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Journal articles on the topic 'Desmosine'

Author: Grafiati

Published: 4 June 2021

Last updated: 8 February 2022

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1

McClintock, Dana E., Barry Starcher, Mark D. Eisner, B. Taylor Thompson, Doug L. Hayden, Gwynne D. Church, and Michael A. Matthay. "Higher urine desmosine levels are associated with mortality in patients with acute lung injury." American Journal of Physiology-Lung Cellular and Molecular Physiology 291, no. 4 (October 2006): L566—L571. http://dx.doi.org/10.1152/ajplung.00457.2005.

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Desmosine is a stable breakdown product of elastin that can be reliably measured in urine samples. We tested the hypothesis that higher baseline urine desmosine would be associated with higher mortality in 579 of 861 patients included in the recent Acute Respiratory Distress Syndrome Network trial of lower tidal volume ventilation ( 1 ). We also correlated urine desmosine levels with indexes of disease severity. Finally, we assessed whether urine desmosine was lower in patients who received lower tidal volumes. Desmosine was measured by radioimmunoassay in urine samples from days 0, 1, and 3 of the study. The data were expressed as a ratio of urine desmosine to urine creatinine to control for renal dilution. The results show that higher baseline ( day 0) urine desmosine-to-creatinine concentration was associated with a higher risk of death on adjusted analysis (odds ratio 1.36, 95% confidence interval 1.02–1.82, P = 0.03). Urine desmosine increased in both ventilator groups from day 0 to day 3, but the average rise was higher in the 12-ml/kg predicted body weight group compared with the 6-ml/kg predicted body weight group ( P = 0.053, repeated-measures model). In conclusion, patients with acute lung injury ventilated with lower tidal volumes have lower urine desmosine levels, a finding that may reflect reduced extracellular matrix breakdown. These results illustrate the value of evaluating urinary biological markers that may have prognostic and pathogenetic significance in acute lung injury.

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2

Starcher, Barry, and Marti Scott. "Fractionation of Urine to Allow Desmosine Analysis by Radioimmunoassay." Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 29, no. 1 (January 1992): 72–78. http://dx.doi.org/10.1177/000456329202900111.

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The present study was designed to re-evaluate the radioimmunoassay for desmosine in urine, which is currently used as a measure of elastin metabolism. Using ion exchange chromatography, gel filtration and affinity chromatography it was shown that at least five other compounds in hydrolysates of human urine competed for desmosine in the RIA. Fractionating the urine prior to hydrolysis with acetone removed one of the major contaminants. The other contaminants could subsequently be removed by extracting the urine hydrolysate with a mixture of chloroform/ethanol (60:40). Samples from nine normal adult urines showed that an average of 45% of the RIA competing material in unfractionated urine was not desmosine. The final extracted residue retained all of the desmosine and only 16% of the original solids. The average adult urine contains approximately 50 pmol desmosine/mg creatinine, reflecting a daily turnover of between 3 and 4 mg of elastin per day.

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3

Murakami, Yuko, Rina Suzuki, Hiroto Yanuma, Jiangtao He, Shuren Ma, Gerard M. Turino, Yong Y. Lin, and Toyonobu Usuki. "Synthesis and LC-MS/MS analysis of desmosine-CH2, a potential internal standard for the degraded elastin biomarker desmosine." Org. Biomol. Chem. 12, no. 48 (2014): 9887–94. http://dx.doi.org/10.1039/c4ob01438c.

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4

Hirose, Mika, Reiko Yokoo, Daisuke Watanabe, Rina Suzuki, Miho Tanigawa, and Toyonobu Usuki. "Synthesis of Multi‐Deuterated Desmosine." ChemistrySelect 5, no. 13 (April 2020): 3843–46. http://dx.doi.org/10.1002/slct.202000507.

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5

Schräder, Christoph U., Andrea Heinz, Petra Majovsky, and Christian E. H. Schmelzer. "Fingerprinting Desmosine-Containing Elastin Peptides." Journal of The American Society for Mass Spectrometry 26, no. 5 (January 21, 2015): 762–73. http://dx.doi.org/10.1007/s13361-014-1075-9.

