Molecular cloning, sequencing, and tissue and developmental expression of mouse cartilage oligomeric matrix protein (COMP)

Abstract

Mouse cartilage oligomeric matrix protein cDNA was cloned and sequenced by a reverse transcription-polymerase chain reaction. The open reading frame encoded a product of 755 amino acids that shares a high degree of identity to and possesses all the characteristic molecular features of both rat and human cartilage oligomeric matrix protein. This suggests that cartilage oligomeric matrix protein is highly conserved during evolution. The clone was 83, 84, and 95% identical to human, bovine, and rat cartilage oligomeric matrix protein cDNA, respectively. In tissues from the adult mouse, cartilage oligomeric matrix protein was expressed not only in cartilage and tendon but in trachea, bone, skeletal muscle, eye, heart, and placenta as well, and no expression was found in other tissues. Immunohistology revealed that cartilage oligomeric matrix was deposited as early as 10 days post coitus in predifferentiated mouse embryo mesenchyme. It was detected in all cartilaginous tissues and in the skeletal muscles of the embryo at day 13. As development progressed, accumulation of cartilage oligomeric matrix protein was marked in the growth plate. At 19 days post coitus, it was prominently deposited in the hypertrophic zone of the growth plate, perichondrium, and periosteum and in the superficial layer of the articular cartilage surface but was absent in the more central areas of the epiphyseal cartilage. The restricted tissue distribution and expression of cartilage oligomeric matrix protein in developing as well as adult mouse tissues suggest the regulation of this protein at the transcriptional level. The findings reported herein are the first detailed characterization of the distribution of cartilage oligomeric matrix protein during early skeletal development of the mouse.

Mutation (D472Y) in the Type 3 Repeat Domain of Cartilage Oligomeric Matrix Protein Affects Its Early Vesicle Trafficking in Endoplasmic Reticulum and Induces Apoptosis

“…The immunohistochemical distribution was very similar to that in a previous study performed with a different COMP-specific antibody 40 ( Figure 1A-C). Immnoreactivity associated with anti-COMP antibody was intracellularly observed in the proliferating zone of the growth plate while it was pronounced in the pericellular and territorial matrix of the hypertrophic zone.…”

“…Note that the distribution of immunoreactivity with this antibody was similar to that with a COMP-specific antibody described in a previous study. 40 PZ, HZ, and CZ represent the proliferating zone, hypertrophic zone, and calcification zone, respectively. D: Western blot showing that anti-COMP antibody specifically recognized native COMP protein synthesized in chondrocytes.…”

Three-Dimensional Culture and Transforming Growth Factor Beta3 Synergistically Promote Tenogenic Differentiation of Equine Embryo-Derived Stem Cells

“…The genes were selected on the basis of having been previously shown to be associated with tendon tissue. [21][22][23][24][25][26] The adult tendon is primarily composed of Collagen Type I, 21 which lacks tissue specificity and is a more general component of multiple ECMs. More robust markers of tenocytes include Scleraxis (SCX), Tenomodulin (TNMD), Tenascin-C (TNC), Cartilage oligomeric matrix protein (COMP), and Thrombospondin-4 (THBS4), which are not only collectively expressed in tendons, but individually also present in other tissue types.…”

“…More robust markers of tenocytes include Scleraxis (SCX), Tenomodulin (TNMD), Tenascin-C (TNC), Cartilage oligomeric matrix protein (COMP), and Thrombospondin-4 (THBS4), which are not only collectively expressed in tendons, but individually also present in other tissue types. [22][23][24][25][26] Developmental studies have also implicated genes such as Six1/2, Eph-A4, Eya1/2, Egr1/2, and Mohawk (Mkx), 25,[27][28][29][30] although it has not been established whether these genes show temporally restricted expression in tendon tissue.…”

Antisense Reduction of Mutant COMP Reduces Growth Plate Chondrocyte Pathology

“…11,[58][59][60][61][62][63] Tolerability and toxicity must be carefully considered with long-term administration, whereas these factors are less important with short-duration therapies. Collectively, the observations reported here demonstrate that early ASO1 systemic administration dampens the MT-COMP growth plate chondrocyte phenotype.…”