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G Plenz

Publications and source records attributed to G Plenz.

32 records · Page 2Linked to original sources
PubMed1998

The effect of tissue expansion on the expression of collagen type I and type III mRNA in distinct areas of skin in the dog as an animal model.

To evaluate the transcriptional response of skin to tissue expansion in the dog, the expression of procollagen alpha 1(I) mRNA and procollagen alpha 1(III) mRNA were analyzed by in situ hybridization. This expression was evaluated in distinct skin areas (subepidermal zone, dermis, capsular zone) after 4-85 days of expansion. Within the first 4 days of expansion expression of procollagen alpha 1(I) and alpha 1(III) mRNA was not affected in the subepidermal and dermal zone. Only a slightly elevated level of type III procollagen mRNA was demonstrated in tissue surrounding the implanted silicone expander. After 7 days of expansion an enhanced level of procollagen alpha 1(III) mRNA was observed in the dermis and capsular zone. A slightly enhanced type I collagen mRNA level occurred in all zones of the dermis that was even stronger in the capsular zone after 9 days of expansion. Concurrently, the number of transcriptionally active cells was significantly higher. Return to the basal level of procollagen alpha 1(I) mRNA was attained after 40 days. At this time a significant expression of procollagenase mRNA was observed. Procollagen III mRNA expression reached its basal level on day 85.

Animals↗
PubMed1998

Nonradioactive in situ hybridization for detection of hydrophobin mRNA in the phytopathogenic fungus Claviceps purpurea during infection of rye.

Hydrophobins are unique fungal extracellular proteins that produce amphipathic films at interfaces, mediate contact to hydrophobic surfaces and are known to be important in phytopathogenicity. In the pathogenic ascomycete Claviceps purpurea, causing ergot disease in grasses and cereals and ergotism in livestock, a gene encoding an extraordinary type of hydrophobin has been detected, which appeared to be induced during alkaloid synthesis in axenic culture of an ergot-alkaloid producing strain of Claviceps (V. Garre and P. Tudzynski, pers. communication; Arntz and Tudzynski, 1997, Curr. Genet. 31, 357-360). To elucidate presence and function of this hydrophobin during infection of rye, the nonradioactive in situ hybridization technique was successfully adapted to the fungal organism and optimized in the pathogenic interaction system. Semithin cryosections proved to be suitable for microscopical gene expression analysis using immune-mediated alkaline-phosphatase staining for detection of digoxigenin-labeled cRNA probes. Specific hybridization of the prepared antisense riboprobe to hydrophobin mRNA was confirmed in nonradioactive Northern blots. While permeabilization by proteinase K had only a minor effect, the inclusion of detergent into the hybridization solutions enhanced specific RNA-RNA hybridization under maximum stringency. Hydrophobin mRNA was found in fungal cells, growing in axenic culture. In the disease cycle, hydrophobin transcripts were localized in abundance during vegetative fructification in conidiophores that actively produced conidia. No signals were observed in sclerotial hyphae during formation of the alkaloid-containing ergots, although they fluoresced intensely during total RNA detection using acridine orange. Notably, in situ hybridization experiments resulted in specific signals during early infection and colonization phases in the external mycelia and in hyphae penetrating the host epidermal layer. The presumed role of the hydrophobin gene product in ergot pathogenicity is discussed with respect to the described spatio-temporal distribution of the hydrophobin transcripts.

Claviceps↗
PubMed1998

Left-ventricular expression of interleukin-6 messenger-RNA higher in idiopathic dilated than in ischemic cardiomyopathy.

