Quantitative Heel Ultrasonography, 25-Hydroxyvitamin D, and Urine Amino-terminal Cross-linking Telopeptide of Type I Collagen in Patients With a Recent Hip Fracture

The purpose of this work was to describe changes in metabolic activity in the bones of young male competitive cyclists (CYC) as compared with age-matched controls (CON) over a one-year period of study. Eight adolescent male cyclists aged between fourteen and twenty, and eight age-matched controls participated in this longitudinal study. Serum osteocalcin (OC), amino-terminal propeptide of type I procollagen (PINP), beta-isomerized C-telopeptides (β-CTx) and plasma 25 hydroxyvitamin D [25(OH)D], were investigated by an electrogenerated chemiluminescence immunoassay. Analysis of variance revealed no significant differences in formation and resorption markers between cyclists and controls. Within the groups, both CYC and CON showed decreased OC at −30% and −24%, respectively, and PINP where the figures were −28% and −30% respectively (all p < 0.05). However, only the CYC group showed a decrease in [25(OH)D], lower by 11% (p < 0.05). The similarity in the concentrations of markers in cyclists and controls seems to indicate that cycling does not modify the process of bone remodeling. The decrease in vitamin D in cyclists might be detrimental to their future bone health.

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Low Serum 25-hydroxyvitamin D Level Does Not Adversely Affect Bone Turnover in Prepubertal Children

Nutrients ◽

10.3390/nu13103324 ◽

2021 ◽

Vol 13 (10) ◽

pp. 3324

Author(s):

Wojciech J. Bilinski ◽

Lukasz Szternel ◽

Joanna Siodmiak ◽

Przemyslaw T. Paradowski ◽

Krzysztof Domagalski ◽

...

Keyword(s):

Bone Turnover ◽

Type I Collagen ◽

Type I ◽

Healthy Children ◽

Strong Positive Correlation ◽

Hydroxyvitamin D ◽

Type I Procollagen ◽

25 Hydroxyvitamin D ◽

Turnover Markers ◽

Low Serum

Both vitamin D and insulin-like growth factor 1 (IGF-1) play essential roles in bone metabolism and may interact during prepubertal bone accrual. We investigated the association of low serum 25-hydroxyvitamin D (25(OH)D) (<20 ng/mL) with the circulating bone turnover markers, when compared to their interaction with IGF-1. Subjects and Methods: Serum 25(OH)D, IGF-I, P1NP (N-terminal propeptide of type I procollagen), and CTX-1 (C-terminal telopeptide of type I collagen) were measured, and the bone turnover index (BTI) was calculated in 128 healthy children, aged 9–11 years. Results: Mean 25(OH)D concentration was 21.9 ± 4.9 ng/mL, but in 30.5% of participants it was <20 ng/mL (<50 nmol/L). We observed a trend for higher P1NP (p < 0.05) and IGF-1 (p = 0.08), towards lower 25(OH)D in tertiles. Levels of P1NP in the lowest 25(OH)D tertile (<20 ng/mL) were the highest, while CTX and BTI remained unchanged. Additionally, 25(OH)D negatively correlated with IGF-1, while the correlation with P1NP was not significant. A strong positive correlation of IGF-1 with P1NP and BTI but weak with CTX was observed. Low 25(OH)D (<20 ng/mL) explained 15% of the IGF-1 variance and 6% of the P1NP variance. Conclusions: Low levels of 25(OH)D do not unfavorably alter bone turnover. It seems that serum 25(OH)D level may not be an adequate predictor of bone turnover in children.

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Abnormal type I collagen glycosylation pattern and cross-linking in a cyclophilin B KO mouse model of recessive osteogenesis imperfecta

Bone Abstracts ◽

10.1530/boneabs.1.pp501 ◽

2013 ◽

Author(s):

Wayne Cabral ◽

Irina Perdivara ◽

MaryAnn Weis ◽

Masahiko Terajima ◽

Angela Blissett ◽

...

