Effects of prostaglandin F2α on intracellular pH, intracellular calcium, cell shortening and L-type calcium currents in rat myocytes

Yew, Su Fong; Reeves, Katherine A.; Woodward, Brian

doi:10.1016/s0008-6363(98)00195-3

Cited by 18 publications

(11 citation statements)

References 37 publications

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“…Originally, a few groups documented PGF2α mediated increase in intracellular calcium and subsequent myocyte shortening suggesting a positive ionotropic effect (Yew et al, 1998; Otani et al, 1988; Ponicke et al, 2000b). In contrast to those early reports, Jovanovic et al (2006) found PGF2α acting through the FP receptor mediated a negative ionotropic effect in isolated right ventricular muscle.…”

Section: Prostaglandin Fmentioning

confidence: 99%

The contribution of prostaglandins versus prostacyclin in ventricular remodeling during heart failure

Harding

Murray

2011

Life Sciences

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Although the role of Cox-2 in the heart’s response to physiologic stress remains controversial (i.e. expression in myocytes versus other resident myocardial cells) the ever expanding role of prostanoids in multiple models of heart failure cannot be denied. Due to the fact that prostanoids are metabolized rather quickly (half life of seconds to minutes) it is believed these signaling mediators act in a paracrine fashion at the site of production. Evidence to date is quite convincing that these bioactive lipid derivatives are involved in physiologic homeostatic regulation as well as beneficial and maladaptive ventricular remodeling in heart failure. Thus, this review will assess the direct contribution of each PG on remodeling in the left ventricle (e.g. hypertrophy, functional effects, and fibrosis).

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Section: Prostaglandin Fmentioning

confidence: 99%

The contribution of prostaglandins versus prostacyclin in ventricular remodeling during heart failure

Harding

Murray

2011

Life Sciences

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“…Signaling pathways that are activated by calcium are important for skeletal muscle growth ( Abbott et al, 1998 ; Dunn et al, 1999 ; Musaro et al, 1999 ; Semsarian et al, 1999 ; Delling et al, 2000 ; Friday et al, 2000 ; Horsley et al, 2001 ; Mitchell et al, 2002 ). PGs have been shown to activate increases in intracellular calcium within a variety of muscle cell types ( Asboth et al, 1996 ; Chen et al, 1997 ; Yew et al, 1998 ; Yousufzai and Abdel-Latif, 1998 ). Specifically, PGF 2α and PGE 2 can activate increases in intracellular calcium through their receptors, PGF 2α receptor (FP) and EP 1 /EP 3 , respectively ( Breyer et al, 2001 ).…”

Section: Introductionmentioning

confidence: 99%

Prostaglandin F2α stimulates growth of skeletal muscle cells via an NFATC2-dependent pathway

Horsley

Pavlath

2003

The Journal of Cell Biology

138

107

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Skeletal muscle growth requires multiple steps to form large multinucleated muscle cells. Molecules that stimulate muscle growth may be therapeutic for muscle loss associated with aging, injury, or disease. However, few factors are known to increase muscle cell size. We demonstrate that prostaglandin F2α (PGF2α) as well as two analogues augment muscle cell size in vitro. This increased myotube size is not due to PGF2α-enhancing cell fusion that initially forms myotubes, but rather to PGF2α recruiting the fusion of cells with preexisting multinucleated cells. This growth is mediated through the PGF2α receptor (FP receptor). As the FP receptor can increase levels of intracellular calcium, the involvement of the calcium-regulated transcription factor nuclear factor of activated T cells (NFAT) in mediating PGF2α-enhanced cell growth was examined. We show that NFAT is activated by PGF2α, and the isoform NFATC2 is required for PGF2α-induced muscle cell growth and nuclear accretion, demonstrating the first intersection between prostaglandin receptor activation and NFAT signaling. Given this novel role for PGF2α in skeletal muscle cell growth, these studies raise caution that extended use of drugs that inhibit PG production, such as nonsteroidal antiinflammatory drugs, may be deleterious for muscle growth.

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“…The presence of FP receptors in mouse heart has been confirmed with Northern blot analysis [12]. In ventricular myocardia it has been reported that PGF 2· [13], as well as other vasoconstrictive agonists such as phenylephrine, endothelin-I and angiotensin-II [14,15], produces a positive inotropic response and a rise in intracellular pH; both effects were inhibited by dimethylamiloride. In the case of the mouse atria, we detected no change in pH on application of PGF 2· under the present experimental conditions.…”

Section: Discussionmentioning

confidence: 85%

Possible Involvement of Prostaglandins F<sub>2α</sub> and D<sub>2</sub> in Acetylcholine-Induced Positive Inotropy in Isolated Mouse Left Atria

Tanaka

Nishimaru²,

Makuta³

et al. 2003

Pharmacology

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The inotropic action of prostaglandins PGF_2α, PGD₂ and PGE₂ on isolated mouse left atria was characterized and compared with the positive inotropic action of acetylcholine, which has previously been shown to be mediated by prostaglandins released from the endocardial endothelium. PGF_2α, PGD₂ and PGE₂ produced positive inotropic responses; the time course of the change in contractile force induced by PGF_2α and PGD₂ was about the same as that by acetylcholine, while that by PGE₂ was slower. Fluprostenol and sulprostone, FP and EP receptor agonists, respectively, had positive inotropic effects while BW-245C, a DP receptor agonist, had no effect. AH-6809, a DP receptor antagonist, had no inhibitory effect on the positive inotropic response to PGD₂. Dimethylamiloride, an inhibitor of Na⁺/H⁺ exchange, inhibited the positive inotropic response to PGF_2α, PGD₂ and acetylcholine, but not PGE₂. Fluorometric pH measurement with carboxy-SNARF-1-loaded atrial myocytes revealed no change in intracellular pH on application of PGF_2α. PGF_2α and PGD₂ significantly prolonged the duration of the atrial action potential while PGE₂ had no significant effect. These findings suggest that prostaglandins induce positive inotropic response in mouse atria through FP and EP receptor stimulation and that the former mechanism mediates in part the positive inotropic response to acetylcholine.

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Effects of prostaglandin F2α on intracellular pH, intracellular calcium, cell shortening and L-type calcium currents in rat myocytes

Abstract: The positive inotropic action of PGF2 alpha appears to be mediated via activation of the Na(+)-H+ exchanger with the possible involvement of PKC. This suggests that PGF2 alpha-produces intracellular alkalosis, which then sensitizes cardiac myofilaments to calcium.

Cited by 18 publications

References 37 publications

The contribution of prostaglandins versus prostacyclin in ventricular remodeling during heart failure

The contribution of prostaglandins versus prostacyclin in ventricular remodeling during heart failure

Prostaglandin F2α stimulates growth of skeletal muscle cells via an NFATC2-dependent pathway

Possible Involvement of Prostaglandins F<sub>2α</sub> and D<sub>2</sub> in Acetylcholine-Induced Positive Inotropy in Isolated Mouse Left Atria

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