Nontranscriptional modulation of intracellular Ca2+ signaling by ligand stimulated thyroid hormone receptor

Saelim, Nuttawut; John, Linu M.; Wu, Jun; Park, Jeong Soon; Bai, Yidong; Camacho, Patricia; Lechleiter, James D.

doi:10.1083/jcb.200409011

Cited by 39 publications

(30 citation statements)

References 63 publications

(95 reference statements)

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“…Additional work demonstrated that application of thyroid hormones to mitochondria increased DpH as well as Ca 2+ efflux [7,29,30]. We noted that the Xenopus TR b A1 had a nearly identical amino-terminus to rTR a DF1 and demonstrated that this receptor was also mitochondrial targeted [31]. Further, we showed that T 3 binding to either of the mitochondrial targeted thyroid hormone receptors acutely increased DW, O 2 consumption and regulated IP 3 -mediated Ca 2+ signaling presumably via their affects on mitochondrial metabolism [31].…”

Section: Introductionmentioning

confidence: 66%

“…We noted that the Xenopus TR b A1 had a nearly identical amino-terminus to rTR a DF1 and demonstrated that this receptor was also mitochondrial targeted [31]. Further, we showed that T 3 binding to either of the mitochondrial targeted thyroid hormone receptors acutely increased DW, O 2 consumption and regulated IP 3 -mediated Ca 2+ signaling presumably via their affects on mitochondrial metabolism [31]. In this previous work, we did not investigate the influence of ligand bound mitochondrial targeted TRs on apoptosis.…”

Section: Introductionmentioning

confidence: 93%

“…Xenopus TR b A1 was amplified by PCR and synthetic mRNA was prepared as previously reported [31]. In brief, the pGEM-HeNot vector containing cDNA template was linearized and mRNA was generated using the T7 promoter (MEGAscript 1 , Ambion 1 , Austin, TX).…”

Section: In Vitro Transcriptions and Oocyte Protein Expressionmentioning

confidence: 99%

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Inhibition of apoptotic potency by ligand stimulated thyroid hormone receptors located in mitochondria

et al. 2007

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We recently reported that shortened thyroid hormone receptor isoforms (TRs) can target mitochondria and acutely modulate inositol 1,4,5 trisphosphate (IP3)-mediated Ca2+ signaling when activated by thyroid hormone 3,5,3'-tri-iodothyronine (T3). Stimulation occurs via an increase in mitochondrial metabolism that is independent of transcriptional activity. Here, we present evidence that T3-bound xTRbetaA1s inhibit apoptotic activity mediated by cytochrome c release. An assay for apoptotic potency was modified to measure the ability of Xenopus oocyte extracts to induce morphological changes in isolated liver nuclei. Apoptotic potency was significantly decreased when oocyte extract was prepared from xTRbetaA1 expressing oocytes and treated with T3. The ability of T3 treatment to inhibit apoptosis was dependent on the expression of xTRbetaA1s in the mitochondrial fraction, not in the cytosolic fraction. T3 treatment also increased the membrane potential of isolated mitochondria prepared from oocytes expressing xTRbetaA1s but not from wildtype controls. We conclude that T3 acutely regulates cytochrome c release in a potential dependent manner by activating TRs located within mitochondria.

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Section: Introductionmentioning

confidence: 66%

Section: Introductionmentioning

confidence: 93%

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Inhibition of apoptotic potency by ligand stimulated thyroid hormone receptors located in mitochondria

et al. 2007

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“…More recent studies performed in different cell types including myoblasts have reported that mtDNA depletion or CCCP treatment influences the expression of a set of nuclear genes through changes in calcium signalling pathways (Biswas et al, 1999;Amuthan et al, 2002). Lastly, in Xenopus ovocyte, p43 overexpression affects both mitochondrial activity and Ca 2þ wave activity (Saelim et al, 2004). As c-myc expression is known to be regulated by calcium levels (Reed et al, 1985;Tsuda et al, 1985), these data well support the possibility that calcium signalling could be involved in the regulation of the cellular oncogene expression by mitochondrial activity.…”

Section: C-myc Is a Target Of Mitochondrial Activitymentioning

confidence: 99%

Mitochondrial activity regulates myoblast differentiation by control of c‐Myc expression

