Mechanical stress stimulates phospholipase C activity and intracellular calcium ion levels in neonatal rat cardiomyocytes

Ruwhof, Cindy; Wamel, Annemieke van; Noordzij, L.A.W.; Aydın, Semiha; Harper, J.C.R.; Laarse, Arnoud van der

doi:10.1054/ceca.2000.0158

Cited by 73 publications

(44 citation statements)

References 43 publications

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“…The contribution of different preload-dependent cellular and/or intracellular sources of additional Ca 2+ , e.g., stretch-activated channels (SAC) [9,33], L-type calcium channels [36,37] or ATP activity of myosin cross-bridges [38] 2+ ] i has been observed in stimulated ferret and mouse cardiac muscle [8,9] and rat atrial or ventricular myocyte [13,26]. On the other hand, stretch of rat trabeculae resulted in a decrease in resting Ca 2+ level [9,17], while stretch of stimulated Guinea-pig trabeculae or isolated myocyte produced a rise in resting [Ca 2+ ] i level [10][11][12]15].…”

Section: Effect Of Preload On Peak Active Tension and Fluorescencementioning

confidence: 99%

Preload-induced changes in isometric tension and [Ca2+]i in rat myocardium

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Protsenko

2011

Open Life Sciences

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Preload-induced changes of active tension and [Ca2+]i are “dissociated” in mammalian myocardium. This study aimed to describe the distinct effects of preload at low and physiological [Ca2+]o. Rat RV papillary muscles were studied in isometric conditions at 25‡C and 0.33 Hz at 1 mM (hypo-Ca group) and 2.5 mM [Ca2+]o (normal-Ca group). [Ca2+]i was monitored with fura-2/AM. Increase of preload caused a rise of active tension in hypo-Ca and normal-Ca groups whereas peak fluorescence rose significantly only at low [Ca2+]o. End-diastolic tension, end-diastolic level of fluorescence, time-to-peak tension, but not time-to-peak of Ca2+ transient, progressively increased with preload. Mechanical relaxation decelerated with preload while Ca2+ transient decay time decreased in the initial phase and increased in the late phase, resulting in a prominent “bump” configuration. The “bump” was assessed as a ratio of its area to the fluorescence trace area. It was a new finding that the preload-induced rise of this ratio was twice as large in hypo-Ca. Our results indicate that preload-induced changes in active tension and [Ca2+]i are “dissociated” in rat myocardium, with relatively higher expression at low [Ca2+]o. Ca-dependence of Ca-TnC association/dissociation kinetics is thought to be a main contributor to these preload-induced effects.

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Section: Effect Of Preload On Peak Active Tension and Fluorescencementioning

confidence: 99%

Preload-induced changes in isometric tension and [Ca2+]i in rat myocardium

Lookin

Protsenko

2011

Open Life Sciences

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“…PLA 2 and Src kinase have also been implicated in the activation of TRPCmediated SOC and ROC activities (Hisatsune et al 2004;Bolotina and Csutora 2005;Vazquez et al 2004b). There is also evidence that indicates PLC may be MS (Brophy et al 1993), with some reports indicating that the mechanosensitivity depends upon Ca 2+ influx (Basavappa et al 1988;Matsumoto et al 1995;Ryan et al 2000;Ruwhof et al 2001;Alexander et al 2004) and others indicating independence of external Ca 2+ and Ca 2+ influx (Mitchell et al 1997;Rosales et al 1997;Moore et al 2002). In either case, the combined evidence indicates that mechanical forces transduced by MscCa and/or by MS enzymes may modulate the gating of all TRP channels.…”

Section: Discussionmentioning

confidence: 93%

“…However, while there are reports that PLC can be mechanically stimulated independent of external Ca 2+ (Rosales et al 1997;Mitchell et al 1997;Moore et al 2002), there are more cases that indicate that the mechanosensitivity of PLC derives from stimulation by Ca 2+ influx via MscCa (Matsumoto et al 1995;Ryan et al 2000;Ruwhof et al 2001). In this case, it becomes important to demonstrate that TRPC6 can be mechanically activated in the absence of external Ca 2+ (e.g., using Ba…”

Section: Trpc6 Role In Myogenic Tonementioning

confidence: 99%

The Mechanosensitive Ca2+ Channel as a Central Regular of Prostate Tumor Cell Migration and Invasiveness