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6

Pai, V., A. Guz, G. J. Phillips, N. T. Cooke, D. C. S. Hutchison, and T. D. Tetley. "Urinary desmosine, elastolysis, and lung disease." Metabolism 40, no. 2 (February 1991): 139–45. http://dx.doi.org/10.1016/0026-0495(91)90164-r.

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7

Janssen, Rob, Jef Serré, Ianthe Piscaer, Ruben Zaal, Henny van Daal, Carolien Mathyssen, Pieter Zanen, Jody M. W. van den Ouweland, and Wim Janssens. "Post hoc analysis of a randomised controlled trial: effect of vitamin D supplementation on circulating levels of desmosine in COPD." ERJ Open Research 6, no. 4 (October 2020): 00128–2019. http://dx.doi.org/10.1183/23120541.00128-2019.

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BackgroundVitamin D supplementation lowers exacerbation frequency in severe vitamin D-deficient patients with COPD. Data regarding the effect of vitamin D on elastin degradation are lacking. Based on the vitamin's anti-inflammatory properties, we hypothesised that vitamin D supplementation reduces elastin degradation, particularly in vitamin D-deficient COPD patients. We assessed the effect of vitamin D status and supplementation on elastin degradation by measuring plasma desmosine, a biomarker of elastin degradation.MethodsDesmosine was measured every 4 months in plasma of 142 vitamin D-naïve COPD patients from the Leuven vitamin D intervention trial (100 000 IU vitamin D3 supplementation every 4 weeks for 1 year).ResultsNo significant association was found between baseline 25-hydroxyvitamin D (25(OH)D) and desmosine levels. No significant difference in desmosine change over time was found between the placebo and intervention group during the course of the trial. In the intervention arm, an unexpected inverse association was found between desmosine change and baseline 25(OH)D levels (p=0.005).ConclusionsVitamin D supplementation did not have a significant overall effect on elastin degradation compared to placebo. Contrary to our hypothesis, the intervention decelerated elastin degradation in vitamin D-sufficient COPD patients and not in vitamin D-deficient subjects.

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8

Sekhon, H. S., and W. M. Thurlbeck. "Lung growth in hypobaric normoxia, normobaric hypoxia, and hypobaric hypoxia in growing rats. I. Biochemistry." Journal of Applied Physiology 78, no. 1 (January 1, 1995): 124–31. http://dx.doi.org/10.1152/jappl.1995.78.1.124.

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Adaptive changes in cellular and connective tissue components of the lung after chronic exposure to reduced ambient oxygen and/or pressure were studied. Four-week-old male Sprague-Dawley rats were randomly divided into five groups (n = 12 each): 1) general control, room air (GC); 2) hypobaric normoxic; 3) normobaric hypoxic; 4) hypobaric hypoxic; and 5) weight-matched control, restricted food intake (WMC; weight matched to hypobaric hypoxic animals). Lung growth (lung weight and DNA, RNA, protein, hydroxyproline, and desmosine contents) diminished in WMC compared with GC. Somatic growth decreased in hypobaric and normobaric hypoxic rats compared with GC. Lung weight; DNA, RNA, protein, hydroxyproline, and desmosine contents; and RNA/DNA, protein/DNA, and desmosine/DNA ratios increased in both hypobaric and normobaric hypoxic rats compared with WMC. Hydroxyproline and desmosine contents and the hydroxyproline/DNA ratio were significantly higher in hypobaric than normobaric hypoxic rats. Hypobaric normoxia caused a slight somatic growth reduction, but biochemical parameters of lung growth remained unaffected. In conclusion, in growing animals, despite inhibition of lung growth due to reduced food consumption, accelerated lung growth in hypobaric or normobaric hypoxia occurs by hyperplastic and hypertrophic changes. Hypobaric normoxia does not affect lung growth, but connective tissue proteins accumulate slightly more in hypobaric hypoxia than in hypoxia alone.

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9

Zay, K., S. Loo, C. Xie, D. V. Devine, J. Wright, and A. Churg. "Role of neutrophils and α1-antitrypsin in coal- and silica-induced connective tissue breakdown." American Journal of Physiology-Lung Cellular and Molecular Physiology 276, no. 2 (February 1, 1999): L269—L279. http://dx.doi.org/10.1152/ajplung.1999.276.2.l269.

