TRPC1 regulates fMLP-stimulated migration and chemotaxis of neutrophil granulocytes

Lindemann, Otto; Strodthoff, C.; Horstmann, Martin; Nielsen, Nikoline Juul; Jung, F; Schimmelpfennig, Sandra; Heitzmann, Marianne; Schwab, Albrecht

doi:10.1016/j.bbamcr.2014.12.037

Cited by 35 publications

(31 citation statements)

References 41 publications

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“…· decreased endothelial transmigration of neutrophils · decreased inflammatory response and ineffective bacterial clearance · no pulmonary hypertension response to chronic hypoxia and reduced vascular muscularisation Lindemann et al, 2015;Malczyk et al, 2013;Zhou et al, 2015 …”

Section: Trpc1 -/-mentioning

confidence: 99%

The role of transient receptor potential channels in joint diseases

Krupková

Zvick²,

Wuertz‐Kozak³

2017

eCM

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Transient receptor potential channels (TRP channels) are cation selective transmembrane receptors with diverse structures, activation mechanisms and physiological functions. TRP channels act as cellular sensors for a plethora of stimuli, including temperature, membrane voltage, oxidative stress, mechanical stimuli, pH and endogenous as well as exogenous ligands, thereby illustrating their versatility. As such, TRP channels regulate various functions in both excitable and non-excitable cells, mainly by mediating Ca 2+ homeostasis. Dysregulation of TRP channels is implicated in many pathologies, including cardiovascular diseases, muscular dystrophies and hyperalgesia. However, the importance of TRP channel expression, physiological function and regulation in chondrocytes and intervertebral disc (IVD) cells is largely unexplored. Osteoarthritis (OA) and degenerative disc disease (DDD) are chronic age-related disorders that significantly affect the quality of life by causing pain, activity limitation and disability. Furthermore, currently available therapies cannot effectively slow-down or stop progression of these diseases. Both OA and DDD are characterised by reduced tissue cellularity, enhanced inflammatory responses and molecular, structural and mechanical alterations of the extracellular matrix, hence affecting load distribution and reducing joint flexibility. However, knowledge on how chondrocytes and IVD cells sense their microenvironment and respond to its changes is still limited. In this review, we introduced six families of mammalian TRP channels, their mechanisms of activation as well as activation-driven cellular consequences. We summarised the current knowledge on TRP channel expression and activity in chondrocytes and IVD cells and the significance of TRP channels as therapeutic targets for the treatment of OA and DDD.

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Section: Trpc1 -/-mentioning

confidence: 99%

The role of transient receptor potential channels in joint diseases

Krupková

Zvick²,

Wuertz‐Kozak³

2017

eCM

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“…fMLP-stimulated increase in [Ca 2+ ] i plays an important role in the functional responses of human neutrophils such as respiratory burst, chemotaxis, and degranulation [454647]. There is some controversy in the effect of NAC on fMLP-induced respiratory burst in human neutrophils.…”

Section: Discussionmentioning

confidence: 99%

N-acetyl-L-cysteine and cysteine increase intracellular calcium concentration in human neutrophils

Hasan

Ahn

Song

2016

Korean J Physiol Pharmacol

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N-acetyl-L-cysteine (NAC) and cysteine have been implicated in a number of human neutrophils' functional responses. However, though Ca2+ signaling is one of the key signalings contributing to the functional responses of human neutrophils, effects of NAC and cysteine on intracellular calcium concentration ([Ca2+]i) in human neutrophils have not been investigated yet. Thus, this study was carried out with an objective to investigate the effects of NAC and cysteine on [Ca2+]i in human neutrophils. We observed that NAC (1 µM ~ 1 mM) and cysteine (10 µM ~ 1 mM) increased [Ca2+]i in human neutrophils in a concentration-dependent manner. In NAC pre-supplmented buffer, an additive effect on N-formyl-methionine-leucine-phenylalanine (fMLP)-induced increase in [Ca2+]i in human neutrophils was observed. In Ca2+-free buffer, NAC- and cysteine-induced [Ca2+]i increase in human neutrophils completely disappeared, suggesting that NAC- and cysteine-mediated increase in [Ca2+]i in human neutrophils occur through Ca2+ influx. NAC- and cysteine-induced [Ca2+]i increase was effectively inhibited by calcium channel inhibitors SKF96365 (10 µM) and ruthenium red (20 µM). In Na+-free HEPES, both NAC and cysteine induced a marked increase in [Ca2+]i in human neutrophils, arguing against the possibility that Na+-dependent intracellular uptake of NAC and cysteine is necessary for their [Ca2+]i increasing activity. Our results show that NAC and cysteine induce [Ca2+]i increase through Ca2+ influx in human neutrophils via SKF96365- and ruthenium red-dependent way.

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“…TRPC1 may primarily function as a regulator of neutrophil migration and chemotaxis. TRPC1 −/− mPMNs were described to display reduced migratory and chemotactic properties following fMLF stimulation . Surprisingly, Ca 2+ influx was not diminished in TRPC1 −/− mPMNs, but rather increased.…”

Section: Other Ion Channels Involved In Ca2+ Signalling In Neutrophilsmentioning

confidence: 94%

Calcium signalling and related ion channels in neutrophil recruitment and function

Immler

Simon

Sperandio

2018

Eur J Clin Investigation

108

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The recruitment of neutrophils to sites of inflammation, their battle against invading microorganisms through phagocytosis and the release of antimicrobial agents is a highly coordinated and tightly regulated process that involves the interplay of many different receptors, ion channels and signalling pathways. Changes in intracellular calcium levels, caused by cytosolic Ca store depletion and the influx of extracellular Ca via ion channels, play a critical role in synchronizing neutrophil activation and function. In this review, we provide an overview of how Ca signalling is initiated in neutrophils and how changes in intracellular Ca levels modulate neutrophil function.

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TRPC1 regulates fMLP-stimulated migration and chemotaxis of neutrophil granulocytes

Cited by 35 publications

References 41 publications

The role of transient receptor potential channels in joint diseases

The role of transient receptor potential channels in joint diseases

N-acetyl-L-cysteine and cysteine increase intracellular calcium concentration in human neutrophils

Calcium signalling and related ion channels in neutrophil recruitment and function

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