Calreticulin in cardiac development and pathology

Michalak, Marek; Lynch, Jeffrey M.; Groenendyk, Jody; Guo, Lei; Parker, J. M. R.; Opas, Michał

doi:10.1016/s1570-9639(02)00441-7

Cited by 41 publications

(34 citation statements)

References 74 publications

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“…CALR protein is a Ca 2+ -binding chaperone localized in the rough endoplasmic reticulum, responsible for the binding of misfolded proteins, stopping their export to the Golgi apparatus [11]. Apart from this function, CALR plays a role in cardiac development [12]. The target genes of calreticulin are unknown, but there is evidence for its involvement in apoptosis and cell survival regulation in cancer cells by promotion of macrophage antitumor activity [13].…”

Section: Discussionmentioning

confidence: 99%

Frequency and Molecular Characteristics of Calreticulin Gene (CALR) Mutations in Patients with JAK2-Negative Myeloproliferative Neoplasms

Wojtaszewska¹,

Iwoła²,

Lewandowski³

2014

Acta Haematol

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In 2013, Nangalia et al. and Klampfl et al. found a recurrent and abundant mutation in the calreticulin gene (CALR), mutually exclusive with JAK2 and MPL alterations. At present, the data concerning the new mutation, i.e. its prevalence, allele burden and clinical significance, are scarce. We report the incidence and molecular characteristics of CALR mutations in a group of 184 Polish patients with myeloproliferative neoplasms (MPNs). Clinical data analysis revealed significant differences between JAK2 V617F-mutated and CALR-mutated groups. In essential thrombocythemia patients, hemoglobin levels and leukocyte counts were significantly higher in JAK2-positive than in CALR-positive patients (p = 0.023 and p = 0.017, respectively), but the CALR-positive patients had significantly higher platelet counts (p = 0.022). Patients harboring CALR mutations were also younger at the time of diagnosis (p = 0.039). In primary myelofibrosis patients, the degree of anemia was less severe in those who were CALR exon 9 mutation-positive than in those who were JAK2 V617F-positive (p = 0.048). © 2014 S. Karger AG, Basel

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Section: Discussionmentioning

confidence: 99%

Frequency and Molecular Characteristics of Calreticulin Gene (CALR) Mutations in Patients with JAK2-Negative Myeloproliferative Neoplasms

Wojtaszewska¹,

Iwoła²,

Lewandowski³

2014

Acta Haematol

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“…SAGE shows downregulation of genes for calreticulin and phospholamban, proteins involved in Ca 2ϩ handling. Calreticulin, a Ca 2ϩ -binding chaperone residing in the lumen of the endoplasmic reticulum, is known to affect intracellular Ca 2ϩ homeostasis by modulating Ca 2ϩ storage and transport (31). As an upstream regulator of calcineurin, the calcium-dependent protein phosphatase calreticulin plays a vital role in cardiac physiology and pathologies (31).…”

Section: Discussionmentioning

confidence: 99%

“…Calreticulin, a Ca 2ϩ -binding chaperone residing in the lumen of the endoplasmic reticulum, is known to affect intracellular Ca 2ϩ homeostasis by modulating Ca 2ϩ storage and transport (31). As an upstream regulator of calcineurin, the calcium-dependent protein phosphatase calreticulin plays a vital role in cardiac physiology and pathologies (31). Phospholamban, a sarcoplasmic reticulum membrane protein, is a regulator of SERCA2a, the cardiac isoform of sarco(endo)plasmic reticulum Ca 2ϩ -ATPase, diminished expression of which is considered to be one of the markers of chronic cardiac overload (19).…”

Section: Discussionmentioning

confidence: 99%

Novel targets of ANG II regulation in mouse heart identified by serial analysis of gene expression

