Serology of Collagen Types I and III in Normal Healing of Tibial Shaft Fractures

Kurdy, Nasser; Bowles, Shirley A; Marsh, David; Davies, Aled

doi:10.1097/00005131-199802000-00010

Cited by 48 publications

(43 citation statements)

References 27 publications

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“…Possible effects of injury on levels of P-III-P also need to be investigated. P-III-P levels increase from day 8 to week 5 following tibial fractures [16] but data on the effects of less severe soft tissue injuries and strains such as those commonly suffered by athletes needs to be obtained. We also need to bear in mind that an athlete with active acromegaly will test positive by this method as would one with fibrosing alveolitis (or similar collagen disorder) and both would need further investigation to confirm this diagnosis.…”

Section: Discussionmentioning

confidence: 99%

Detection of growth hormone abuse in sport

Powrie

Bassett

Rosén

et al. 2007

Growth Hormone & IGF Research

136

140

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Section: Discussionmentioning

confidence: 99%

Detection of growth hormone abuse in sport

Powrie

Bassett

Rosén

et al. 2007

Growth Hormone & IGF Research

136

140

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“…However, biological mediators can also be causative factors of nonunion. Several bone turnover markers such as bone-specific alkaline phosphatase [5–8], osteocalcin [5, 6, 9] and fragments of type-I and type-III procollagen [7] have been suggested as potential markers of nonunion. Levels of leptin, interleukin-6, platelet-derived growth factor-BB, stem cell factor and insulin-like growth factor-1 were found altered in nonunion compared to healthy volunteers [2].…”

Section: Introductionmentioning

confidence: 99%

Biomarkers of inflammation and innate immunity in atrophic nonunion fracture

et al. 2016

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BackgroundNonunion is a failure of healing following a bone fracture. Its physiopathology remains partially unclear and the discovery of new mediators could promote the understanding of bone healing.MethodsThirty-three atrophic nonunion (NU) patients that failed to demonstrate any radiographic improvement for 6 consecutive months were recruited for providing serum samples. Thirty-five healthy volunteers (HV) served as the control group. Proteomics studies were performed using SELDI-TOF–MS and 2D-DIGE approaches, associated or not with Proteominer® preprocessing, to highlight biomarkers specific to atrophic nonunion pathology. Peak intensities were analyzed by two statistical approaches, a nonparametric Mann–Whitney U tests (univariate approach) and a machine-learning algorithm called extra-trees (multivariate approach). Validation of highlighted biomarkers was performed by alternative approaches such as microfluidic LC–MS/MS, nephelometry, western blotting or ELISA assays.ResultsFrom the 35 HV and 33 NU crude serum samples and Proteominer® eluates, 136 spectra were collected by SELDI-TOF–MS using CM10 and IMAC-Cu2+ ProteinChip arrays, and 665 peaks were integrated for extra-trees multivariate analysis. Accordingly, seven biomarkers and several variants were identified as potential NU biomarkers. Their levels of expression were found to be down- or up-regulated in serum of HV vs NU. These biomarkers are inter-α-trypsin inhibitor H4, hepcidin, S100A8, S100A9, glycated hemoglobin β subunit, PACAP related peptide, complement C3 α-chain. 2D-DIGE experiment allowed to detect 14 biomarkers as being down- or up-regulated in serum of HV vs NU including a cleaved fragment of apolipoprotein A-IV, apolipoprotein E, complement C3 and C6. Several biomarkers such as hepcidin, complement C6, S100A9, apolipoprotein E, complement C3 and C4 were confirmed by an alternative approach as being up-regulated in serum of NU patients compared to HV controls.ConclusionTwo proteomics approaches were used to identify new biomarkers up- or down-regulated in the nonunion pathology, which are involved in bone turn-over, inflammation, innate immunity, glycation and lipid metabolisms. High expression of hepcidin or S100A8/S100A9 by myeloid cells and the presence of advanced glycation end products and complement factors could be the result of a longstanding inflammatory process. Blocking macrophage activation and/or TLR4 receptor could accelerate healing of fractured bone in at-risk patients.Electronic supplementary materialThe online version of this article (doi:10.1186/s12967-016-1019-1) contains supplementary material, which is available to authorized users.

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“…A multinational team, the GH-2000, has proposed the combined application of IGF-I and P3NP for detection of rhGH doping (13,15,16). P3NP levels rise after a bone fracture or soft tissue muscle injury (9,(33)(34)(35). P3NP response to rhGH administration may be affected by the age, gender, and stage of pubertal maturation, whereas ethnicity has only a small effect (6,17,36).…”

Section: Discussionmentioning

confidence: 99%

N-Terminal Propeptide of Type III Procollagen as a Biomarker of Anabolic Response to Recombinant Human GH and Testosterone

Meikle¹

2010

Yearbook of Endocrinology

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Context:Biomarkers that predict musculoskeletal response to anabolic therapies should expedite drug development. During collagen synthesis in soft lean tissue, N-terminal propeptide of type III procollagen (P3NP) is released into circulation. We investigated P3NP as a biomarker of lean body mass (LBM) and muscle strength gains in response to testosterone and GH.Design: Community-dwelling older men received GnRH agonist plus 5 or 10 g testosterone gel plus 0, 3, or 5 g recombinant human GH daily. P3NP levels were measured at baseline and wk 4, 8, 12, and 16.LBMandappendicularskeletalmusclemass(ASM)weremeasuredbydual-energyx-rayabsorptiometry. Results:One hundred twelve men completed treatment; 106 underwent serum P3NP measurements. P3NP levels were higher at wk 4 than baseline (6.61 Ϯ 2.14 vs. 4.51 Ϯ 1.05, P Ͻ 0.0001) and reached plateau by wk 4 in men receiving testosterone alone. However, wk 8 P3NP levels were higher than wk 4 levels in men receiving testosterone plus recombinant human GH. Increases in P3NP from baseline to wk 4 and 16 were significantly associated with gains in LBM (r ϭ 0.26, P ϭ 0.007; r ϭ 0.53, P Ͻ 0.001) and ASM (r ϭ 0.17, P ϭ 0.07; r ϭ 0.40, P Ͻ 0.0001). Importantly, for participants receiving only testosterone, P3NP increases at wk 4 and 16 were related to muscle strength gains (r ϭ 0.20, P ϭ 0.056 and r ϭ 0.36, P ϭ 0.04). In stepwise regression, change in P3NP explained 28 and 30% of the change in ASM and LBM, respectively, whereas change in testosterone but not IGF-I and age provided only small improvements in the models. Conclusion:Early changes in serum P3NP levels are associated with subsequent changes in LBM and ASM during testosterone and GH administration. Serum P3NP may be a useful early predictive biomarker of anabolic response to GH and testosterone. The past decade has witnessed substantial pharmaceutical and academic investment in the development of function promoting anabolic therapies that improve physical function and health-related outcomes (1). The leading function promoting anabolic molecules that are under development, androgens, myostatin inhibitors, and GH, are potential promyogenic agents that are expected to improve physical function primarily by increasing skeletal muscle mass. Considering the enormous resources required for conducting large efficacy trials, serum biomar-

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Serology of Collagen Types I and III in Normal Healing of Tibial Shaft Fractures

Cited by 48 publications

References 27 publications

Detection of growth hormone abuse in sport

Detection of growth hormone abuse in sport

Biomarkers of inflammation and innate immunity in atrophic nonunion fracture

N-Terminal Propeptide of Type III Procollagen as a Biomarker of Anabolic Response to Recombinant Human GH and Testosterone

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