During end-stage heart failure, plasma levels of interleukin-6 (IL6) are elevated. This cytokine exerts a negative inotropic influence on the myocardium. The production site of IL6 is unclear. We examined the hypothesis that IL6 in end-stage heart-failure patients is produced in the myocardium itself and is differentially regulated according to etiology. Cardiac tissue was obtained from 27 patients (idiopathic dilated cardiomyopathy, (DCM) 9/6 m/f, age 46 +/- 14 y; ischemic cardiomyopathy (ICM), 11/1 m/f, age 55 +/- 8 y) at the time of transplantation. The tissue was subjected to IL6 Northern-blot analysis. Signals were quantified by densitometric scanning after normalization to G3 PDH mRNA. Data were compared by Mann-Whitney test between DCM and ICM patients, divided by chamber origin. IL6 transcripts were found in all patients. In DCM, left-ventricular IL6 mRNA expression was higher than in ICM (p = 0.006). Median right-ventricular as well as left- and right-atrial IL6 mRNA expression was not significantly different in both groups. In summary, in end-stage heart failure, IL6 mRNA is consistently expressed in the myocardium. Left-ventricular expression is higher in DCM than in ICM. These data support the concept of a potentially reversible inflammatory component in the etiology of DCM which is more pronounced than in patients with ICM of comparable clinical severity.

Adult↗
PubMed1998

Monocytes/macrophages in atherosclerosis.

The realization that the monocyte/macrophage is central to both atherogenesis and the progression of the atherosclerotic plaque has arisen only recently. In this chapter the role of the monocyte/macrophage in the genesis of the atherosclerotic plaque will be discussed. As will be demonstrated, the pivotal role of the macrophage in atherosclerosis depends not only on its ability to handle lipids but also on its physical and secretory functions and its role as a mediator of inflammation.

Animals↗
PubMed1997

[Proinflammatory cytokines and cardiac pump function].

In situations of depressed myocardial function, the role of immunological mechanisms has been studied recently. In different pathophysiological situations, such as chronic heart failure, open heart surgery with extracorporal circulation, cardiac transplantation, myocardial infarction and angina pectoris, patterns have been described with elevation of proinflammatory cytokines, such as tumor necrosis factor-alpha, interleukin-1, interleukin-6, and reversible myocardial dysfunction, which may represent a final common pathway. The available data suggest a modulation of important determinants of pump function, i.e., contractility, preload, afterload, and heart rate, by cytokines. Potential mechanisms include the beta-adrenoceptor- and nitric oxide pathway, as well as a direct impact on intracellular calcium homeostasis. Interventional strategies based on this understanding are beginning to emerge.

Animals↗
PubMed1997

Smooth muscle cells express granulocyte-macrophage colony-stimulating factor in the undiseased and atherosclerotic human coronary artery.

Granulocyte-macrophage colony-stimulating factor (GM-CSF), one of a family of cytokines that regulate proliferation in macrophages and other types of cells, has been implicated in the inflammatory-fibroproliferative response of atherosclerosis. However, previous studies have been restricted to cultured cells and animal models. In the present study, we investigated GM-CSF expression in undiseased and atherosclerotic human coronary arteries at both the mRNA and protein levels. Dual in situ hybridization/cell-marking experiments demonstrated that subpopulations of intimal smooth muscle cells (SMCs) and endothelial cells express the cytokine in the histologically normal human coronary artery and that augmented expression occurs at these sites, and in macrophage accumulations and medial SMCs, in the atherosclerotic vessel. Corresponding data were obtained by in situ hybridization and reverse transcription-polymerase chain reaction and Northern analyses of cultured cells. Cultured human coronary arterial SMCs showed constitutive expression of GM-CSF in cells that had adopted an activated synthetic phenotype. Electron microscope immunocytochemistry revealed that GM-CSF is a protein localized in the cytoplasmic matrix of SMCs of both the undiseased and atherosclerotic vessel wall; extracellular matrix was largely unlabeled, with only occasional small patches of amorphous immunopositive material. The expression of GM-CSF by subpopulations of intimal SMCs in the undiseased artery and the marked upregulation of GM-CSF apparent in atherosclerotic lesions suggest roles for the cytokine in the cellular events underlying initiation and progression of the human atherosclerotic lesion.

Adolescent↗
PubMed1996

Two additional 5' exons in the human Vigilin gene distinguish it from the chicken gene and provide the structural basis for differential routes of gene expression.