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Mineral dusts produce emphysema, and administration of dust to rats results in the rapid appearance of desmosine and hydroxyproline in lavage fluid, confirming that dusts directly induce connective tissue breakdown. To examine the role of neutrophils and α1-antitrypsin (α1-AT) in this process, we instilled silica or coal into normal rats or rats that had been pretreated with antiserum against neutrophils. One day after dust exposure, lavage fluid neutrophils and desmosine and hydroxyproline levels were all elevated; treatment with antiserum against neutrophils reduced neutrophils by 75%, desmosine by 40–50%, and hydroxyproline by 25%. By 7 days, lavage fluid neutrophils and desmosine level had decreased, whereas macrophages and hydroxyproline level had increased. By ELISA analysis, lavage fluid α1-AT levels were increased four- to eightfold at both times. On Western blot, some of the α1-AT appeared as degraded fragments, and by HPLC analysis, 5–10% of the methionine residues were oxidized. At both times, lavage fluid exhibited considerably elevated serine elastase inhibitory capacity and also showed elevations in metalloelastase activity. We conclude that, in this model, connective tissue breakdown is initially driven largely by neutrophil-derived proteases and that markedly elevated levels of functional α1-AT do not prevent breakdown, thus providing in vivo support for the concept of quantum proteolysis proposed by Liou and Campbell (T. G. Liou and E. J. Campbell. Biochemistry 34: 16171–16177, 1995). Macrophage-derived proteases may be of increasing importance over time, especially in coal-treated animals.

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10

TETLEY, T. D., G. J. PHILLIPS, A. GUZ, and B. FOX. "The Blotchy Mouse, Lung Desmosine, and Emphysema." Annals of the New York Academy of Sciences 624, no. 1 (May 1991): 358. http://dx.doi.org/10.1111/j.1749-6632.1991.tb17048.x.

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11

Guay, M., G. Lagace, and F. Lamy. "Photolysis and Ozonolysis of Desmosine and Elastolytic Peptides." Connective Tissue Research 14, no. 2 (January 1985): 89–107. http://dx.doi.org/10.3109/03008208509015016.

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12

Dhital, Basant, Philip Durlik, Pratikkumar Rathod, Farhana Gul-E-Noor, Zhixiao Wang, Cheng Sun, Emmanuel J. Chang, Boris Itin, and Gregory S. Boutis. "Ultraviolet radiation reduces desmosine cross-links in elastin." Biochemistry and Biophysics Reports 10 (July 2017): 172–77. http://dx.doi.org/10.1016/j.bbrep.2017.04.002.

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13

Leppert, Phyllis C., Shiu Yeh Yu, Stephen Keller, Joseph Cerreta, and Ines Mandl. "Decreased elastic fibers and desmosine content in incompetent cervix." American Journal of Obstetrics and Gynecology 157, no. 5 (November 1987): 1134–39. http://dx.doi.org/10.1016/s0002-9378(87)80277-6.

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14

Fill, J. A., J. T. Brandt, H. P. Wiedemann, B. L. Rinehart, C. F. Lindemann, J. J. Komara, R. R. Bowsher, M. C. Spence, and B. G. Zeiher. "Urinary desmosine as a biomarker in acute lung injury." Biomarkers 11, no. 1 (January 2006): 85–96. http://dx.doi.org/10.1080/13547500500343225.

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15

Sulaiman, Mazdida, Marie-Therese Martin, Mary Pais, A. Hamid A. Hadi, and Khalijah Awang. "ChemInform Abstract: Desmosine, an Artefact Alkaloid from Desmos dumosus." ChemInform 30, no. 18 (June 16, 2010): no. http://dx.doi.org/10.1002/chin.199918205.

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16

Usuki, Toyonobu, Haruka Yamada, Takahiro Hayashi, Hiroto Yanuma, Yohei Koseki, Noriyuki Suzuki, Yoshiro Masuyama, and Yong Y. Lin. "Total synthesis of COPD biomarker desmosine that crosslinks elastin." Chemical Communications 48, no. 26 (2012): 3233. http://dx.doi.org/10.1039/c2cc17958j.

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17

Giummelly, Philippe, Bernard Botton, Raphaëlle Friot, Deddi Prima-Putra, and Jeffrey Atkinson. "Measurement of desmosine and isodesmosine by capillary zone electrophoresis." Journal of Chromatography A 710, no. 2 (September 1995): 357–60. http://dx.doi.org/10.1016/0021-9673(95)00487-4.

