Insulin-like growth factor binding protein (IGFBP6) is a cross-species tendon marker.

The main challenge in tendon injury management is suboptimal tissue healing that fails to re-establish original tendon function. Tissue bioengineering is a promising approach for tendon therapy, with potential to improve its functional outcomes. However, evaluation criteria for tissue-engineered tendon are unclear due to the lack of specific markers of differentiated tendon. The study aim was to identify a panel of genes that characterised tendons in comparison to cartilage or muscles and validate those genes, both in human and key species used as models for tendon diseases. Gene expression profiling of rat tendon and cartilage in whole-tissue samples and primary tenocytes and chondrocytes was undertaken using two independent microarray platforms. Genes that demonstrated high expression correlation across two assays were validated by qRT-PCR in rat tendon relative to cartilage and muscle. Five genes demonstrating the highest tendon-related expression in the validation experiment (ASPN, ECM1, IGFBP6, TNMD, THBS4) were further evaluated by qRT-PCR in ovine, equine and human tissue. The group of tendon markers, identified by unbiased transcriptomic analysis of rat musculoskeletal tissues, demonstrated species-dependent profiles of expression. Insulin-like growth factor binding protein 6 (IGFBP6) was identified as the only universal tendon marker. Further investigation in equine tendon showed that IGFBP6 expression was not affected by ageing or tendon function but decreased in anatomical regions subjected to elevated compressive force. IGFBP6 is a robust cross-species marker of tendon phenotype and may find application in evaluation of tendon physiology and guided differentiation of permissive cells towards functional tenocytes.

Reference intervals for selected hematological and biochemical variables in Hucul horses.

BACKGROUND: Hucul horses are the unique, genetically distinct breed of Carpathian Mountains. Even though they are recognized as primitive breed, many morphological differences between them and other primitive horses have been reported. Neither hematological nor blood biochemical studies in this breed have been conducted so far. OBJECTIVES: The aim of this study was to establish the reference intervals for basic hematological and selected biochemical variables and to compare them with other breeds. MATERIAL AND METHODS: Blood samples were collected from 168 Hucul horses and the analyses were performed using routine methods. Mainly nonparametric method was used to establish reference intervals. RESULTS: The following reference intervals have been established (rounded to two significant digits): RBC: 7.0-13×1012/l; HGB: 106.1-195.8 g/l; HCT: 0.3-0.6 l/l; MCV: 35-50 fl; MCH 11.9-17.1 pg; MCHC: 31.9-34.8 g/dl; WBC: 7.5-22×109/l, bands: 0-0.5×109/l; segmented neutrophils: 3.3-10×109/l; eosinophils: 0-1.1×109/l; basophils: 0-0.3×109/l; lymphocytes: 1.9-12×109/l; monocytes: 0-0.2×109/l; PLT 95-350×109/l; MPV 5.2-7.0; ALP: 98-425 U/l; AST: 220-470 U/l; GGT: 9.1-31 U/l; total bilirubin: 6.5-29 µmol/l; CPK: 120-640 U/l; triglycerides: 0.1-0.9 mmol/l; urea: 3.8-11 mmol/l; creatinine: 44 -140 µmol/l; serum amyloid A: 130-5200 µg/l. CONCLUSIONS: Hematological and biochemical variables in Hucul horses were closer to hot-blooded then to cold-blooded and primitive horses or wild equidae. The reference intervals presented in this study pose clinically useful tool for evaluation of blood check-up in Hucul horses.

Post-exercise dynamics of serum amyloid A blood concentration in thoroughbred horses classified as injured and non-injured after the race.

The aim of this study was to evaluate serum amyloid A (SAA) concentration in horses with orthopedic injuries acquired during racing and in healthy ones after completing the race. Injuries of bone and tendon did not cause radical increase in SAA concentration observed in other inflammatory conditions. SAA concentration correlated positively with white blood cell count (WBC) on the 3rd-4th days after race being significantly higher in the injured horses than in the control group in that time. It was suggested that racing effort may cause increase in SAA level, more pronounced in horses manifesting clinical signs of orthopedic injury after the race.