Hamill¹

2011

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Public reporting burden for this collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing this collection of information. Send comments regarding this burden estimate or any other aspect of this collection of information, including suggestions for reducing this burden to Department of Defense, Washington Headquarters Services, Directorate for Information Operations and Reports (0704-0188), 1215 Jefferson Davis Highway, Suite 1204, Arlington, VA 22202-4302. Respondents should be aware that notwithstanding any other provision of law, no person shall be subject to any penalty for failing to comply with a collection of information if it does not display a currently valid OMB control number. PLEASE DO NOT RETURN YOUR FORM TO THE ABOVE ADDRESS. REPORT DATE (DD-MM-YYYY)2. REPORT TYPE 3. DATES COVERED (From -To) 4. TITLE AND SUBTITLE 5a. CONTRACT NUMBER 5b. GRANT NUMBER 5c. PROGRAM ELEMENT NUMBER 6. AUTHOR(S) 5d. PROJECT NUMBER 5e. TASK NUMBER E-Mail:5f. WORK UNIT NUMBER 4 Introduction A major challenge for treating prostate cancer (PC) is to discover new therapies that will prevent the spread of PC cells from the prostate to distal sites. Our research focuses on the stretch-activated mechanosensitive Ca 2+ permeant channel (MscCa) as a central regulator of prostate tumor cell migration. Our experiments are designed to address the two most basic issues of the disease: the mechanism(s) that trigger progression of PC to malignancy and the urgent need for new therapeutic targets to block or reverse this progression. Our original experiments funded by DOD were aimed to test whether MscCa is expressed in human prostate tumor cells and whether MscCa activity is required for prostate tumor cell migration. We confirmed both results. In the course of these experiments we also discovered that the predominate gating mode of the MscCa differs between noninvasive and invasive PC cells, may be the most powerful determinate of the [Ca 2+ ]i dynamics required to coordinate cell locomotion. The aims of the current award were three-fold. First, determine the mechanisms underlying MscCa gating. Second, determine the cancer-related processes that switch MscCa gating, and third determine whether anti-MscCa conditions that suppress PC migration in vitro also block PC cell invasion in vivo. Insights into these aspects would provide added motivation for developing more selective therapies that target MscCa and its regulatory mechanisms. The basic results supporting our hypothesis have been published (Maroto, R. & Hamill, O.P. MscCa regulation of tumor cell migration and metastasis. Current Topics in Membranes.59, 485-509, 2007). Also included in the Appendix are other manuscripts and abstracts Gotlieb et al., 2008; Maroto & Hamill, 2011; and Maroto, Kurosky and Hamill, 2011) that include specific results described in body of the text. PERFORMING ORGANIZATION NAME(S) AND AD...

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“…Cellular signalling drives SF remodelling and the exponentially decaying signal in the current study is based on the observations of Roberts et al (2001) and Ruwhof et al (2001). In these studies, an approximately exponentially decaying calcium signal is detected following mechanical loading.…”

Section: Simulations Reveal Thatmentioning

confidence: 98%

Cellular contractility and substrate elasticity: a numerical investigation of the actin cytoskeleton and cell adhesion

Ronan

Deshpande

McMeeking

et al. 2013

Biomech Model Mechanobiol

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Publication InformationRonan, William, Deshpande, Vikram S., McMeeking, Robert M., & McGarry, J. Patrick. (2014). Cellular contractility and substrate elasticity: a numerical investigation of the actin cytoskeleton and cell adhesion. Biomechanics found to alter the range of substrate stiffness that cause the most significant changes in stress fibre and focal adhesion formation. Furthermore, stress fibre and focal adhesion formation evolve as a cell spreads on a substrate and leading to the formation of bands of fibres leading from the cell periphery over the nucleus. Inhibiting the formation of FAs during cell spreading is found to limit stress fibre formation. The predictions of this mutually dependent material-interface framework are strongly supported by experimental observations of cells adhered to elastic substrates and offer insight into the interdependent biomechanical processes regulating stress fibre and focal adhesion formation.

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Mechanical stress stimulates phospholipase C activity and intracellular calcium ion levels in neonatal rat cardiomyocytes

Cited by 73 publications

References 43 publications

Preload-induced changes in isometric tension and [Ca2+]i in rat myocardium

Preload-induced changes in isometric tension and [Ca2+]i in rat myocardium

The Mechanosensitive Ca2+ Channel as a Central Regular of Prostate Tumor Cell Migration and Invasiveness

Cellular contractility and substrate elasticity: a numerical investigation of the actin cytoskeleton and cell adhesion

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