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18

Sabirin, Rahmaningsih Mara, Prasetyastuti, and Denny Agustiningsih. "Rosuvastatin Attenuated Elastic Fiber Degradation in Chronic Obstructive Pulmonary Disease Sprague-Dawley Rats." Jurnal Kedokteran Brawijaya 30, no. 3 (February 28, 2019): 175. http://dx.doi.org/10.21776/ub.jkb.2019.030.03.2.

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<p>Chronic obstructive pulmonary disease (COPD) is an incurable disease which causes disability and death. The main pathogenesis of COPD is oxidative stress due to cigarette smoke which initiates various reactions and lead to lung elastic fibers destruction. Statins are known to have antioxidant effects and reduce mortality in COPD. We studied the effects of cigarette smoke exposure cessation and rosuvastatin on oxidative stress and the level of elastic fiber destruction in COPD model rats. Thirty 10-week old male Sprague-Dawley rats were divided into 2 groups: Control (n=6, did not received fumigation nor treatment) and Smoking (n=24, received fumigation for 70 days) groups. Afterwards, the smoking group was divided into 4 groups: Sham, R2, R5,R10, and received 0.9% NaCl, 2.5, 5 and 10 mg/kg/day of rosuvastatin, respectively. Examination of malondialdehyde (MDA) and desmosine serum were conducted to measure oxidative stress and elastic fiber degradation level, respectively. After smoke exposure, MDA and desmosine levels of COPD rats were found to be significantly higher (p=0.000 and 0.000) than controls. The MDA level in Sham, R2, R5 and R10 groups decreased significantly after therapy (p=0.000; 0.033; 0.015; 0.002). However, the post-treatment desmosine level was increase significantly in Sham and R2 groups (p=0.006 dan 0.012) and insignificantly (p=0.117 dan 0.278) in the R5 and R10 groups. It can be concluded that the cessation of exposure to cigarette smoke can reduce oxidative stress, but not elastic degradation process. The administration of rosuvastatin of 5 or 10 mg/kg/day attenuated elastic degradation process.</p>

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19

AIKAWA, JUNICHIRO, HIROSHI MUNAKATA, MAMORU ISEMURA, and ZENSAKU YOSIZAWA. "Sulfated glycopeptides, containing desmosine and isodesmosine, isolated from porcine aorta." Tohoku Journal of Experimental Medicine 145, no. 2 (1985): 175–83. http://dx.doi.org/10.1620/tjem.145.175.

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20

Ma, Shuren, Yong Y. Lin, and Gerard M. Turino. "Measurements of Desmosine and Isodesmosine by Mass Spectrometry in COPD." Chest 131, no. 5 (May 2007): 1363–71. http://dx.doi.org/10.1378/chest.06-2251.

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21

Luisetti, M., J. Stolk, and P. Iadarola. "Desmosine, a biomarker for COPD: old and in the way." European Respiratory Journal 39, no. 4 (March 31, 2012): 797–98. http://dx.doi.org/10.1183/09031936.00172911.

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22

Adgate, John L., Holly F. Reid, Robin Morris, Ronald W. Helms, Richard A. Berg, Ping-Chuan Hu, Pi-Wan Cheng, et al. "Nitrogen Dioxide Exposure and Urinary Excretion of Hydroxyproline and Desmosine." Archives of Environmental Health: An International Journal 47, no. 5 (October 1992): 376–84. http://dx.doi.org/10.1080/00039896.1992.9938378.

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23

Cantor, Jerome, Arnulfo Ochoa, Shuren Ma, Xingjian Liu, and Gerard Turino. "Free Desmosine is a Sensitive Marker of Smoke-Induced Emphysema." Lung 196, no. 6 (September 14, 2018): 659–63. http://dx.doi.org/10.1007/s00408-018-0163-1.

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24

Cumiskey, Wayne R., Edward D. Pagani, and Donald C. Bode. "Enrichment and analysis of desmosine and isodesmosine in biological fluids." Journal of Chromatography B: Biomedical Sciences and Applications 668, no. 2 (June 1995): 199–207. http://dx.doi.org/10.1016/0378-4347(95)00092-w.

