Capture Type II Collagen ELISA Kit (DEIA11776)

Regulatory status: For research use only, not for use in diagnostic procedures.

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Size
96T
Sample
cells, tissues culture, cartilage
Species Reactivity
Human, Horse, Dog
Intended Use
The Capture Type II Collagen ELISA Kit is to be used for measuring native type II collagen, and will not measure denatured collagen.
Contents of Kit
1. Anti-type II collagen-coated strips: 10 strips
2. Standard coated strips: 4 strips
3. Reagent Diluent Buffer 1 x : 50 mL
4. Wash Buffer 10X: 50 mL
5. Anti-type II collagen (Conjugated to biotin): 2 vials
6. Standard: 1 vial
7. Purified type II collagen: 200 ng
8. Collagen Sample/Standard Dilution Buffer 1 x : 20 mL
9. Avidin-Peroxidase: 2 vials
10. TMB (1X): 10 mL
11. Stop Solution (1X): 5 mL
Storage
For more detailed information, please download the following document on our website.
Detection Range
0-200 ng/mL

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References


Hydrostatic Pressure Regulates Oxidative Stress through microRNA in Human Osteoarthritic Chondrocytes

INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES

Authors: Cheleschi, Sara; Barbarino, Marcella; Gallo, Ines; Tenti, Sara; Bottaro, Maria; Frati, Elena; Giannotti, Stefano; Fioravanti, Antonella

Hydrostatic pressure (HP) modulates chondrocytes metabolism, however, its ability to regulate oxidative stress and microRNAs (miRNA) has not been clarified. The aim of this study was to investigate the role of miR-34a, miR-146a, and miR-181a as possible mediators of HP effects on oxidative stress in human osteoarthritis (OA) chondrocytes. Chondrocytes were exposed to cyclic low HP (1-5 MPa) and continuous static HP (10 MPa) for 3 similar to h. Metalloproteinases (MMPs), disintegrin and metalloproteinase with thrombospondin motif (ADAMTS)-5, type II collagen (Col2a1), miR-34a, miR-146a, miR-181a, antioxidant enzymes, and B-cell lymphoma 2 (BCL2) were evaluated by quantitative real-time polymerase chain reaction qRT-PCR, apoptosis and reactive oxygen species ROS production by cytometry, and beta-catenin by immunofluorescence. The relationship among HP, the studied miRNA, and oxidative stress was assessed by transfection with miRNA specific inhibitors. Low cyclical HP significantly reduced apoptosis, the gene expression of MMP-13, ADAMTS5, miRNA, the production of superoxide anion, and mRNA levels of antioxidant enzymes. Conversely, an increased Col2a1 and BCL2 genes was observed. beta-catenin protein expression was reduced in cells exposed to HP 1-5 MPa. Opposite results were obtained following continuous static HP application. Finally, miRNA silencing enhanced low HP and suppressed continuous HP-induced effects. Our data suggest miRNA as one of the mechanisms by which HP regulates chondrocyte metabolism and oxidative stress, via Wnt/beta-catenin pathway.

Kat2a and Kat2b Acetyltransferase Activity Regulates Craniofacial Cartilage and Bone Differentiation in Zebrafish and Mice

JOURNAL OF DEVELOPMENTAL BIOLOGY

Authors: Sen, Rwik; Pezoa, Sofia A.; Shull, Lomeli Carpio; Hernandez-Lagunas, Laura; Niswander, Lee A.; Artinger, Kristin Bruk

Cranial neural crest cells undergo cellular growth, patterning, and differentiation within the branchial arches to form cartilage and bone, resulting in a precise pattern of skeletal elements forming the craniofacial skeleton. However, it is unclear how cranial neural crest cells are regulated to give rise to the different shapes and sizes of the bone and cartilage. Epigenetic regulators are good candidates to be involved in this regulation, since they can exert both broad as well as precise control on pattern formation. Here, we investigated the role of the histone acetyltransferases Kat2a and Kat2b in craniofacial development using TALEN/CRISPR/Cas9 mutagenesis in zebrafish and the Kat2a(hat/hat) (also called Gcn5) allele in mice. kat2a and kat2b are broadly expressed during embryogenesis within the central nervous system and craniofacial region. Single and double kat2a and kat2b zebrafish mutants have an overall shortening and hypoplastic nature of the cartilage elements and disruption of the posterior ceratobranchial cartilages, likely due to smaller domains of expression of both cartilage- and bone-specific markers, including sox9a and col2a1, and runx2a and runx2b, respectively. Similarly, in mice we observe defects in the craniofacial skeleton, including hypoplastic bone and cartilage and altered expression of Runx2 and cartilage markers (Sox9, Col2a1). In addition, we determined that following the loss of Kat2a activity, overall histone 3 lysine 9 (H3K9) acetylation, the main epigenetic target of Kat2a/Kat2b, was decreased. These results suggest that Kat2a and Kat2b are required for growth and differentiation of craniofacial cartilage and bone in both zebrafish and mice by regulating H3K9 acetylation.

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