Schwartz¹,

Duka²,

Duka³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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Schwartz, Faina, Arvi Duka, Irena Duka, Jing Cui, and Haralambos Gavras. Novel targets of ANG II regulation in mouse heart identified by serial analysis of gene expression. Am J Physiol Heart Circ Physiol 287: H1957-H1966, 2004. First published July 8, 2004 doi:10.1152/ajpheart.00568.2004.-Although the central role of ANG II in cardiovascular homeostasis is well appreciated, the molecular circuitry of its many actions is not completely understood. With the use of serial analysis of gene expression to assess global transcriptional changes in the heart of mice after continuous 7-day ANG II administration, we identified patterns of gene expression indicative of cardiac remodeling, including coordinate regulation of genes previously described in a context of processes associated with hypertrophy and fibrosis. In addition, we discovered several novel ANG II targets, including characterized genes of known function, recently annotated genes of unknown function, and the putative genes not yet present in current databases. The serial analysis of gene expression approach to assess the role of ANG II presented in this report provides new venues for inquiries into ANG II-mediated cardiac function.genome-wide transcriptional profiling; hypertension; cardiac remodeling; hypertrophy; fibrosis THE KEY ROLE of ANG II in cardiovascular homeostasis is well documented. Although initially known for its vasoconstrictive action, the adverse effects of ANG II elevation on the heart independent of its hemodynamic influence were recognized in the early 1970s (7, 16), and the cardioprotective outcomes of the pharmacological interventions that either prevent the ANG II formation from the inactive angiotensinogen precursor (14) or inhibit its interaction with specific receptors (15, 48) are now well appreciated in clinical practice (6,13,17).Experimental animal studies have shown that ANG II administration can cause multifocal myocardial lesions (16, 47), and, via ANG II type 1 receptors, directly induce cardiac remodeling that involves myocyte hypertrophy (9, 25), fibroblast proliferation, and subsequent fibrosis (47), thus leading to the development of pathological cardiac hypertrophy and, ultimately, heart failure. Both in vivo and in vitro studies revealed that the ANG II effects in the heart are accompanied by changes in gene expression in the cardiac myocytes, fibroblasts, and endothelial cells (24). While the queries of selected ANG II targets supplied important information on several molecular pathways underlying the physiological and pathophysiological actions of ANG II, an all-inclusive view is provided by the genome-wide transcriptional profiling that offers an opportunity to connect separate pieces of the puzzle through the identification of the new players not intuitively obvious from our present understanding of physiology. Thus simultaneous evaluation of 4,000 genes by the use of microarray technology to query the quantitative changes in left ventricular RNA in response to ANG II-induced progression, and, subsequently, regre...

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“…Calreticulin binds to misfolded proteins, preventing them from being exported from the endoplasmic reticulum to the Golgi apparatus (Michalak et al 2012), whereas the lethal protein Efl21 is related to the heat shock protein family, playing the role of a chaperonin (Kurzik-Dumke and Lohmann 1995). According to Ki et al (2012), oxidative stress plays a central role in fipronil-induced cytotoxicity.…”

Section: Discussionmentioning

confidence: 99%

Modification of the brain proteome of Africanized honeybees (Apis mellifera) exposed to a sub‐lethal doses of the insecticide fipronil

et al. 2014

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Fipronil is a phenylpyrazole insecticide that is widely used in Brazilian agriculture for pest control. Although honeybees are not targets of fipronil, studies indicate that this pesticide can be harmful to honeybees. To assess the effects of fipronil in the brain of Africanized Apis mellifera workers, this study focused on the toxico-proteome profiling of the brain of newly emerged and aged honeybee workers that were exposed to a sub-lethal dose (10 pg fipronil per day. i.e. (1)/100 of LD50/bee/day during 5 days) of the insecticide. Proteomic analysis identified 25 proteins that were differentially up-regulated or down-regulated when the fipronil-exposed and non-exposed groups were compared. These proteins are potentially related to pathogen susceptibility, neuronal chemical stress, neuronal protein misfolding, and occurrence of apoptosis, ischemia, visual impairment, damaged synapse formation, brain degeneration, memory and learning impairment. The exposure of honeybees to a very low dose of fipronil, even for a short period of time (5 days), was sufficient to cause a series of important neuroproteomic changes in the brains of honeybees.

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Calreticulin in cardiac development and pathology

Cited by 41 publications

References 74 publications

Frequency and Molecular Characteristics of Calreticulin Gene <b><i>(CALR)</i></b> Mutations in Patients with <b><i>JAK2</i></b>-Negative Myeloproliferative Neoplasms

Frequency and Molecular Characteristics of Calreticulin Gene <b><i>(CALR)</i></b> Mutations in Patients with <b><i>JAK2</i></b>-Negative Myeloproliferative Neoplasms

Novel targets of ANG II regulation in mouse heart identified by serial analysis of gene expression

Modification of the brain proteome of Africanized honeybees (Apis mellifera) exposed to a sub‐lethal doses of the insecticide fipronil

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