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25

Myers, B. A., M. A. Dubick, R. D. Reynolds, and R. B. Rucker. "Effect of vitamin B-6 (pyridoxine) deficiency on lung elastin cross-linking in perinatal and weanling rat pups." Biochemical Journal 229, no. 1 (July 1, 1985): 153–60. http://dx.doi.org/10.1042/bj2290153.

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Weanling and perinatal rats were rendered vitamin B-6 (pyridoxine)-deficient. The rat pups were nursed from vitamin B-6-deficient or -sufficient dams and were killed at day 15 after parturition. The weanling rats were fed vitamin B-6-deficient or -sufficient diets and were killed after 5 weeks of treatment. Lung elastin from the groups of rats was then studied with respect to its content of lysine-derived cross-linking amino acids. Lung lysyl oxidase activity was also measured. B-6 deficiency decreased the number of lysine residues in elastin that were converted into the cross-linking amino acid precursor allysine. However, a more significant defect in cross-link formation was an apparent block in the condensation steps leading to the formation of desmosine. Desmosine was decreased, with an increase in the amounts of aldol condensation products (aldol CP) in elastin. It is proposed that the elevation in aldol CP results from the formation of thiazines, which are produced from the reaction between aldehyde and homocysteine. The concentration of homocysteine is significantly elevated in vitamin B-6-deficient rats.

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26

Low, R. B., W. S. Stirewalt, P. Hultgren, E. S. Low, and B. Starcher. "Changes in collagen and elastin in rabbit right-ventricular pressure overload." Biochemical Journal 263, no. 3 (November 1, 1989): 709–13. http://dx.doi.org/10.1042/bj2630709.

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Collagen content, the ratio of collagen types I and III and elastin content were measured in 5-6- and 10-12-week-old rabbits with and without right-ventricular pressure overload. Significant and equivalent hypertrophy occurred in both age groups. A 2-day pressure overload caused a fall in collagen concentration below control levels in right-ventricular tissue from the older animals, but no change in the younger ones. A 2-week pressure overload in the older animals resulted in a rise in collagen concentration, a decreased ratio of type III to type I plus III [III/(I + III)] collagens, a fall in desmosine concentration and a fall in the desmosine/hydroxyproline ratio in the right ventricle. None of these changes occurred in the younger age group. We hypothesize that the changes in connective-tissue proteins after overload in the older group may contribute to previously observed changes in mechanical performance. The divergent connective-tissue responses in the two groups suggest the importance of age in determining outcome, as well as the possibility of separate regulatory mechanisms for contractile and for architectural elements of the heart.

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27

Mackey, K., M. C. Meyer, W. S. Stirewalt, B. C. Starcher, and M. K. McLaughlin. "Composition and mechanics of mesenteric resistance arteries from pregnant rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 263, no. 1 (July 1, 1992): R2—R8. http://dx.doi.org/10.1152/ajpregu.1992.263.1.r2.

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We tested the hypothesis that the systemic resistance vasculature of the rat is remodeled during pregnancy as evidenced by significant alterations in the passive mechanical properties and extracellular matrix proteins in mesenteric arteries. Mechanical characteristics were determined for arteries from 20-day pregnant rats (n = 6) and age-matched controls (n = 5). Lumen diameter and wall thickness were measured in pressurized arteries (250-microns diameter) using a dimension analyzing system. Distensibility (the relative change in diameter per unit change in pressure) was less in the arteries from the pregnant rats (P less than 0.01). The calculated stress-strain relationships and elastic moduli indicated that the arteries were less stiff by late gestation (P less than 0.05). Ultramicro amino acid analysis and radioimmunoassay were used to measure hydroxyproline, desmosine, and leucine as indicators of collagen, elastin, and total protein, respectively, in similar-sized arteries. Hydroxyproline/leucine (index of collagen) and desmosine/leucine (elastin concentration) decreased 19 and 15% by late gestation (P less than 0.05). The significant alterations in passive mechanics and in extracellular protein content support the concept that arterial wall remodeling in the peripheral vasculature may be one component of the cardiovascular adaptations during pregnancy.

