails to sequester cytosolic Ca 2ϩ into the endoplasmic reticulum (ER) lumen, thereby disturbing the otherwise normal Ca 2ϩ homeostasis circuitry within the cells (Zhao et al., 2001;Ahn et al., 2003). Although oral retinoids, such as isotretinoin, have been shown to reduce hyperkeratosis (Burge and Wilkinson, 1992), the mechanism behind dysfunction of SERCA2 resulting in keratosis remains elusive.Ca 2ϩ is an integral signaling element that regulates numerous cellular processes (Clapham, 1995;Berridge e...

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“…Conditions for SDS-PAGE and Western blotting were as described previously (27). Polyvinylidene difluoride membranes were blocked and incubated for 1 hour with rabbit IgG anti-eNOS phosphorylated at Ser 1179 of the bovine eNOS (corresponding to human Ser 1177 ) antibody (Zymed, Invitrogen).…”

Section: Protein Extraction and Western Blot Analysismentioning

confidence: 99%

Multiple Roles of Protein Kinase A in Arachidonic Acid–Mediated Ca2+ Entry and Tumor-Derived Human Endothelial Cell Migration

Fiorio

Genova

Pupo

et al. 2010

Molecular Cancer Research

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We recently showed that arachidonic acid (AA) triggers calcium signals in endothelial cells derived from human breast carcinoma (B-TEC). In particular, AA-dependent Ca 2+ entry is involved in the early steps of tumor angiogenesis in vitro. Here, we investigated the multiple roles of the nitric oxide (NO) and cyclic AMP/protein kinase A (PKA) pathways in AA-mediated Ca 2+ signaling in the same cells. B-TEC stimulation with 5 μmol/L AA resulted in endothelial NO synthase (NOS) phosphorylation at Ser 1177 , and NO release was measured with the fluorescent NO-sensitive probe DAR4M-AM. PKA inhibition by the use of the membrane-permeable PKA inhibitory peptide myristoylated PKI 14-22 completely prevented both AA-and NOinduced calcium entry and abolished B-TEC migration promoted by AA. AA-dependent calcium entry and cell migration were significantly affected by both the NOS inhibitor N G -nitro-L-arginine methyl ester and the NO scavenger 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl 3-oxide, suggesting that NO release is functionally involved in the signaling dependent on AA. Moreover, pretreatment with carboxyamidotriazole, an antiangiogenic compound that interferes with agonist-activated calcium entry, prevented AA-dependent B-TEC motility. Interestingly, even in the absence of AA, enhancement of the cyclic AMP/PKA pathway with the adenylyl cyclase activator forskolin evoked a calcium entry dependent on NOS recruitment and NO release. The functional relevance of AA-induced calcium entry could be restricted to tumor-derived endothelial cells (EC) because AA evoked a smaller calcium entry in normal human microvascular ECs compared with B-TECs, and even more importantly, it was unable to promote cell motility in wound healing assay. This evidence opens an intriguing opportunity for differential pharmacologic treatment between normal and tumor-derived human ECs.

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Canonical Transient Receptor Potential 1 Plays a Role in Basic Fibroblast Growth Factor (bFGF)/FGF Receptor-1-Induced Ca²+ Entry and Embryonic Rat Neural Stem Cell Proliferation

Cited by 144 publications

References 46 publications

Arachidonic Acid–Induced Ca2+ Entry Is Involved in Early Steps of Tumor Angiogenesis

Arachidonic Acid–Induced Ca2+ Entry Is Involved in Early Steps of Tumor Angiogenesis

Up-Regulation of Transient Receptor Potential Canonical 1 (TRPC1) following Sarco(endo)plasmic Reticulum Ca²⁺ATPase 2 Gene Silencing Promotes Cell Survival: A Potential Role for TRPC1 in Darier's Disease

Multiple Roles of Protein Kinase A in Arachidonic Acid–Mediated Ca2+ Entry and Tumor-Derived Human Endothelial Cell Migration

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Canonical Transient Receptor Potential 1 Plays a Role in Basic Fibroblast Growth Factor (bFGF)/FGF Receptor-1-Induced Ca2+ Entry and Embryonic Rat Neural Stem Cell Proliferation

Cited by 144 publications

References 46 publications

Arachidonic Acid–Induced Ca2+ Entry Is Involved in Early Steps of Tumor Angiogenesis

Arachidonic Acid–Induced Ca2+ Entry Is Involved in Early Steps of Tumor Angiogenesis

Up-Regulation of Transient Receptor Potential Canonical 1 (TRPC1) following Sarco(endo)plasmic Reticulum Ca2+ATPase 2 Gene Silencing Promotes Cell Survival: A Potential Role for TRPC1 in Darier's Disease

Multiple Roles of Protein Kinase A in Arachidonic Acid–Mediated Ca2+ Entry and Tumor-Derived Human Endothelial Cell Migration

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Canonical Transient Receptor Potential 1 Plays a Role in Basic Fibroblast Growth Factor (bFGF)/FGF Receptor-1-Induced Ca²+ Entry and Embryonic Rat Neural Stem Cell Proliferation

Up-Regulation of Transient Receptor Potential Canonical 1 (TRPC1) following Sarco(endo)plasmic Reticulum Ca²⁺ATPase 2 Gene Silencing Promotes Cell Survival: A Potential Role for TRPC1 in Darier's Disease