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Abstract Chronic kidney disease is a significant health problem worldwide, affecting the adult population with significant social and economic burdens. Calcium synthesis is also affected in patients with CKD and those with multiple conditions, including vascular calcifications, mineral bone disorders, and cardiovascular diseases, is included in this group. In the current research, we wanted to investigate serum total UCMA levels and its relationships with calcium metabolism factors in CKD patients, including hemodialysis patients. For the first time, we provide an insight into the potential biomarker role of UCMA in CKD, as well as HD. Patients with CKD, HD patients, and healthy controls had significantly higher serum UCMA levels than the healthy controls. Increased total UCMA levels may be a factor in the Ca metabolism disorder and closely connected to Vascular Calcification in patients with CKD.
Source link: https://doi.org/10.1590/1678-4324-2020190594
We investigated the combined effects of IGF-II and SOX9 transgene expression on Col-III and GAG production by cultured human articular chondrocytes. On day 9 post-transfection, the chondrocytes that were over-expressing IGF-III gene and a 57% rise in Col-III protein were over-expressing by the Col-III gene, as well as a 57% decrease in Col-III protein, while type I collagen expression was down by 53% relative to controls. These cells' production of GAG in these cells increased significantly in comparison to the controls at day 9. So, IGF-I/SOX9 cotransfected chondrocytes may be useful for cell-based cartilage therapy.
Source link: https://doi.org/10.1590/1414-431x20154732
The absence of -1,3-galactosyl glycoprotein is hypothesized to prevent rejection due to foreign-body immunogenicity. The composite hydrogels were characterized in a variety of ways, including aqueous swelling, structural deposition, response under compression, and morphology, e. g. in vitro biocompatibility by the CCK-8 and live-dead assays and cytoskeleton staining/microscopy. To determine the chondrogenic induction capacity of the hydrogels, Alcian blue staining and real-time PCR RT-PCR were conducted. In addition, a rod TM defect simulator was used to determine the hydrogels' in vivo results in this particular case.
Source link: https://doi.org/10.3389/fbioe.2021.811652
Mice lacking the Runx2 gene in hypertrophic chondrocytes survive, but limb dwarfism remains. In mutant mice, pro-apoptotic Bax expression decreased significantly, but anti-apoptotic Bcl2 was unchanged, resulting in a fourfold rise in the Bcl2/Bax ratio. Both collagen type 2 and aggrecan were similar among Runx2HC/HC and WT littermates, but this was not due to improved synthesis of the cartilage matrix. According to our qPCR analysis, the increased amount of cartilage matrix is due to a lack of cartilage degrading enzymes such as metalloproteinase and aggrecanase, as well as a tissue inhibitor of metalloproteinases. Using micro-CT and Von Kossa, we determine if increasing cartilage matrix in Runx2HC/HC mice serves as a template for bone and mineral deposition. Compared to littermates, the mutant mice have a substantial rise in trabecular bone mass.
Source link: https://doi.org/10.1016/j.mbplus.2021.100088
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