FKBP12.6 and cADPR regulation of Ca<sup>2+</sup> release in smooth muscle cells

Wang, Yong-Xiao; Zheng, Yun‐Min; Mei, Qibing; Wang, Qinq-Song; Collier, Mei Lin; Fleischer, Sidney; Xin, Hong‐Bo; Kotlikoff, Michael I.

doi:10.1152/ajpcell.00106.2003

Cited by 126 publications

(95 citation statements)

References 71 publications

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“…1A, 1B, 2A, and 2B). The inhibitory effect of CaN in C 2 C 12 cells is thought to depend on CaN, RyR, and the 12-kDa FK-506-binding protein (FKBP 12) being associated in a trimeric complex (37); however, within ASMCs, FKBP 12 does not bind to RyRs (44), providing support that CaN regulates ASMC RyR activity through a novel regulatory mechanism. As shown in Fig.…”

Section: Discussionmentioning

confidence: 99%

“…Muscle contraction in isolated tracheal rings was measured using the organ bath technique, as described previously (44), with isometric transducers (Harvard Apparatus, South Natick, MA) and a PowerLab/4SP recording system (AD Instruments, Colorado Springs, CO). Tracheas were quickly removed from mice and transferred into ice-cold 1.8 mM PSS.…”

Section: Methodsmentioning

confidence: 99%

“…Ca 2ϩ sparks have been observed in equine (44), guinea pig (51), porcine (32), mouse (26), and human ASMCs (10). These local Ca 2ϩ events are known to regulate ASMC membrane potential through the activation of hyperpolarizing spontaneous transient outward currents (STOCs) or depolarizing spontaneous transient inward currents (STICs) (49).…”

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confidence: 99%

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Calcineurin upregulates local Ca²⁺signaling through ryanodine receptor-1 in airway smooth muscle cells

Savoia

Liu

Zheng

et al. 2014

American Journal of Physiology-Lung Cellular and Molecular Phys

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Calcineurin upregulates local Ca²⁺signaling through ryanodine receptor-1 in airway smooth muscle cells

Savoia

Liu

Zheng

et al. 2014

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…In this context, Wang and colleagues have provided evidence relevant to the mechanisms by which calcium release through RyR channels is brought forth in airway myocytes (23). The open state of the RyR channels in cardiac muscle cells is regulated by FK506-binding proteins (33).…”

Section: Cyclic Adp-ribose As An Endogenous Ligand For the Ryanodine mentioning

confidence: 99%

“…The open state of the RyR channels in cardiac muscle cells is regulated by FK506-binding proteins (33). Specifically, FKBP12.6 is known to associate with the RyR2 isoform in smooth muscle cells to regulate its function (23,34). In ASM cells, Wang and coworkers showed that, although both FKBP12 and FKBP12.6 mRNAs are expressed, the FKBP12.6 fusion proteins only associate with the RyR2 (23).…”