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28

Afdhal, Nezam H., Andrew P. Keaveny, Steven B. Cohen, David P. Nunes, Norris Maldonado, Michael O'Brien, and Phillip J. Stone. "Urinary assays for desmosine and hydroxylysylpyridinoline in the detection of cirrhosis." Journal of Hepatology 27, no. 6 (December 1997): 993–1002. http://dx.doi.org/10.1016/s0168-8278(97)80142-0.

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29

Boutin, Michel, Carl Berthelette, François G. Gervais, Mary-Beth Scholand, John Hoidal, Mark F. Leppert, Kevin P. Bateman, and Pierre Thibault. "High-Sensitivity NanoLC−MS/MS Analysis of Urinary Desmosine and Isodesmosine." Analytical Chemistry 81, no. 5 (March 2009): 1881–87. http://dx.doi.org/10.1021/ac801745d.

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30

Laguna, Theresa A., Brandie D. Wagner, Heidi K. Luckey, Shelley A. Mann, Scott D. Sagel, Warren Regelmann, and Frank J. Accurso. "Sputum Desmosine During Hospital Admission for Pulmonary Exacerbation in Cystic Fibrosis." Chest 136, no. 6 (December 2009): 1561–68. http://dx.doi.org/10.1378/chest.09-0217.

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31

Minkin, Ruth, Gagangeet Sandhu, Horiana Grosu, Lori Tartell, Shuren Ma, Yong Y. Lin, Edward Eden, and Gerard M. Turino. "Desmosine and Isodesmosine as a Novel Biomarker for Pulmonary Arterial Hypertension." American Journal of Therapeutics 24, no. 4 (2017): e399-e404. http://dx.doi.org/10.1097/mjt.0000000000000260.

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32

Tanaka, Nao, Manami Kurita, Yuko Murakami, and Toyonobu Usuki. "Chichibabin and IsoChichibabin Pyridinium Syntheses of Isodesmosine, Desmosine, and their Derivatives." European Journal of Organic Chemistry 2018, no. 43 (October 24, 2018): 6002–9. http://dx.doi.org/10.1002/ejoc.201801156.

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33

FIORENZA, D., S. VIGLIO, A. LUPI, J. BACCHESCHI, C. TINELLI, R. TRISOLINI, P. IADAROLA, M. LUISETTI, and G. L. SNIDER. "Urinary desmosine excretion in acute exacerbations of COPD: a preliminary report." Respiratory Medicine 96, no. 2 (February 2002): 110–14. http://dx.doi.org/10.1053/rmed.2001.1224.

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34

Stone, P. J., E. C. Lucey, G. L. Snider, and C. Franzblau. "Effect of diet on urinary excretion of desmosine and hydroxylysyl pyridinoline." American Journal of Respiratory and Critical Care Medicine 149, no. 1 (January 1994): 174–77. http://dx.doi.org/10.1164/ajrccm.149.1.8111578.

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35

Starcher, Barry, Michael Green, and Marti Scott. "Measurement of Urinary Desmosine as an Indicator of Acute Pulmonary Disease." Respiration 62, no. 5 (1995): 252–57. http://dx.doi.org/10.1159/000196458.

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36

Sato, Takaji, Takashi Kajikuri, Yoshihiro Saito, Masahiko Chikuma, and Sonoko Nagai. "Determination of desmosine in bronchoalveolar lavage fluids by time-resolved fluoroimmunoassay." Clinica Chimica Acta 387, no. 1-2 (January 2008): 113–19. http://dx.doi.org/10.1016/j.cca.2007.09.015.

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37

Stone, Phillip J., Julianne Bryan-Rhadfi, Edgar C. Lucey, David E. Ciccolella, George Crombie, Barbara Faris, Gordon L. Snider, and Carl Franzblau. "Measurement of Urinary Desmosine by Isotope Dilution and High Performance Liquid Chromatography: Correlation between Elastase-induced Air-Space Enlargement in the Hamster and Elevation of Urinary Desmosine." American Review of Respiratory Disease 144, no. 2 (August 1991): 284–90. http://dx.doi.org/10.1164/ajrccm/144.2.284.

