scholarly journals The effect of human growth hormone on the carbohydrate units in arterial basement membrane-like material

2000 ◽  
pp. 631-635 ◽  
Author(s):  
T Ledet ◽  
L Heickendorff
Keyword(s):  
Growth Hormone ◽  
Smooth Muscle ◽  
Basement Membrane ◽  
Smooth Muscle Cells ◽  
Human Growth Hormone ◽  
Human Growth ◽  
Muscle Cells ◽  
Carbohydrate Composition ◽  
Large Vessel Disease

OBJECTIVE: The present study focuses on the pathogenesis of the large vessel disease in diabetes. The arterial wall from diabetic individuals displays characteristic alterations of the extracellular matrix. Other observations show that the metabolism is changed with increased levels of growth hormone in diabetes. DESIGN: The effects of growth hormone on the carbohydrate composition in the basement membrane around the arterial smooth muscle cells were investigated. METHODS: Basement membrane material was obtained from cultures of smooth muscle cells by sonication and differential centrifugation after labeling with either [(3)H]glucose or [(3)H]glucosamine. The proportions of galactose, glucose, mannose, xylose, fucose and glucosamine were evaluated after addition of 45.45pmol/l human growth hormone. Also, the proportion of glycopeptides generated from the basement membrane was analyzed after fractionation on a combination of a Concanavalin A and a Pea Sepharose column. RESULTS: The proportion of galactose and glucose was changed, and the incorporation of [(3)H]glucosamine was reduced. The proportion of glycopeptides containing high mannose moities was increased as well as that of triantinary glycopeptides with internal fucose residues. CONCLUSION: The current in vitro data indicates that growth hormone may change the carbohydrate composition of the arterial basement membrane.

scholarly journals Production of hyaluronan and chondroitin sulphate proteoglycans from human arterial smooth muscle--the effect of glucose, insulin, IGF-I or growth hormone

2001 ◽  
pp. 193-198 ◽  
Author(s):  
C Erikstrup ◽  
LM Pedersen ◽  
L Heickendorff ◽  
T Ledet ◽  
LM Rasmussen
Keyword(s):  
Growth Hormone ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Chondroitin Sulphate ◽  
Human Growth ◽  
Muscle Cells ◽  
Arterial Smooth Muscle ◽  
Chondroitin Sulphate Proteoglycans ◽  
Igf I

BACKGROUND: Although it is recognized that the extracellular matrix is important for cell proliferation, migration and metabolism of growth factors, the regulation of the synthesis of hyaluronan and chondroitin sulphate proteoglycan (CSPG) in the vessel wall is poorly understood. OBJECTIVE: To examine the role of glucose, insulin, IGF-I and human growth hormone (hGH) on the accumulation of hyaluronan and CSPG using cultures of human aortic smooth muscle cells. METHODS: The cultures were exposed for 36 h. The CSPG content in the incubation medium was measured by a combination of digestion with testicular hyaluronidase and precipitation of [35SO4(2-)]-labelled material with ethanol and trichloroacetic acid. Hyaluronan was estimated using a radiometric assay. RESULTS: Glucose and insulin reduced the amount of synthesized hyaluronan (2P<0.01). Stimulation of synthesis was seen with hGH (2P<0.01), whereas no effect was observed with IGF-I. The production of CSPG was increased with glucose and hGH (2P<0.01), but showed no change with insulin. CONCLUSIONS: The present data obtained with human arterial smooth muscle cells in vitro showed that glucose, insulin and hGH can influence the accumulation of hyaluronan and CSPG. These observations may be relevant for an understanding of diabetic macroangiopathy.

Phenotypic Modulation of Smooth Muscle Cells after Arterial Injury Is Associated with Changes in the Distribution of Laminin and Fibronectin

1997 ◽  
Vol 45 (6) ◽  
pp. 837-846 ◽  
Author(s):  
Johan Thyberg ◽  
Karin Blomgren ◽  
Joy Roy ◽  
Phan Kiet Tran ◽  
Ulf Hedin
Keyword(s):  
Smooth Muscle ◽  
Basement Membrane ◽  
Smooth Muscle Cells ◽  
Actin Filaments ◽  
Cell Structure ◽  
Muscle Cells ◽  
Arterial Injury ◽  
Internal Elastic Lamina ◽  
Contractile Phenotype

Earlier in vitro studies suggest opposing roles of laminin and fibronectin in regulation of differentiated properties of vascular smooth muscle cells. To find out if this may also be the case in vivo, we used immunoelectron microscopy to study the distribution of these proteins during formation of intimal thickening after arterial injury. In parallel, cell structure and content of smooth muscle α-actin was analyzed. The results indicate that the cells in the normal media are in a contractile phenotype with abundant α-actin filaments and an incomplete basement membrane. Within 1 week after endothelial denudation, most cells in the innermost layer of the media convert into a synthetic phenotype, as judged by loss of actin filaments, construction of a large secretory apparatus, and destruction of the basement membrane. Some of these cells migrate through fenestrae in the internal elastic lamina and invade a fibronectin-rich network deposited on its luminal surface. Within another few weeks a thick neointima forms, newly produced matrix components replace the strands of fibronectin, and a basement membrane reappears. Simultaneously, the cells resume a contractile phenotype, recognized by disappearance of secretory organelles and restoration of α-actin filaments. These findings support the notion that laminin and other basement membrane components promote the expression of a differentiated smooth muscle phenotype, whereas fibronectin stimulates the cells to adopt a proliferative and secretory phenotype.