Vigilin, a 150-kDa protein, contains 14 tandemly arranged domains, each consisting of a KH RNA-binding motif and a spacer region. Here, we report on the physical structure of the human Vigilin gene with 29 exons, thereby outnumbering the chicken gene by two additional 5' exons. These additional exons, 1A and 1B, are alternatively though concurrently spliced to exon 1C which is homologous to the first exon in the chicken gene. None of the additional human exons code for an amino-terminal extension of Vigilin, due to in-frame stop codons. Structural features of exon 1A, however, would allow the translation of a 13-amino-acid peptide from an upstream open reading frame preceding the vigilin open reading frame. We suggest that exons 1A and 1B have been gained during evolution, allowing alternative routes of expression control of the human Vigilin gene.

Alternative Splicing↗
PubMed1995

Experimental tissue expansion induces changes in expression of procollagen I and III messenger RNA.

Experimental tissue expansion was performed in nine dogs following placement of subcutaneous silicone balloons. The balloon expander was then filled with 300 ml saline immediately after implantation. Duration of expansion varied from 3 days to 124 days. Unaffected skin and skin over an empty expander served as control tissue. Dermal procollagen I and procollagen III gene expression in response to tissue expansion was investigated by dot-blot analysis using digoxigenin-labeled RNA probes complementary to either human procollagen-alpha 1(I) mRNA or procollagen-alpha 1(III) mRNA. Cross-hybridization of human probes with canine procollagen mRNA was demonstrated by Northern blot analysis. In response to the trauma of surgery, procollagen I and III mRNA transcriptions were found to be decreased significantly within the first few days after implantation. After 9 days of expansion, increased levels of procollagen I mRNA were found, while after 16 days increased levels of procollagen III mRNA were evident. The present study is the first to demonstrate changes in dermal collagen gene expression as a reaction to tissue expansion.

Animals↗
PubMed1994

The human vigilin gene: identification, chromosomal localization and expression pattern.

Chick vigilin cRNA clones were used to isolate the cognate human gene, by screening a pWE15 genomic library. Three independent cosmid clones were isolated and characterized by restriction mapping. The gene was identified by sequencing an internal EcoRI fragment containing two exons homologous to exon 24 and 25 of the chicken vigilin gene and corresponding to nucleotides 1973-2104 of the human HBP-cDNA. The homology between the chicken and human sequences was 77% and 82% at the cDNA level, and 91% and 100% at the amino acid level. In addition, the analyzed intron/exon boundaries were invariantly conserved. The 5' and 3' regions of the human gene were mapped by Southern analysis of the respective clones with synthetic oligonucleotides. The entire vigilin gene spans a region of about 50 kb and has been assigned to chromosome 2q36-q37.2 (FL-pter value of 0.96 +/- 0.03) by fluorescence in situ hybridization to metaphase spreads from normal peripheral blood lymphocytes. The vigilin gene is localized in a chromosomal region comprising a cluster of collagen genes (COLIVA3, COLVIA3) and the locus of the Waardenburg syndrome I. Only one mRNA species of 4.4 kb is transcribed from the human vigilin gene. In accordance with previous observations on chicken mRNA, the expression of the human vigilin mRNA depends on the stage of cytodifferentiation both in vitro and in situ.

Blotting, Northern↗
PubMed1993

Expression of vigilin in chicken cartilage and bone.

The expression of vigilin was followed during chick embryonal development by in situ hybridization. Vigilin mRNA is abundantly expressed in tissues of mesenchymal and ectomesenchymal origin. The mesenchymal primordial cells of cartilage and bone did not show any significant expression of vigilin. As tissue differentiation proceeded, vigilin mRNA levels increased in hyaline cartilage and in both endochondral as well as intramembranous bone. The results suggest that the expression of vigilin mRNA in cartilage- and bone-forming cells, chondrocytes and osteoblasts, is dependent on the stage of development and cellular differentiation, although not a unique process of bone formation. Most striking is the correlation of the maximum vigilin mRNA expression in osteoblasts and hypertrophic chondrocytes to periods when cell-specific genes were highly transcribed and substantially translated, e.g., synthesis of procollagen and formation of extracellular matrix in bone and cartilage.

Animals↗