Transient receptor potential canonical channel 1 impacts on mechanosignaling during cell migration

Fabian, Anke; Bertrand, Jessica; Lindemann, Otto; Pap, Thomas; Schwab, Albrecht

doi:10.1007/s00424-012-1169-9

Cited by 29 publications

(20 citation statements)

References 33 publications

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“…We determined the intracellular Ca 2+ concentration ([Ca 2+ ] i ) ratiometrically with the fluorescent Ca 2+ indicator fura-2 as described previously [54]. Cells were plated on glass bottom dishes (Willco, Amsterdam, The Netherlands) coated with a basement membrane-like matrix and pretreated in the same way as for migration experiments.…”

Section: Methodsmentioning

confidence: 99%

Ion channels in control of pancreatic stellate cell migration

Storck¹,

Hild²,

Schimmelpfennig³

et al. 2016

Oncotarget

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Pancreatic stellate cells (PSCs) play a critical role in the progression of pancreatic ductal adenocarcinoma (PDAC). Once activated, PSCs support proliferation and metastasis of carcinoma cells. PSCs even co-metastasise with carcinoma cells. This requires the ability of PSCs to migrate. In recent years, it has been established that almost all “hallmarks of cancer” such as proliferation or migration/invasion also rely on the expression and function of ion channels. So far, there is only very limited information about the function of ion channels in PSCs. Yet, there is growing evidence that ion channels in stromal cells also contribute to tumor progression. Here we investigated the function of KCa3.1 channels in PSCs. KCa3.1 channels are also found in many tumor cells of different origin. We revealed the functional expression of KCa3.1 channels by means of Western blot, immunofluorescence and patch clamp analysis. The impact of KCa3.1 channel activity on PSC function was determined with live-cell imaging and by measuring the intracellular Ca2+ concentration ([Ca2+]i). KCa3.1 channel blockade or knockout prevents the stimulation of PSC migration and chemotaxis by reducing the [Ca2+]i and calpain activity. KCa3.1 channels functionally cooperate with TRPC3 channels that are upregulated in PDAC stroma. Knockdown of TRPC3 channels largely abolishes the impact of KCa3.1 channels on PSC migration. In summary, our results clearly show that ion channels are crucial players in PSC physiology and pathophysiology.

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Section: Methodsmentioning

confidence: 99%

Ion channels in control of pancreatic stellate cell migration

Storck¹,

Hild²,

Schimmelpfennig³

et al. 2016

Oncotarget

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“…We showed that the composition of the mRNA maternal pool of X. tropicalis includes the transcripts of eight non selective cation mechanosen sitive TRP channels. It is essential that the activity of these channels is not only able to depolarize or indi rectly hyperpolarize cell membranes (which itself can regulate cell motility and differentiation) but is also able to regulate the dynamics of cytoplasmic Ca 2+ concentration of [12,14,15], which is an extremely TRPV1 TRPV2 TRPV4 TRPM7 TRPC3 TRPC5 TRPC6 TRPM4 TRPC1 TRPA1 PKD1 PKD2 ODC RT- important secondary messenger. Note that we found the mRNA expression of these channels but not the protein expression.…”

Section: Discussionmentioning

confidence: 99%

“…Almost all TRP channels are expressed in the nervous system of vertebrates, and may be involved in the perception of mechanical influ ences, cold, heat, pH or chemical factors. An analysis of the scientific literature revealed TRP ion channels that can be activated in response to a mechanical stim ulus, which, in turn, leads to the regulation of mor phogenesis and differentiation [11][12][13][14][15]. Today, it is known that the following TRP channels are mecha nosensitive: TRPC1, 3, 5, 6, TRPV1, 2, 4, TRPM4, 7, TRPP2 (PKD2) and TRPA1, although, for some of them, this fact is not yet proven conclu sively [11,12].…”

Section: Introductionmentioning

confidence: 99%

Spatio-temporal expression pattern of mechanosensitive TRP ion channels during early development of Xenopus tropicalis

Silina

Никишин

Kremnyov

2015

Biochem. Moscow Suppl. Ser. A

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It is known that endogenous mechanical stress in the tissues of developing organisms is involved in regulating both morphogenesis and cell differentiation. These processes can be regulated by bioelectrical signals. Mechanosensitive ion channels are the structures that transform the mechanical stimulus into the bioelectrical signal. In this work we study the expression of mechanosensitive TRP ion channels during early development of Xenopus tropicalis. Real time RT PCR and PCR show the spatio temporal expression of mRNA of mechanosensitive TRP ion channels during the early development of Xenopus tropicalis.

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“…TRPC1 was found to mediate mechanosensitive currents in neuronal cells (Kerstein et al 2013), migrating Madin-Darby canine kidney (MDCK) cells (Fabian et al 2008(Fabian et al , 2012, mouse brain microvessel endothelial cells (Berrout et al 2012), and primary afferent sensory neurons (Garrison et al 2012). …”

Section: Functionmentioning

confidence: 99%

Trpc1

Nesin

Tsiokas

2014

Handbook of Experimental Pharmacology

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The TRPC1 ion channel was the first mammalian TRP channel to be cloned. In humans, it is encoded by the TRPC1 gene located in chromosome 3. The protein is predicted to consist of six transmembrane segments with the N- and C-termini located in the cytoplasm. The extracellular loop connecting transmembrane segments 5 and 6 participates in the formation of the ionic pore region. Inside the cell, TRPC1 is present in the endoplasmic reticulum, plasma membrane, intracellular vesicles, and primary cilium, an antenna-like sensory organelle functioning as a signaling platform. In human and rodent tissues, it shows an almost ubiquitous expression. TRPC1 interacts with a diverse group of proteins including ion channel subunits, receptors, and cytosolic proteins to mediate its effect on Ca(2+) signaling. It primarily functions as a cation nonselective channel within pathways controlling Ca(2+) entry in response to cell surface receptor activation. Through these pathways, it affects basic cell functions, such as proliferation and survival, differentiation, secretion, and cell migration, as well as cell type-specific functions such as chemotropic turning of neuronal growth cones and myoblast fusion. The biological role of TRPC1 has been studied in genetically engineered mice where the Trpc1 gene has been experimentally ablated. Although these mice live to adulthood, they show defects in several organs and tissues, such as the cardiovascular, central nervous, skeletal and muscular, and immune systems. Genetic and functional studies have implicated TRPC1 in diabetic nephropathy, Parkinson's disease, Huntington's disease, Duchenne muscular dystrophy, cancer, seizures, and Darier-White skin disease.

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Transient receptor potential canonical channel 1 impacts on mechanosignaling during cell migration

Cited by 29 publications

References 33 publications

Ion channels in control of pancreatic stellate cell migration

Ion channels in control of pancreatic stellate cell migration

Spatio-temporal expression pattern of mechanosensitive TRP ion channels during early development of Xenopus tropicalis

Trpc1

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