Keyword(s):

Mouse Model ◽

Osteogenesis Imperfecta ◽

Type I Collagen ◽

Cross Linking ◽

Type I ◽

Glycosylation Pattern ◽

Cyclophilin B

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Role of the amino-terminal extrahelical region of type I collagen in directing the 4D overlap in fibrillogenesis

Biopolymers ◽

10.1002/bip.1979.360181208 ◽

1979 ◽

Vol 18 (12) ◽

pp. 3005-3014 ◽

Cited By ~ 93

Author(s):

Donald L. Helseth ◽

Joseph H. Lechner ◽

Arthur Veis

Keyword(s):

Type I Collagen ◽

Type I ◽

Amino Terminal

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Electroacupuncture Ameliorates Subchondral Bone Deterioration and Inhibits Cartilage Degeneration in Ovariectomised Rats

Acupuncture in Medicine ◽

10.1136/acupmed-2016-011258 ◽

2018 ◽

Vol 36 (1) ◽

pp. 37-43 ◽

Cited By ~ 3

Author(s):

Jun Zhou ◽

Peirui Zhong ◽

Ying Liao ◽

Jing Liu ◽

Yuan Liao ◽

...

Keyword(s):

Subchondral Bone ◽

Type I Collagen ◽

Cartilage Degeneration ◽

Cross Linking ◽

Control Group ◽

Sham Operation ◽

Type I ◽

Trabecular Thickness ◽

Ovx Rats ◽

Time Point

Objectives To investigate the effects of electroacupuncture (EA) on subchondral bone mass and cartilage degeneration in an experimental animal model of osteoarthritis (OA) induced by ovariectomy (OVX). Methods Ninety 3-month-old female Sprague-Dawley rats were randomly divided into the following three groups (n = 30 each): sham operation without treatment (control group); OVX without treatment (OVX group);, and ovariectomy with EA treatment (EA group). Rats in the EA group received EA treatment from the day of OVX. Ten rats in each group were randomly killed at 4, 8 and 12 weeks after operation. Results EA reduced urine C-terminal cross-linking telopeptide of type I collagen from 4 weeks after OVX, reduced C-terminal cross-linking telopeptide of type II collagen and body weight from 8 weeks after OVX, and increased serum 17β-oestradiol from 4 weeks after OVX compared with the OVX group (all p<0.01). In the EA group, trabecular bone volume ratio, trabecular thickness and trabecular number increased, and trabecular separation were reduced at each time point compared with the OVX group (p<0.05, p<0.01, respectively). In the EA group, osteoprotegerin (OPG) expression was increased and receptor activator of nuclear factor kappa-B ligand (RANKL) expression was reduced at each time point compared with the OVX group (p<0.05, p<0.01, respectively). Mankin scores and mRNA expression of matrix metalloproteinase-13 (MMP-13) were lower in EA versus OVX groups at 12 weeks after OVX (both p<0.01). Conclusion The results suggest that EA inhibits subchondral bone loss by regulating RANK/RANKL/OPG signalling and protects articular cartilage by inhibiting MMP-13 in OVX rats.

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Atrial natriuretic peptide, B-type natriuretic peptide, and serum collagen markers after acute myocardial infarction

Journal of Applied Physiology ◽

10.1152/japplphysiol.00557.2003 ◽

2004 ◽

Vol 96 (4) ◽

pp. 1306-1311 ◽

Cited By ~ 24

Author(s):

Jarkko Magga ◽

Mikko Puhakka ◽

Seppo Hietakorpi ◽

Kari Punnonen ◽

Paavo Uusimaa ◽

...

Keyword(s):

Myocardial Infarction ◽

Acute Myocardial Infarction ◽

Atrial Natriuretic Peptide ◽

Natriuretic Peptide ◽

Type I Collagen ◽

Left Ventricular ◽

Type I ◽

Amino Terminal ◽

Collagen Markers ◽

Atrial Natriuretic

Experimental data suggest that atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) act locally as antifibrotic factors in heart. We investigated the interrelationships of natriuretic peptides and collagen markers in 93 patients receiving thrombolytic treatment for their first acute myocardial infarction (AMI). Collagen formation following AMI, evaluated as serum levels of amino terminal propeptide of type III procollagen, correlated with NH2-terminal proANP ( r = 0.45, P < 0.001), BNP ( r = 0.55, P < 0.001) and NH2-terminal proBNP ( r = 0.50, P < 0.01) on day 4 after thrombolysis. Levels of intact amino terminal propeptide of type I procollagen decreased by 34% ( P < 0.001), and levels of carboxy terminal cross-linked telopeptide of type I collagen (ICTP) increased by 65% ( P < 0.001). ICTP levels correlated with NH2-terminal proBNP ( r = 0.25, P < 0.05) and BNP ( r = 0.28, P < 0.05) on day 4. Our results suggest that ANP and BNP may act as regulators of collagen scar formation and left ventricular remodeling after AMI in humans. Furthermore, degradation of type I collagen is increased after AMI and may be regulated by BNP.