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38

Iskandar, Zaid, Ify Mordi, Jeffrey T. J. Huang, David Newby, James Chalmers, Matt Bown, Chim Lang, and Anna Maria Choy. "PLASMA DESMOSINE, AN ELASTIN DEGRADATION PRODUCT, PREDICTS OUTCOMES IN AT RISK POPULATIONS." Journal of the American College of Cardiology 73, no. 9 (March 2019): 1805. http://dx.doi.org/10.1016/s0735-1097(19)32411-8.

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39

LOW, R., P. HULTGREN, B. STARCHER, W. STIREWALT, B. MACLEOD, and E. LOW. "Collagen and desmosine in three models of rabbit right ventricular pressure overload." Journal of Molecular and Cellular Cardiology 19 (1987): S53. http://dx.doi.org/10.1016/s0022-2828(87)80783-6.

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40

OSAKABE, Toru, Eiji USAMI, Akira SATO, Shigeru SASAKI, Tetsuo WATANABE, and Yoshiyuki SEYAMA. "Characteristic Change of Urinary Elastin Peptides and Desmosine in the Aortic Aneurysm." Biological & Pharmaceutical Bulletin 22, no. 8 (1999): 854–57. http://dx.doi.org/10.1248/bpb.22.854.

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41

Laguna, Theresa A., Brandie D. Wagner, Barry Starcher, Heidi K. Luckey Tarro, Shelley A. Mann, Scott D. Sagel, and Frank J. Accurso. "Urinary desmosine: A biomarker of structural lung injury during CF pulmonary exacerbation." Pediatric Pulmonology 47, no. 9 (March 19, 2012): 856–63. http://dx.doi.org/10.1002/ppul.22525.

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42

Usuki, Toyonobu, Haruka Yamada, Takahiro Hayashi, Hiroto Yanuma, Yohei Koseki, Noriyuki Suzuki, Yoshiro Masuyama, and Yong Y. Lin. "ChemInform Abstract: Total Synthesis of COPD Biomarker Desmosine (I) that Crosslinks Elastin." ChemInform 43, no. 29 (June 21, 2012): no. http://dx.doi.org/10.1002/chin.201229212.

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43

Rathod, Pratikkumar, Manjeet Kaur, Hsin-Pin Ho, Marissa E. Louis, Basant Dhital, Philip Durlik, Gregory S. Boutis, Kevin J. Mark, Jong I. Lee, and Emmanuel J. Chang. "Quantification of desmosine and isodesmosine using MALDI-ion trap tandem mass spectrometry." Analytical and Bioanalytical Chemistry 410, no. 26 (July 31, 2018): 6881–89. http://dx.doi.org/10.1007/s00216-018-1288-z.

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Salomoni, M., M. Muda, E. Zuccato, and E. Mussini. "High-performance liquid chromatographic determination of desmosine and isodesmosine after phenylisothiocyanate derivatization." Journal of Chromatography B: Biomedical Sciences and Applications 572, no. 1-2 (December 1991): 312–16. http://dx.doi.org/10.1016/0378-4347(91)80496-y.

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Piscaer, Ianthe, Jody M. W. van den Ouweland, Kristina Vermeersch, Niki L. Reynaert, Frits M. E. Franssen, Spencer Keene, Emiel F. M. Wouters, Wim Janssens, Cees Vermeer, and Rob Janssen. "Low Vitamin K Status Is Associated with Increased Elastin Degradation in Chronic Obstructive Pulmonary Disease." Journal of Clinical Medicine 8, no. 8 (July 27, 2019): 1116. http://dx.doi.org/10.3390/jcm8081116.

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Elastin degradation is accelerated in chronic obstructive pulmonary disease (COPD) and is partially regulated by Matrix Gla Protein (MGP), via a vitamin K-dependent pathway. The aim was to assess vitamin K status in COPD as well as associations between vitamin K status, elastin degradation, lung function parameters and mortality. A total of 192 COPD patients and 186 age-matched controls were included. In addition to this, 290 COPD patients from a second independent longitudinal cohort were also included. Vitamin K status was assessed by measuring plasma inactive MGP levels and rates of elastin degradation by measuring plasma desmosine levels. Reduced vitamin K status was found in COPD patients compared to smoking controls (p < 0.0005) and controls who had never smoked (p = 0.001). Vitamin K status was inversely associated with desmosine (cohort 1: p = 0.001; cohort 2: p = 0.004). Only few significant associations between vitamin K status and lung function parameters were found. Mortality was higher in COPD patients within the quartile with the lowest vitamin K status compared to those within the other quartiles (hazard ratio 1.85, 95% confidence interval (CI), 1.21–2.83, p = 0.005). In conclusion, we demonstrated reduced vitamin K status in COPD and an inverse association between vitamin K status and elastin degradation rate. Our results therefore suggest a potential role of vitamin K in COPD pathogenesis.