Section: Cyclic Adp-ribose As An Endogenous Ligand For the Ryanodine mentioning

confidence: 99%

Calcium Signaling in Airway Smooth Muscle

Jude¹,

Wylam²,

Walseth³

et al. 2008

Proceedings of the American Thoracic Society

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Contractility of airway smooth muscle requires elevation of intracellular calcium concentration. Under resting conditions, airway smooth muscle cells maintain a relatively low intracellular calcium concentration, and activation of the surface receptors by contractile agonists results in an elevation of intracellular calcium, culminating in contraction of the cell. The pattern of elevation of intracellular calcium brought about by agonists is a dynamic process and involves the coordinated activities of ion channels located in the plasma membrane and the sarcoplasmic reticulum. Among the signaling molecules involved in this dynamic calcium regulation in airway smooth muscle cells are inositol 1,4,5-trisphosphate and cyclic ADPribose, which mobilize calcium from the sarcoplasmic reticulum by acting via the inositol 1,4,5-trisphosphate and ryanodine receptors, respectively. In addition, calcium influx from the extracellular space is critical for the repletion of the intracellular calcium stores during activation of the cells by agonists. Calcium influx can occur via voltage-and receptor-gated channels in the plasma membrane, as well as by influx that is triggered by depletion of the intracellular stores (i.e., store-operated calcium entry mechanism). Transient receptor potential proteins appear to mediate the calcium influx via receptor-and store-operated channels. Recent studies have shown that proinflammatory cytokines regulate the expression and activity of the pathways involved in intracellular calcium regulation, thereby contributing to airway smooth muscle cell hyperresponsiveness. In this review, we will discuss the specific roles of cyclic ADP-ribose/ryanodine receptor channels and transient receptor potential channels in the regulation of intracellular calcium in airway smooth muscle cells. DYNAMIC INTRACELLULAR CALCIUM REGULATION IN AIRWAY SMOOTH MUSCLE CELLSExposure of airway smooth muscle (ASM) cells to contractile agonists results in a biphasic elevation of intracellular calcium concentration ([Ca 21 ] i ) that is characterized by an initial rapid and transient rise in calcium, followed by a decline to a lower, sustained steady-state concentration above the basal level (1-3). This biphasic [Ca 21 ] i response results from calcium influx from the extracellular space and release of calcium from the intracellular stores (i.e., the sarcoplasmic reticulum [SR]). Earlier studies have attributed the initial rapid and transient phase of the [Ca 21 ] i response to release from the SR, while the sustained phase of the response was thought to be due to influx from the extracellular space (2-6). Recent investigations using the improved temporal and spatial resolution features of real-time confocal microscopy have shed light on the dynamics of the [Ca 21 ] i response in ASM cells. These studies have shown that the biphasic [Ca 21 ] i response of ASM cells elicited by contractile agonists in reality consists of propagating regenerative calcium oscillations that originate at a location within a cell and propagate...

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Abnormal tracheal smooth muscle function in the CF mouse

et al. 2013

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Increased airway smooth muscle (ASM) contractility is thought to underlie symptoms of airway hyperresponsiveness (AHR). In the cystic fibrosis (CF) airway, ASM anomalies have been reported, but have not been fully characterized and the underlying mechanisms are largely unknown. We examined ASM in an adult CF mouse tracheal ring preparation, and determined whether changes in contractility were associated with altered ASM morphology. We looked for inherent changes in the cellular pathways involved in contractility, and characterized trachea morphology in the adult trachea and in an embryonic lung culture model during development. Results showed that that there was a reduction in tracheal caliber in CF mice as indicated by a reduction in the number of cartilage rings; proximal cross-sectional areas of cftr−/− tracheas and luminal areas were significantly smaller, but there was no difference in the area or distribution of smooth muscle. Morphological differences observed in adult trachea were not evident in the embryonic lung at 11.5 days gestation or after 72 h in culture. Functional data showed a significant reduction in the amplitude and duration of contraction in response to carbachol (CCh) in Ca-free conditions. The reduction in contraction was agonist specific, and occurred throughout the length of the trachea. These data show that there is a loss in the contractile capacity of the CF mouse trachea due to downregulation of the pathway specific to acetylcholine (ACh) activation. This reduction in contraction is not associated with changes in the area or distribution of ASM.

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FKBP12.6 and cADPR regulation of Ca²⁺ release in smooth muscle cells

Abstract: . FKBP12.6 and cADPR regulation of Ca 2ϩ release in smooth muscle cells.

Cited by 126 publications

References 71 publications

Calcineurin upregulates local Ca²⁺signaling through ryanodine receptor-1 in airway smooth muscle cells

Calcineurin upregulates local Ca²⁺signaling through ryanodine receptor-1 in airway smooth muscle cells

Calcium Signaling in Airway Smooth Muscle

Abnormal tracheal smooth muscle function in the CF mouse

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FKBP12.6 and cADPR regulation of Ca2+ release in smooth muscle cells

Abstract: . FKBP12.6 and cADPR regulation of Ca 2ϩ release in smooth muscle cells.

Cited by 126 publications

References 71 publications

Calcineurin upregulates local Ca2+signaling through ryanodine receptor-1 in airway smooth muscle cells

Calcineurin upregulates local Ca2+signaling through ryanodine receptor-1 in airway smooth muscle cells

Calcium Signaling in Airway Smooth Muscle

Abnormal tracheal smooth muscle function in the CF mouse

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FKBP12.6 and cADPR regulation of Ca²⁺ release in smooth muscle cells

Calcineurin upregulates local Ca²⁺signaling through ryanodine receptor-1 in airway smooth muscle cells

Calcineurin upregulates local Ca²⁺signaling through ryanodine receptor-1 in airway smooth muscle cells