Epicardial Cells of Human Adults Can Undergo an Epithelial-to-Mesenchymal Transition and Obtain Characteristics of Smooth Muscle Cells In Vitro

Stem Cells ◽  
2007 ◽  
Vol 25 (2) ◽  
pp. 271-278 ◽  
Author(s):  
John van Tuyn ◽  
Douwe E. Atsma ◽  
Elizabeth M. Winter ◽  
Ietje van der Velde-van Dijke ◽  
Daniel A. Pijnappels ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Epithelial To Mesenchymal Transition ◽  
Muscle Cells ◽  
Mesenchymal Transition ◽  
Epicardial Cells ◽  
Human Adults

Characterization and confocal imaging of calponin in gastrointestinal smooth muscle

1993 ◽  
Vol 265 (5) ◽  
pp. C1371-C1378 ◽  
Author(s):  
M. P. Walsh ◽  
J. D. Carmichael ◽  
G. J. Kargacin
Keyword(s):  
Smooth Muscle ◽  
Protein Kinase ◽  
Smooth Muscle Cells ◽  
Thin Filament ◽  
Muscle Cells ◽  
Biochemical Properties ◽  
Confocal Imaging ◽  
Isolated Cells ◽  
Independent Manner

Calponin isolated from chicken gizzard smooth muscle binds in vitro to actin in a Ca(2+)-independent manner and thereby inhibits the actin-activated Mg(2+)-adenosinetriphosphatase of smooth muscle myosin. This inhibition is relieved when calponin is phosphorylated by protein kinase C or Ca2+/calmodulin-dependent protein kinase II, suggesting that calponin is involved in thin filament-associated regulation of smooth muscle contraction. To further examine this possibility, calponin was isolated from toad stomach smooth muscle, characterized biochemically, and localized in intact isolated cells. Toad stomach calponin had the same basic biochemical properties as calponin from other sources. Confocal immunofluorescence microscopy revealed that calponin in intact smooth muscle cells was localized to long filamentous structures that were colabeled by antibodies to actin or tropomyosin. Preservation of the basic biochemical properties of calponin from species to species suggests that these properties are relevant for its in vivo function. Its colocalization with actin and tropomyosin indicates that calponin is associated with the thin filament in intact smooth muscle cells.

Reduced and S-carboxymethylated human growth hormone: a probe for diabetogenic action

1984 ◽  
Vol 247 (5) ◽  
pp. E639-E644
Author(s):  
C. M. Cameron ◽  
J. L. Kostyo ◽  
J. A. Rillema ◽  
S. E. Gennick
Keyword(s):  
Growth Hormone ◽  
Amino Acid ◽  
Human Growth Hormone ◽  
Human Growth ◽  
Mouse Mammary Gland ◽  
Amino Acid Incorporation ◽  
Acid Incorporation ◽  
Hypophysectomized Rats

The biological activity profile of reduced and S-carboxymethylated human growth hormone (RCM-hGH) was determined to establish its suitability for study of the diabetogenic property of hGH. RCM-hGH was found to have greatly attenuated in vivo growth-promoting activity in the 9-day weight-gain test in hypophysectomized rats (approximately 1%) and to have a similar low order of in vitro activity in stimulating amino acid incorporation into the protein of the isolated rat diaphragm. RCM-hGH also only had approximately 1% of the in vitro insulin-like activity of the native hormone on isolated adipose tissue from hypophysectomized rats. In contrast, RCM-hGH retained substantial in vivo diabetogenic activity in the ob/ob mouse, appearing to have approximately 50% of the activity of the native hormone. RCM-hGH was also found to retain significant, although attenuated (25%), in vitro lactogenic activity when tested for the ability to stimulate amino acid incorporation into a casein-rich protein fraction in mouse mammary gland explants. Because RCM-hGH exhibits a high degree of diabetogenic activity, although lacking significant anabolic or insulin-like activities, it will be useful as a "monovalent" probe for the study of the molecular mechanism of the diabetogenic action of GH.

Bioactivity of human growth hormone in serum: validation of an in vitro bioassay.

Endocrinology ◽  
1993 ◽  
Vol 132 (5) ◽  
pp. 2073-2082 ◽  
Author(s):  
C M Foster ◽  
M Borondy ◽  
V Padmanabhan ◽  
J Schwartz ◽  
G B Kletter ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Human Growth Hormone ◽  
Human Growth ◽  
In Vitro Bioassay

Light and dark smooth muscle cells in estrogen-stimulated rat myometrium

1976 ◽  
Vol 54 (6) ◽  
pp. 822-833 ◽  
Author(s):  
R. E. Garfield ◽  
E. E. Daniel
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Atp Depletion ◽  
Metabolic Inhibitors ◽  
Volume Control ◽  
Control Mechanisms ◽  
Dark Cells ◽  
Light Cells

Smooth muscle cells of different densities to transmission of electrons (termed light and dark cells) were found in rat myometrium examined in the electron microscope following fixation by immersion in glutaraldehyde. Light cells accounted for about 4% of the total population of cells. No light cells were found in tissues fixed in situ by intraarterial perfusion with glutaraldehyde. In addition to staining differences, light cells were distinguished from most dark cells by differences in nuclear, mitochondrial, endoplasmic reticular, and surface structures. The relative number of light and dark cells after in vitro fixation was not changed in tissues relaxed with adrenaline or contracted with oxytocin. Mechanical injury resulted in increased numbers of light cells. Similarly, chemical injury with metabolic inhibitors resulted in ATP depletion, followed by increased numbers of light cells and gain in water content. We concluded that light cells were produced by mechanical or metabolic damage, leading to loss of volume control mechanisms, swelling, and leakage of protein. Light cells found after fixation in vitro in numerous prior studies represent cells damaged during isolation, and not a physiological variant among smooth muscle cells.

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