Seyer¹,

Grandemange²,

Busson³

et al. 2005

Journal Cellular Physiology

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We have previously shown that mitochondrial activity is an important regulator of myoblast differentiation, partly through processes targeting myogenin expression. Here, we investigated the possible involvement of c-myc in these processes. Inhibition of mitochondrial activity by chloramphenicol abrogated the decrease in c-myc mRNA and protein levels occurring at the onset of terminal differentiation. Conversely, stimulation of mitochondrial activity by overexpression of the T3 mitochondrial receptor (p43) down-regulated c-myc expression. In addition, c-myc overexpression mimicked the influence of mitochondrial activity inhibition on myoblast differentiation. Moreover, like chloramphenicol, c-myc overexpression strongly inhibited the myogenic influence of p43 overexpression. These data suggest that c-Myc is an important target of mitochondrial activity involved in the myogenic influence of the organelle. Lastly, we found that chloramphenicol influence is negatively related to the frequency of post-mitotic myoblasts in the culture at the onset of treatment, and cell cycle analyses demonstrated that the frequency of myoblasts in G0-G1 phase at cell confluence is increased by p43 overexpression and decreased by chloramphenicol or c-myc overexpression. These results suggest that irreversible myoblast withdrawal from the cell cycle is a target of mitochondrial activity by control of c-Myc expression.

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“…The nongenomic actions of thyroid hormones are dependent on the activation of plasma membrane receptor(s) or subcellular located receptor(s), mainly found at the cytoplasm, nucleus, and mitochondria (Bassettt et al, 2003;Farach-Carson and Davis, 2003;Saelim et al, 2004). Although the cell surface receptor(s) for thyroid hormone has not been sequenced or cloned yet, it has been suggested that this receptor could be distinct from the nuclear one (Bassettt et al, 2003;FarachCarson and Davis, 2003).…”

Section: General Vision Of Nongenomic Signaling Pathwaymentioning

confidence: 99%

Nongenomic signaling pathways triggered by thyroid hormones and their metabolite 3‐iodothyronamine on the cardiovascular system

Axelband

Dias

Ferrão

et al. 2010

Journal Cellular Physiology

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Thyroid hormones play a wide range of important physiological activities in almost all organism. As changes in these hormones levels-observed in hypothyroidism and hyperthyroidism-promote serious derangements of the cardiovascular system, it is important to know their mechanisms of action. Although the classic genomic actions which are dependent on interaction with nuclear receptors to modulate cardiac myocytes genes expression, there is growing evidence about T(3) and T(4)-triggered nongenomic pathways, resulted from their binding to plasma membrane, cytoplasm, or mitocondrial receptors that leads to a rapidly regulation of cardiac functions. Interestingly both actions converge to amplify thyroid hormone effects on cardiovascular system. T(3) and T(4) nongenomic actions modify inotropic and chronotropic effects, cardiac action potential duration, cardiac growth, and myocyte shape by protein translation through protein kinases-dependent signaling cascades, which include PKA, PKC, PI3K, and MAPK, and changes on ion channels and pumps activity. In respect to the decreased systemic vascular resistance seen in hyperthyroidism, T(3) appears to activate NOS or ATP-sensitive K(+) channels. In addition, a novel biologically active T(4)-derived metabolite has been described, 3-iodothyronamine, T(1)AM, which also acts through membrane receptors to mediate nongenomic cardiac effects. This metabolite influences the physiological manifestations of thyroid hormone actions by inducing opposite effects from those stimulated by T(3) and T(4), such as negative inotropic and chronotropic effects. Therefore, beyond genomic and nongenomic effects of thyroid hormones, it is crucial for there to be an equilibrium between T(3) or T(4) and T(1)AM levels for maintaining cardiac homeostasis.

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Nontranscriptional modulation of intracellular Ca2+ signaling by ligand stimulated thyroid hormone receptor

Cited by 39 publications

References 63 publications

Inhibition of apoptotic potency by ligand stimulated thyroid hormone receptors located in mitochondria

Inhibition of apoptotic potency by ligand stimulated thyroid hormone receptors located in mitochondria

Mitochondrial activity regulates myoblast differentiation by control of c‐Myc expression

Nongenomic signaling pathways triggered by thyroid hormones and their metabolite 3‐iodothyronamine on the cardiovascular system

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