Annexins V and VI: major calcium-dependent atrial secretory granule-binding proteins.

Doubell, Anton; Bester, A J; Thibault, Gaétan

doi:10.1161/01.hyp.18.5.648

Cited by 23 publications

(8 citation statements)

References 65 publications

(41 reference statements)

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“…1F, F′, arrow), respectively. Furthermore, we observe localization of Annexin A6 to the chick heart (data not shown), corroborating prior studies showing that Annexin A6 is a major protein in atrial myocytes [29]. Interestingly, Annexin A6 expression (Fig.…”

Section: Resultssupporting

confidence: 92%

Differential expression pattern of Annexin A6 in chick neural crest and placode cells during cranial gangliogenesis

Shah

Taneyhill

2015

Gene Expression Patterns

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The cranial trigeminal and epibranchial ganglia are components of the peripheral nervous system that possess an important somatosensory role. These ganglia arise from the intermixing and coalescence of two different migratory cell types, neural crest cells and neurogenic placodes cells, and thus typify the phenomena of cell migration and intercellular interactions for their creation. The underlying molecular mechanisms of ganglia formation, however, are still poorly understood. To address this, we have analyzed the spatio-temporal expression profile of Annexin A6 during chick gangliogenesis, as Annexin proteins play important, conserved roles in ganglia development and physiology. We observe Annexin A6 protein in cranial neural crest cells prior to, during and after their emergence from the neural tube. Fully migratory cranial neural crest cells, however, are devoid of Annexin A6. Interestingly, we note Annexin A6 protein in trigeminal and epibranchial placode cells as these cells ingress from the ectoderm to initiate ganglia formation. This expression is also maintained in the sensory placodes later on when they coalesce with neural crest cells to assemble the cranial ganglia. These results suggest that the dynamic expression of Annexin A6 in various embryonic cell types may allow Annexin A6 to serve distinct functions throughout embryonic development.

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Section: Resultssupporting

confidence: 92%

Differential expression pattern of Annexin A6 in chick neural crest and placode cells during cranial gangliogenesis

Shah

Taneyhill

2015

Gene Expression Patterns

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“…Annexin 6 is localized around individual myofibrils and is associated with the terminal cisternae of isolated SR membranes. In this context, it has been suggested that annexin 6 is involved in atrial secretary granule binding (21) and the cycle of calcium release/uptake in the SR (9,22,23).…”

Section: Resultsmentioning

confidence: 99%

Altered mechanical properties and intracellular calcium signaling in cardiomyocytes from annexin 6 null‐mutant mice

et al. 2002

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Annexin 6 is one of a widely expressed family of calcium-binding proteins found in most mammalian tissues, including the heart. Several studies have implicated annexin 6 in the regulation of intracellular Ca2+ signaling, and it has been shown in vitro to act as a modulator of the sarcoplasmic reticulum Ca2+-release channel, cardiac L-type calcium channel, and Na+/Ca2+ exchanger. To investigate the role of annexin 6 in intact cardiomyocytes, we used mice containing a targeted disruption of the annexin 6 gene. Compared with controls, the myocytes of annexin 6 null-mutant mice demonstrated a significant increase in the rates of shortening and relengthening. Intracellular Ca2+ transients in fura-2-loaded cardiomyocytes induced by caffeine showed a normal baseline and amplitude, whereas the rate of decay was doubled in annexin 6-/- myocytes compared with control mice. These results show that annexin 6 knockout in the mouse leads to an increase in myocyte contractility and faster diastolic Ca2+ removal from the cytoplasm. In light of published findings showing annexin 6 to be down-regulated in end-stage heart failure, these results are consistent with a role for annexin 6 as a negative inotropic factor in the regulation of cardiomyocyte mechanics.

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“…Annexin A6, like annexin A5, is known to form an active Ca 2+ channel [18] and has been involved in exocytosis and release of atrial natriuretic peptide from atrial granules [58]. Regulation by annexin A6 of membrane trafficking and endocytosis has been recently reported by Grewal et al [73].…”

Section: Annexin A6mentioning

confidence: 97%

“…3) [41,57]. Interestingly, annexin A5 has previously been detected in specific atrial granules where atrial natriuretic peptide is stored, and suggested to play a role as mediating atrial natriuretic peptide secretion [58].…”

Section: Annexin A5mentioning

confidence: 99%

Annexins and Ca handling in the heart

Camors

Monceau

Charlemagne

2005

Cardiovascular Research

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Annexins are a family of 13 proteins known to bind phospholipids (PL) in a Ca(2+)-dependent way. They are ubiquitous proteins and share a similar structure characterized by a conserved C-terminal domain with Ca(2+) binding sites and a variable N-terminal domain. Depending on Ca(2+) concentration, they have been reported to participate in a variety of membrane-related events such as exocytosis, endocytosis, apoptosis and binding to cytoskeletal proteins. They have also been reported to regulate protein activities. This review will focus on annexins in the heart, and particularly on annexins A2, A5, A6 and A7. Annexin A2 has been found in endothelial cells and reported to play a central role in control of plasmin-mediated processes. Annexin A5 is mainly localized in cardiomyocytes. However, it could be relocated to interstitial tissue in ischemic and failing hearts or it could be externalized and exhibit a proapoptotic effect in cardiomyocytes. Annexin A6 is the most abundant annexin in the heart, and has been localized in various cell types including myocytes. Overexpression of annexin A6 has underlined physiological alterations in contractile mechanics leading to dilated cardiomyopathy, whereas knockout has been found to induce faster changes in Ca(2+) transient and increased contractility, suggesting a negative inotropic role for annexin A6. Annexin A7 is expressed in heart and skeletal muscle. In annexin A7 null mutant mice decreases in the force-frequency relationship were observed in adult cardiomyocytes, consistent with regulation of Ca(2+) handling. In conclusion, while annexin A2 was involved in regulation of fibrin homeostasis, alterations in expression and activity of annexins A5, A6 and A7 have been associated with regulation of Ca(2+) handling in the heart, but the target of each annexin has not yet been identified.

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Annexins V and VI: major calcium-dependent atrial secretory granule-binding proteins.

Cited by 23 publications

References 65 publications

Differential expression pattern of Annexin A6 in chick neural crest and placode cells during cranial gangliogenesis

Differential expression pattern of Annexin A6 in chick neural crest and placode cells during cranial gangliogenesis

Altered mechanical properties and intracellular calcium signaling in cardiomyocytes from annexin 6 null‐mutant mice

Annexins and Ca handling in the heart

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