The organisation of the mouse chromogranin B (secretogranin I) gene

Pohl, Thomas; Phillips, Elizabeth A.; Song, Kyuyong; Gerdes, Hans‐Hermann; Huttner, Wieland B.; Rüther, Ulrich

doi:10.1016/0014-5793(90)80194-n

Cited by 66 publications

(44 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We used FSK as a positive control as the CgB promoter contains a cAMP response element. 24 NE has been found to activate cAMP response element transcription sites through both ␣ 1 -and ␤-adrenergic receptor signaling, 25,26 and NE-induced increase in CgB gene expression may reflect CgB stimulustranscription-secretion coupling in the myocardium during HF, a mechanism known to be important for CgB production and secretion in nonmyocardial tissue. 21 Because circulating NE levels in HF are increased in proportion to patient NYHA functional class, 27 the effect of NE on cardiomyocyte CgB production, and possibly also secretion, may explain the close association found between CgB levels in the myocardium and plasma and indices of severity of HF.…”

Section: Discussionmentioning

confidence: 99%

Chromogranin B in Heart Failure

Røsjø

Husberg

Dahl

et al. 2010

Circ: Heart Failure

View full text Add to dashboard Cite

Background-Chromogranin B (CgB) is a member of the granin protein family. Because CgB is often colocalized with chromogranin A (CgA), a recently discovered cardiac biomarker, we hypothesized that CgB is regulated during heart failure (HF) development. Methods and Results-CgB regulation was investigated in patients with chronic HF and in a post-myocardial infarction HF mouse model. Animals were phenotypically characterized by echocardiography and euthanized 1 week after myocardial infarction. CgB mRNA levels were 5. Key Words: heart failure Ⅲ molecular biology Ⅲ biological markers Ⅲ chromogranin B A dvances in treatment of acute coronary syndromes have reduced short-term mortality following acute myocardial infarction (MI), but at the cost of a higher incidence of post-MI heart failure (HF). 1 Improved pathophysiological understanding of HF and better tools for risk prediction and diagnostic purposes are therefore needed. 2 The cardiac biomarkers used routinely in clinical practice today are proteins specific to the diseased myocardium, either released during cell necrosis (cardiac specific troponins) 3 or secreted secondary to cardiomyocyte strain (B-type natriuretic peptide, BNP). 4 However, there is still a need for markers reflecting other pathophysiological processes in heart disease. 5 Thus, identifying new proteins regulated in the failing myocardium may potentially improve both the understanding of HF development and lead to the discovery of novel cardiac biomarkers. Clinical Perspective on p 511Chromogranin B (CgB) is a 50-kDa protein belonging to a group of acidic proteins called the granin protein family. 6 The most extensively studied and well-known member of the granin family is chromogranin A (CgA), a protein currently used clinically as a biomarker in patients with neuroendocrine tumors. 7 Recently, CgA has been shown to increase with the severity of HF 8 and to be an independent predictor of mortality in patients with acute coronary syndrome. 9 -11 Moreover, increased CgA production has been demonstrated in cardiomyocytes of the failing myocardium. 12 However, a confounding factor possibly reducing CgA's merit as a cardiac biomarker is the increase in CgA levels seen with the use of proton pump inhibitors (PPIs). 13 In contrast, CgB Methods Mouse Model of HFA permanent ligation of the left main coronary artery were performed in mice in the HF group, whereas sham-operated (sham) animals underwent the same procedure except ligation of the coronary artery. 16 Echocardiographic examination was performed 1 week after the primary operation. The criteria for including animals in the HF group have previously been validated. 17

show abstract

Section: Discussionmentioning

confidence: 99%

Chromogranin B in Heart Failure

Røsjø

Husberg

Dahl

et al. 2010

Circ: Heart Failure

View full text Add to dashboard Cite

show abstract

“…In particular, the disulfide loop of CGB is also contained in exon three of the CGB gene and the final exon of CGB contains sequences of the protein highly homologous to CGA [31]. The structures of the CGA and CGB genes suggest that they may be related via a gene duplication event.…”