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Rabinovich, Roberto A., Bruce E. Miller, Karolina Wrobel, Kareshma Ranjit, Michelle C. Williams, Ellen Drost, Lisa D. Edwards, et al. "Circulating desmosine levels do not predict emphysema progression but are associated with cardiovascular risk and mortality in COPD." European Respiratory Journal 47, no. 5 (March 23, 2016): 1365–73. http://dx.doi.org/10.1183/13993003.01824-2015.

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Elastin degradation is a key feature of emphysema and may have a role in the pathogenesis of atherosclerosis associated with chronic obstructive pulmonary disease (COPD). Circulating desmosine is a specific biomarker of elastin degradation. We investigated the association between plasma desmosine (pDES) and emphysema severity/progression, coronary artery calcium score (CACS) and mortality.pDES was measured in 1177 COPD patients and 110 healthy control subjects from two independent cohorts. Emphysema was assessed on chest computed tomography scans. Aortic arterial stiffness was measured as the aortic–femoral pulse wave velocity.pDES was elevated in patients with cardiovascular disease (p<0.005) and correlated with age (rho=0.39, p<0.0005), CACS (rho=0.19, p<0.0005) modified Medical Research Council dyspnoea score (rho=0.15, p<0.0005), 6-min walking distance (rho=−0.17, p<0.0005) and body mass index, airflow obstruction, dyspnoea, exercise capacity index (rho=0.10, p<0.01), but not with emphysema, emphysema progression or forced expiratory volume in 1 s decline. pDES predicted all-cause mortality independently of several confounding factors (p<0.005). In an independent cohort of 186 patients with COPD and 110 control subjects, pDES levels were higher in COPD patients with cardiovascular disease and correlated with arterial stiffness (p<0.05).In COPD, excess elastin degradation relates to cardiovascular comorbidities, atherosclerosis, arterial stiffness, systemic inflammation and mortality, but not to emphysema or emphysema progression. pDES is a good biomarker of cardiovascular risk and mortality in COPD.

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Jules-Elysee, Kethy M., Sarah E. Wilfred, Stavros G. Memtsoudis, David H. Kim, Jacques T. YaDeau, Michael K. Urban, Michael L. Lichardi, Alexander S. McLawhorn, and Thomas P. Sculco. "Steroid Modulation of Cytokine Release and Desmosine Levels in Bilateral Total Knee Replacement." Journal of Bone & Joint Surgery 94, no. 23 (December 2012): 2120–27. http://dx.doi.org/10.2106/jbjs.k.00995.

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Ongay, Sara, Marijke Sikma, Peter Horvatovich, Jos Hermans, Bruce E. Miller, Nick H. T. ten Hacken, and Rainer Bischoff. "Free Urinary Desmosine and Isodesmosine as COPD Biomarkers: The Relevance of Confounding Factors." Chronic Obstructive Pulmonary Diseases: Journal of the COPD Foundation 3, no. 2 (2016): 560–69. http://dx.doi.org/10.15326/jcopdf.3.2.2015.0159.

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DAVRIL, MONIQUE, MIREILLE GUAY, KIA-KI HAN, and FRANCOIS LAMY. "Photolysis and ozonolysis of (iso) desmosine-containing crosslinked peptides from porcine aorta elastin." International Journal of Peptide and Protein Research 29, no. 1 (January 12, 2009): 68–77. http://dx.doi.org/10.1111/j.1399-3011.1987.tb02231.x.

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Viglio, S., P. Iadarola, A. Lupi, R. Trisolini, C. Tinelli, B. Balbi, V. Grassi, et al. "MEKC of desmosine and isodesmosine in urine of chronic destructive lung disease patients." European Respiratory Journal 15, no. 6 (June 2000): 1039. http://dx.doi.org/10.1034/j.1399-3003.2000.01511.x.

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