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Ιδιοπαθής υπερασβεστιουρία στην παιδική ηλικία

10.12681/eadd/44686 ◽

2017 ◽

Author(s):

Μαρία Παύλου

Keyword(s):

Type I Collagen ◽

Cross Linking ◽

Type I ◽

Nuclear Factor ◽

Soluble Receptor ◽

Calcium Sensing Receptor ◽

Calcium Sensing ◽

Receptor Activator ◽

Carboxy Terminal ◽

Nuclear Factor Kb

Η ιδιοπαθής υπερασβεστιουρία (ΙΥΑ) στα παιδιά έχει επιπολασμό 2,2-17,7%. Ποσοστό 2635% των ασθενών εμφανίζει μειωμένη οστική πυκνότητα, που αποδίδεται μάλλον σε αυξημένη οστική απορρόφηση και/ή οστικό ανασχηματισμό, καθώς καταγράφεται φυσιολογική κατά μήκος αύξηση των οστών στα περισσότερα παιδιά με ΙΥΑ. Περιορισμένες είναι οι μελέτες εκτίμησης βιοχημικών δεικτών οστικού μεταβολισμού, αλλά και γονιδιακού ελέγχου σε παιδιά με ΙΥΑ στην διεθνή βιβλιογραφία και καμία στην ελληνική. Επίσης, δεν πραγματοποιήθηκαν μελέτες εκτίμησης των κυτταροκινών οστεοκλαστογένεσης οστεοπροτεγερίνη (osteoprotegerin, OPG) και sRANKL (soluble receptor activator of nuclear factor kB ligand) σε ασθενείς με ΙΥΑ. Σκοπός της μελέτης ήταν η εκτίμηση των βιοχημικών δεικτών οστικής παραγωγής, αλκαλική φωσφατάση (alkaline phosphatase, ALP) και οστεοκαλσίνη (osteocalcin, OC) και οστικής απορρόφησης β-Crosslaps (serum Carboxy-terminal cross-linking telopeptide of type I collagen) και της OPG και sRANKL στον ορό σε παιδιά με ΙΥΑ. Επίσης έγινε γονιδιακή ανάλυση των πολυμορφισμών του γονιδίου του ασβεστιοευαίσθητου υποδοχέα (Calcium sensing Receptor, CaSR). Πενήντα παιδιά με ΙΥΑ αποτέλεσαν την ομάδα ασθενών και 60 υγιή παιδιά την ομάδα ελέγχου. Οι ασθενείς εκτιμήθηκαν κατά τον χρόνο της διάγνωσης και 3 μήνες μετά την εφαρμογή διαιτητικών οδηγιών αντιμετώπισης της ΙΥΑ. Οι ασθενείς της μελέτης μας είχαν σχετικά ήπια προς μέτρια υπερασβεστιουρία (6,49±2,03 mg/Kg/day) κατά την ένταξη στην μελέτη. Μετά την εφαρμογή των διατροφικών οδηγιών, μείωσαν σημαντικά τα επίπεδα του Ca στα ούρα 24ώρου και τον λόγο του Ca προς κρεατινίνη στα δείγματα ούρων, χωρίς όμως να φτάνουν τις φυσιολογικές τιμές. Τα επίπεδα της ALP και OC και το ύψος των ασθενών δεν διέφεραν από της ομάδας ελέγχου, που δείχνει ανεπηρέαστη οστική παραγωγή στους ασθενείς. Τα επίπεδα των β-Crosslaps των ασθενών, στους δύο χρόνους εκτίμησης, ήταν υψηλότερα από των μαρτύρων, ενώ καταγράφηκε τάση μείωσης της μέσης τιμής μετά την τρίμηνη παρέμβαση. Το εύρημα δείχνει αυξημένη οστική απορρόφηση στους ασθενείς με τάση βελτίωσης κατά τον επανέλεγχο. Ο λόγος β-Crosslaps/OC στους ασθενείς κατά την ένταξη στην μελέτη ήταν αυξημένος συγκριτικά με των μαρτύρων, καταγράφοντας υψηλότερο ρυθμό οστικής απορρόφησης συγκριτικά με οστικής παραγωγής. Τα επίπεδα των OPG και sRANKL των ασθενών, στους δύο χρόνους εκτίμησης δε διέφεραν από των μαρτύρων. Ωστόσο, ο λόγος sRANKL/OPG στους ασθενείς κατά την ένταξη στην μελέτη ήταν ελαφρά χαμηλότερος, πιθανά σαν απάντηση αντιρρόπησης του υψηλότερου ρυθμού οστεοκλαστογένεσης. Από την γονιδιακή ανάλυση των πολυμορφισμών A986S, R990G και Q1011E του CaSR, καταγράφηκε συσχέτιση μόνο του A986S με την ΙΥΑ στα παιδιά της μελέτης. Συμπερασματικά οι ασθενείς της μελέτης μας φαίνεται να έχουν φυσιολογική οστική παραγωγή, αλλά αυξημένη οστική απορρόφηση, που βελτιώθηκε μετά την παρέμβαση. Βρέθηκε συσχέτιση μόνο του πολυμορφισμού A986S του CaSR με την ΙΥΑ. Θεωρούμε χρήσιμη την εκτίμηση των βιοχημικών δεικτών οστικής παραγωγής ALP και OC και απορρόφησης β-Crosslaps στον ορό στα παιδιά με ΙΥΑ, ως μια μη επεμβατική μέθοδο ανίχνευσης διαταραχών οστικού μεταβολισμού και παρακολούθησης της αντιμετώπισης της.

