Clinical Efficacy of Glucosamine plus Sodium Hyaluronate for Osteoporosis Complicated by Knee Osteoarthritis and Its Influence on Joint Function and Bone Metabolic Markers.

Background: Osteoporosis (OP) associated with knee osteoarthritis (KOA) is common in older men and postmenopausal women, and it is important to find reliable and effective treatments for this disease to improve joint function and bone metabolism in this population. Objective: To clarify the clinical efficacy of glucosamine (GlcN) plus sodium hyaluronate (SH) for OP complicated by KOA (OP + KOA) and its influence on joint function and bone metabolic markers (BMMs). Methods: Admitted from July 2019 to July 2021, 126 patients with OP + KOA were selected, including 76 cases (observation group) treated with GlcN plus SH and 50 cases (control group) given GlcN alone. The pain, joint function, BMMs, and clinical efficacy were evaluated and compared. Pain and joint function assessments employed the Visual Analogue Scale (VAS) and the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) plus Lysholm Knee Scoring Scale, respectively. BMMs mainly measured bone gla protein (BGP), serum tartrate-resistant acid phosphatase variant (TRACP)-5b, type I collagen cross-linked C-telopeptide (CTX-1), and bone-specific alkaline phosphatase (BALP). Results: Higher posttreatment VAS scores were determined in observation group as compared to control group; observation group showed lower WOMAC scores of joint function and higher Lysholm scores than control group; in terms of BMMs, TRACP-5b and CTX-1 were lower while BGP and BALP were higher in observation group; the curative effect was also higher in observation group. All the above differences were statistically significant. Conclusions: GlcN plus SH has definite clinical efficacy in the treatment of OP + KOA, which can not only significantly improve patients' joint function and bone metabolism but also relieve pain, with high clinical popularization value.

LncRNA KCNQ1OT1 promotes osteogenic differentiation via miR-205-5p/RICTOR axis.

Osteoporosis is a prevalent degenerative disease that is characterized by decreased bone density and strength, resulting in gradually increasing bone fragility. Osteoporosis is caused by an imbalance between osteoblastic bone formation and osteoclastic bone resorption. Recently, increasing evidence has suggested that long non-coding RNAs (lncRNAs) participate in the occurrence and development of osteoporosis. Herein, we explored the role of lncRNA KCNQ1OT1 in osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs). QPCR results indicated that KCNQ1OT1 and RICTOR were down-regulated, while miR-205-5p was up-regulated in the osteoporotic patients, as compared with non-osteoporotic controls. During the osteogenic differentiation of BMSCs, the expression of KCNQ1OT1 and RICTOR was upregulated, whereas miR-205-5p was downregulated. The interaction among KCNQ1OT1, miR-205-5p and RICTOR was validated by dual luciferase reporter system. KCNQ1OT1 promoted RICTOR expression via inhibiting miR-205-5p, therefore promoting osteogenesis as demonstrated by ALP assay, alizarin red staining and the increased expression of osteogenic markers (OPN, RUNX2 and OCN). Furthermore, KCNQ1OT1 overexpression or miR-205-5p inhibition could promote ALP activity and mineralization of BMSCs, while overexpressed miR-205-5p could reverse the effects of overexpressed KCNQ1OT1, and knockdown of RICTOR could reverse the effects of miR-205-5p inhibition. In conclusion, our study illustrated that KCNQ1OT1 might inhibit miR-205-5p in BMSCs, thus upregulating the expression of RICTOR and promoting osteogenic differentiation.

LncRNA GAS5 activates the HIF1A/VEGF pathway by binding to TAF15 to promote wound healing in diabetic foot ulcers.

A diabetic foot ulcer (DFU) is one of the most devastating complications of diabetes. It has been reported that lncRNA GAS5 plays a vital role in wound healing in DFUs. However, the specific mechanism remains unclear. In this research, we aimed to investigate the role of GAS5 in wound healing in DFUs as well as the underlying mechanism. qPCR or western blotting was performed to measure the expression levels of GAS5, HIF1A, VEGF and TAF15. CCK-8 or EdU assays, flow cytometry, wound healing assays and tube formation assays were carried out to assess the proliferation, apoptosis, wound healing and in vitro angiogenesis of HUVECs, respectively. RNA pull-down and RIP assays were performed to verify the interaction between GAS5 and TAF15. ChIP and luciferase assays were conducted to verify the binding of TAF15 to the HIF1A promoter. In the DFU mouse model, H&E and Masson staining were used to determine epidermal and dermal thickness and collagen formation. GAS5 and HIF1A were downregulated in the skin tissues of DFU patients, and GAS5 overexpression promoted cell proliferation, wound healing and tubule formation in HG-treated HUVECs. In addition, GAS5 facilitated HIF1A expression by interacting with TAF15. Rescue assays demonstrated that the suppression of HIF1A/VEGF pathway activation partially reversed the functional roles of GAS5 in HUVECs. Furthermore, GAS5 accelerated wound healing by activating the HIF1A/VEGF pathway in mice with DFUs. GAS5 activates the HIF1A/VEGF pathway by binding to TAF15, resulting in accelerated wound healing in DFUs. Our findings may provide a theoretical basis for the clinical treatment of DFUs.

Complete chloroplast genome sequence of Nicotiana tabacum TN90 (Solanaceae).

This study reported the complete nucleotide sequence of the Nicotiana tabacum TN90 chloroplast (cp) genome. The cpDNA was 155 992 bp in length and contained 133 individual genes (79 protein encoding genes, 30 tRNA genes and four rRNA genes). Maximum-likelihood (ML) phylogenetic tree for 17 species with Arabidopsis thaliana, Oryza sativa, and Anomochloa marantoidea as an outgroup resulted in a single tree with - lnL =542 222.71, where the Nicotiana tabacum TN90 plastid was clustered with three previous reported Nicotiana species: N. tomentosiformis, N. undulata and N. tabacum. The TN90 variety of tobacco cp genome sequence reported in this study will accelerate tobacco improvement in the future.

The angiogenic peptide vascular endothelial growth factor-basic fibroblast growth factor signaling is up-regulated in a rat pressure ulcer model.

The purpose of this study is to investigate the mRNA and protein expression levels of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) in pressure ulcers, and to elucidate the molecular mechanism by which VEGF and bFGF are involved in pressure ulcer formation. A rat model of ischemia-reperfusion pressure ulcer was established by magnetic disk circulating compression method. Real-time fluorescence quantitative PCR and Western blot assays were conducted to detect the mRNA and protein expression of VEGF and bFGF in the tissues of rat I-, II-, and III-degree pressure ulcers, the surrounding tissues, and normal skin. Our study confirmed that the mRNA and protein expression levels of VEGF and bFGF in the tissues of rat I-degree pressure ulcer were significantly higher than that in the II- and III-degree pressure ulcer tissues (P < 0.05). The expression of VEGF and bFGF in the tissues surrounding I- and II-degree pressure ulcers were higher than the rats with normal skin. The expression of VEGF and bFGF in the tissues of rat III-degree pressure ulcer was lower than that in the surrounding tissues and normal skin (P < 0.05). There was a significant positive correlation between change in the VEGF and bFGF. The results showed that with an increase in the degree of pressure ulcers, the expression of VEGF and bFGF in pressure ulcers tissue are decreased. This leads to a reduction in angiogenesis and may be a crucial factor in the formation of pressure ulcers.