Section: Structure Of the Cga Gene And Regulation Of Cga Gene Transcrmentioning

confidence: 99%

“…Although the CGA gene contains a consensus CRE, stimulation of the protein kinase A pathway elicits only modest increases in CGA mRNA levels in chromaffin cells and neuroblastoma cell lines [25,50] (Table 1), although both genes contain consensus CREs in the proximal promoter [31]. The structural basis for CGB gene expression awaits detailed analysis.…”

Section: Structure Of the Cga Gene And Regulation Of Cga Gene Transcrmentioning

confidence: 99%

Chromogranin A: current status as a precursor for bioactive peptides and a granulogenic/sorting factor in the regulated secretory pathway

Iacangelo

Eiden

1995

Regulatory Peptides

165

115

View full text Add to dashboard Cite

“…Plasmids OVEC, S P 6 ' S and JH514ref were described recently (Thiel et al, 1994). To construct plasmid pCgBCAT-1, we used plasmid pUCmCgBpro which contains a 6-kb fragment of the promoter region of the mouse chromogranin B gene flanked by a HindIII site at the 5' end and by a SstI site of exon 1 at the 3' end (Pohl et al, 1990). This plasmid was characterized and kindly provided by Angus King (University of Heidelberg).…”

Section: Reporter Constructsmentioning

confidence: 99%

Differential Regulation of Chromogranin B and Synapsin I Gene Promoter Activity by cAMP and cAMP‐Dependent Protein Kinase

Jüngling

Cibelli

Czardybon

et al. 1994

European Journal of Biochemistry

Self Cite

View full text Add to dashboard Cite

cAMP has neurotrophic effects in the nervous system. We have investigated whether there is a correlation between CAMP-induced neurite outgrowth and induction of chromogranin B and synapsin I gene expression. These genes encode marker proteins of distinct populations of vesicles in neurons, neuroendocrine and endocrine cells, and in addition, they contain a cAMP response element (CRE) in their upstream regions, making it likely that CAMP-induced neuronal differentiation might be accompanied by increased transcription of these genes. We increased intracellular CAMP levels in neuronal and neuroendocrine cells and analyzed the levels of chromogranin B and synapsin I mRNA. Our data revealed that, while chromogranin B mRNA was in fact induced following cAMP stimulation, synapsin I mRNA was not affected. To analyze the cis-acting sequences, we constructed hybrid genes containing the upstream region of the mouse chromogranin B gene fused to a reporter gene. Similar plasmids containing the synapsin I or the glucagon promoter were constructed. Transfections of neuronal and endocrine cells, together with deletion mutagenesis, revealed that the CRE of the chromogranin B gene mediated the effect of cAMP upon transcription. This effect was mimicked by overexpression of the catalytic subunit of the CAMP-dependent protein kinase. In addition, overexpression of the negative-acting CRE-binding protein CREB-2 revealed that the chromogranin B CRE functions as a bifunctional genetic regulatory element in that it mediates basal as well as CAMP-stimulated transcription. Synapsin I gene expression, however, was not induced by either elevated intracellular cAMP concentration or by overexpression of protein kinase A, although a similar pattern of proteins, including CREB, bound to the synapsin I and chromogranin B CRE in vitro. Thus while the CRE element in the chromogranin B gene promoter is responsive to CAMP, the same element, when present in the synapsin I promoter, does not confer cAMP inducibility.

show abstract

The organisation of the mouse chromogranin B (secretogranin I) gene

Cited by 66 publications

References 28 publications

Chromogranin B in Heart Failure

Chromogranin B in Heart Failure

Chromogranin A: current status as a precursor for bioactive peptides and a granulogenic/sorting factor in the regulated secretory pathway

Differential Regulation of Chromogranin B and Synapsin I Gene Promoter Activity by cAMP and cAMP‐Dependent Protein Kinase

Contact Info

Product

Resources

About