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Abstract 17388: Loss of Bone Morphogenetic Protein 9 (BMP9) Limits Survival and Paradoxically Increases Collagen Abundance, but Limits Collagen Cross-Linking in a Murine Model of Acute Myocardial Infarction

Circulation ◽

10.1161/circ.142.suppl_3.17388 ◽

2020 ◽

Vol 142 (Suppl_3) ◽

Author(s):

Shreyas Bhave ◽

Michele Esposito ◽

Lija Swain ◽

Xiaoying QIAO ◽

Gregory Martin ◽

...

Keyword(s):

Myocardial Infarction ◽

Bone Morphogenetic Protein ◽

Murine Model ◽

Cardiac Remodeling ◽

Type I Collagen ◽

Cross Linking ◽

Type I ◽

Morphogenetic Protein ◽

Bone Morphogenetic Protein 9 ◽

Collagen Cross Linking

Myocardial infarction (MI) is a major cause of heart failure (HF). HF is associated with adverse cardiac remodeling that is primarily driven by Transforming growth factor beta (TGFb1) mediated fibrosis and myocyte hypertrophy. We previously reported that loss of bone morphogenetic protein 9 (BMP9) promotes cardiac fibrosis in pressure-overload induced HF. No studies have explored a role for BMP9 in post MI cardiac remodeling. We hypothesize that loss of BMP9 may promote cardiac healing by stabilizing LV scar formation. To test this hypothesis, we subjected whole body BMP9 knockout (-/-) mice to left coronary artery ligation for two weeks followed by PV loop analysis and studied indices of cardiac remodeling. Compared to wild type (WT) controls BMP9-/- mice had significantly lower survival (83% vs 61%, p<0.001, respectively) with a higher rate of cardiac rupture(15% vs 90%). Compared to WT controls, surviving BMP9-/- mice had higher LVEDP, reduced LV dP/dt, and higher lung weight. Compared to WT mice, BMP9-/- mice had significantly higher levels of Type I collagen (2 fold p<0.05). Compared to WT mice, BMP9-/- mice had increased matrix metalloproteinases (MMP)-2 and MMP-9 (2.5 fold p<0.05) activity levels in the LV. Treatment of cultured primary human cardiac fibroblasts with recombinant BMP9 attenuated TGFb1-mediated Type I collagen and MMP-9 protein expression. To assess collagen content and cross-linking, two-photon excitation fluorescence imaging was performed and identified an increase in collagen abundance, but a trend towards lower collagen cross-linking in the LV of BMP9-/- mice compared to WT mice 2 weeks after MI. Our central finding is that loss of BMP9 is associated with reduced survival, increased propensity towards cardiac rupture, and increased LV collagen abundance, but reduced collagen integrity in a murine model of acute MI. These identify a potentially important functional role for BMP9 in post-infarct cardiac remodeling.

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