The mechanisms and functions of TGF-β1 in tendon healing.

Diabetic complications, especially diabetic retinopathy, diabetic nephropathy and painful diabetic neuropathy, account for a large portion of patients with diabetes and display rising global prevalence. They are the leading causes of blindness, kidney failure and hypersensitivity to pain caused by diabetes. Current approved therapeutics against the diabetic complications are few and exhibit limited efficacy. The enhanced cell-specificity, stability, biocompatibility, and loading capacity of drugs are essential for the mitigation of diabetic complications. In the article, we have critically discussed the recent studies over the past two years in material sciences and biochemistry. The insightful concepts in these studies drive the development of novel nanoparticles and mesenchymal stem cells-derived extracellular vesicles to meet the need for treatment of diabetic complications. Their underlying biochemical principles, advantages and limitations have been in-depth analyzed. The nanoparticles discussed in the article include double-headed nanodelivery system, nanozyme, ESC-HCM-B system, soft polymer nanostars, tetrahedral DNA nanostructures and hydrogels. They ameliorate the diabetic complication through attenuation of inflammation, apoptosis and restoration of metabolic homeostasis. Moreover, mesenchymal stem cell-derived extracellular vesicles efficiently deliver therapeutic proteins to the retinal cells to suppress the angiogenesis, inflammation, apoptosis and oxidative stress to reverse diabetic retinopathy. Collectively, we provide a critical discussion on the concept, mechanism and therapeutic applicability of new delivery tools to treat these three devastating diabetic complications. 

New concepts drive the development of delivery tools for sustainable treatment of diabetic complications.

Background: Sporadic inclusion body myositis (s-IBM) represents a unique disease within idiopathic inflammatory myopathies with a dual myodegenerative–autoimmune physiopathology and a lack of an efficacious treatment. Circulating miRNA expression could expand our knowledge of s-IBM patho-mechanisms and provide new potential disease biomarkers. To evaluate the expression of selected pre-amplified miRNAs in the serum of s-IBM patients compared to those of a sex- and age-matched healthy control group, we enrolled 14 consecutive s-IBM patients and 8 sex- and age-matched healthy controls. By using two different normalization approaches, we found one downregulated and three upregulated miRNAs. hsa-miR-192-5p was significantly downregulated, while hsa-miR-372-3p was found to be upregulated more in the s-IBM patients compared to the level of the controls. The other two miRNAs had a very low expression levels (raw Ct data > 29). hsa-miR-192-5p and hsa-miR-372-3p were found to be significantly dysregulated in the serum of s-IBM patients. These miRNAs are involved in differentiation and regeneration processes, thus possibly reflecting pathological mechanisms in s-IBM muscles and potentially representing disease biomarkers.

/pdf/serum-circulating-micrornas-in-sporadic-inclusion-body-2hjhinxm.pdf

Serum-Circulating microRNAs in Sporadic Inclusion Body Myositis

[This retracts the article DOI: 10.1155/2022/6481846.].

Retracted: Mir-192-5p Alleviated Fibrosis and Inflammatory Responses of Tendon Cells by Targeting NFAT5

Electrochemical and imaging-based analysis of composite hydrogel for monitoring the prevention of postoperative adhesion of chest wall in mice with lung cancer

Objective To explore the effect of microRNA (miR)-192-5p on the inflammatory and fibrotic responses of tendon cells. Methods Tendon cells were treated with transforming growth factor-β1 (TGF-β1). The expression of miR-192-5p and nuclear factor of activated T cells 5 (NFAT5) in tendon cells were detected by RT-qPCR. The expressions of inflammatory and fibrosis-related factors were detected by RT-qPCR and Western blot. MiR-192-5p binds to NFAT5 targeting by TargetScan and dual-luciferase reporter gene assay. The expression of the NFAT5 gene was detected by RT-qPCR and Western blot. Detection of apoptosis in tendon cells by flow cytometry. Results MiR-192-5p was downregulated in tendon cells, and the expression level gradually decreased with the prolong of TGF-β1 treatment. The expression of NFAT5 increased with the treatment time of TGF-β1. The expression of miR-192-5p decreased collagen III (COLIII), α smooth muscle actin (α-SMA), matrix metalloproteinase- (MMP-) 1, and MMP-8 expression, thereby inhibiting TGF-β1-induced fibrosis in tendon cells. The expression of miR-192-5p decreased the expression of tumor necrosis factor-α (TNF-α), interleukin (IL)-6, and IL-1β, thereby alleviating TGF-β1-induced inflammatory response and reduce apoptosis in tendon cells. NFAT5 is a direct target of miR-192-5p in tendon cells. The upregulation of NFAT5 reversed the effect of miR-192-5p on the fibrotic activity and inflammatory response of TGF-β1-stimulated tendon cells. Conclusions MiR-192-5p alleviates fibrosis and inflammatory responses of tendon cells by targeting NFAT5.

/pdf/mir-192-5p-alleviated-fibrosis-and-inflammatory-responses-of-3c2yncvv.pdf

MiR-192-5p Alleviated Fibrosis and Inflammatory Responses of Tendon Cells by Targeting NFAT5

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MiR-192-5p Alleviated Fibrosis and Inflammatory Responses of Tendon Cells by Targeting NFAT5