Human/Monkey Anti-Type I and Type II Collagen IgG Antibody ELISA Kit

Pyruvate kinase M2 (PKM2) has been wildly verified to modulate glycolysis in tumor cells. However, the role of PKM2 on the glycolysis of osteoarthritis (OA) chondrocytes is still unclear. In present study, we investigate the function of PKM2 on OA chondrocyte glycolysis and the collagen matrix generation in vitro. Results showed that PKM2 was upregulated in OA chondrocytes compared with healthy control chondrocytes. In OA chondrocytes, ATP expression was lower compared with healthy control chondrocytes. Loss-of-function experiment showed that PKM2 knockdown mediated by lentivirus transfection could significantly suppress the glucose consumption and lactate secretion levels and decrease glucose transporter-1 (Glut-1), lactate dehydrogenase A (LDHA), and hypoxia inducible factor 1-alpha (HIF-1), indicating the inhibition of PKM2 knockdown on glycolysis. Moreover, Cell Counting Kit-8 (CCK-8), flow cytometry, and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay showed that PKM2 knockdown inhibited OA chondrocyte proliferation and promoted the apoptosis. Western blot and immunocytochemical staining showed that PKM2 knockdown downregulated the expression levels of COL2A1 and SOX-9. In summary, our results conclude that PKM2 modulates the glycolysis and extracellular matrix generation, providing the vital role of PKM2 on OA pathogenesis and a novel therapeutic target for OA.

In our previous study, potential pathological mutations of RetNet genes were detected in 23.8% (71/298) of probands with early-onset high myopia (eoHM), based on whole exome sequencing (WES). The current study aimed to confirm this finding in an additional 325 probands with eoHM and to clarify its specificity by comparison of 195 probands with late-onset high myopia (loHM). Variants in the 234 RetNet genes were selected from whole-exome sequencing data and were filtered using multistep bioinformatics analyses. Potential pathological variants in 33 genes were detected in 76 of 325 (23.4%) probands with eoHM and 14 of 195 (7.2%) probands with loHM. Thirty-five of the 76 (46.1%) probands with eoHM had mutations in COL2A1, COL11A1, RPGR, and CACNAIF, while only 2/14 (14.3%) probands with eoHM were detected. The mutation frequency and spectrum of RetNet genes in the 325 probands with eoHM were similar to our previous study but were significantly different in 195 probands with loHM (P = 2 x 10(-6) and 0.04). Data from eoHM and loHM strongly suggest that a significant proportion of eoHM is caused by mutations in RetNet genes. These results also provide initial genetic evidence that eoHM is different from loHM. The presence of mutations in 7.2% probands with loHM raises questions about pathogenicity and the variable manifestation of some mutations. The functional studies of the mutations in question and more extensive investigations of related phenotypes in the mutation carriers and their family members may provide valuable information to address these questions.