Retinoic Acid Receptor Gamma (RARγ) Promotes Cartilage Destruction through Positive Feedback Activation of NF-κB Pathway in Human Osteoarthritis.

Osteoarthritis (OA) is a severe inflammation-related disease which leads to cartilage destruction. The retinoic acid receptor gamma (RARγ) has been indicated to be involved in many inflammation processes. However, the role and mechanism of RARγ in cartilage destruction caused by inflammation in OA are still unknown. Here, we demonstrated that the RARγ was highly expressed in chondrocytes of OA patients compared with healthy people and was positively correlated with the damage degree of cartilage in OA. Cytokine TNF-α promoted the transcription and expression of RARγ through activating the NF-κB pathway in OA cartilage. In addition, the overexpression of RARγ resulted in the upregulation of matrix degradation and inflammation associated genes and downregulation of differentiation and collagen production genes in human normal chondrocyte C28/I2 cells. Mechanistically, overexpression of RARγ could increase the level of p-IκBα and p-P65 to regulate the expression of downstream genes. RARγ and IκBα also could interact with each other and had the same localization in C28/I2 cells. Moreover, the SD rats OA model induced by monosodium iodoacetate indicated that CD437 (RARγ agonist) and TNF-α accelerated the OA progression, including more severe cartilage layer destruction, larger knee joint diameter, and higher serum ALP levels, while LY2955303 (RARγ inhibitor) showed the opposite result. RARγ was also highly expressed in OA group and even higher in TNF-α group. In conclusion, RARγ/NF-κB positive feedback loop was activated by TNF-α in chondrocyte to promote cartilage destruction. Our data not only propose a novel and precise molecular mechanism for OA disease but also provide a prospective strategy for the treatment.

The increase of osteopontin and ß-carboxy-terminal cross-linking telopeptide of type I collagen enhances the risk of hip fracture in the elderly.

BACKGROUND: Hip fracture in the elderly is a health burden worldwide due to its high mortality rate. This study was conducted to determine the possible mechanisms of osteopontin (OPN) and ß-carboxy-terminal cross-linking telopeptide of type I collagen (ß-CTX) in hip fracture in the elderly. MATERIALS AND METHODS: In the study, we recruited 108 elderly patients with hip fracture diagnosed from May 2012 to May 2015 at the Third Hospital of Xiamen and 86 healthy individuals without a history of hip fracture were taken as controls. Serum levels of OPN and ß-CTX were then determined. The T and Z values for bone mineral density (BMD) were also measured. Moreover, logistic regression analysis was performed to assess the risk and protective factors for hip fracture in the elderly. RESULTS: Serum levels of both OPN and ß-CTX were increased in elderly patients with hip fracture. OPN was positively correlated with ß-CTX. In addition, the levels of OPN and ß-CTX shared a positive association with the age, and a negative association with the BMD, in terms of T and Z values of the hip. In addition, increased BMD and outdoor sports might be protective factors for hip fracture, and an increase in levels of OPN and ß-CTX might be associated with a higher risk of hip fracture in the elderly population. DISCUSSION: Collectively, increased serum levels of OPN and ß-CTX might be correlated with a higher risk of a hip fracture and have predictive values in the occurrence of hip fracture in the elderly.

MicroRNA-874 targeting SUFU involves in osteoblast proliferation and differentiation in osteoporosis rats through the Hedgehog signaling pathway.

Osteoporosis is widely viewed as a major public health concern, but the exact magnitude of the problem is uncertain. MicroRNAs play a key role in maintaining bone development and metabolism. This study aims to investigate the effects that microRNA-874 (miR-874) has on osteoblast proliferation and differentiation in osteoporosis rats by targeting SUFU through the Hedgehog signaling pathway. Twenty Wistar female rats were selected for following experiment, and another 20 rats were served as the normal group. Their osteogenic tissues were obtained and the positive expression of SUFU in tissues was determined. Rat osteoblasts were isolated and. The targeting relationship between SUFU and miR-874 was verified and the expression of miR-874, SUFU, Sonic Hedgehog (Shh), Ptch, Smoothened (Smo), bone morphogenetic protein (BMP2), Runx2, proliferating cell nuclear antigen (PCNA) and Bcl-2 associated X protein (Bax) were identified. Besides, cell viability apoptosis, and differentiation were confirmed respectively. Moreover, calcium nodules were observed. Overexpression of SUFU and Bax but lower expression of miR-874, Shh, Ptch, Smo, BMP2, Runx2, and PCNA were found in osteoporosis mice. Besides, elevated expression of miR-874, Shh, Ptch, Smo, BMP2, Runx2 and PCNA, as well as increased cell viability, ALP activity and calcium nodules but decreased expression of SUFU and Bax, and reduced cell apoptosis were confirmed when treated with miR-874 mimic. And it is reciprocal when miR-874 was inhibited. Our study demonstrated that through targeted inhibition of SUFU and activation of Hedgehog signaling pathway, miR-874 could promote the proliferation and differentiation of osteoblasts in osteoporosis rats.

Copper Phthalocyanine-Functionalized Graphitic Carbon Nitride: A Hybrid Heterostructure toward Photoelectrochemical and Photocatalytic Degradation Applications.

In this work, alcian blue 8GX (AB), a copper(II) phthalocyanine derivative, was employed to functionalize graphitic carbon nitride (g-C3 N4 ) for the preparation of a highly efficient photocatalyst. The approach relies on a facile AB-assisted ethanol/water mixed-solvent exfoliation of bulk g-C3 N4 . The as-prepared g-C3 N4 /AB hybrid possesses significantly enhanced solution dispersibility and photoelectrochemical performance resulting from the synergistic effect between g-C3 N4 and AB, which involves the optimization of intimate interfacial contact, extension of light absorption range, and enhancement of charge-transfer efficiency. This synergy contributes enormously to the photocatalytic degradation of rhodamine 6G (R6G) under light irradiation.

Facile Preparation of Bright-Fluorescent Soft Materials from Small Organic Molecules.

Highly fluorescent and biocompatible soft materials are desirable for many potential applications, but their synthetic processes are somehow complicated. Herein, we have explored the feasibility of synthesis of unconventional fluorescence soft materials from small organic molecules under mild conditions. A new blue-fluorescent soft material with high quantum yield (89.6 %) and eutectic feature prepared by simple heat treatment of citric acid (CA) and cysteine (Cys) aqueous mixtures below 100 °C in air was reported. The as-prepared fluorescent material has the features of facile preparation, low cost, scalable production and easy to process, making it suitable for applications like fluorescent labeling and light-emitting devices. This new finding opens a new venue for the preparation of fluorescent soft materials.

Graphene oxide/carbon dot composite: a new photoelectrode material for photocurrent response enhancement.

Low-dimensional carbon nanocomposite-based architectures and anchoring zero-dimensional carbon dots on two-dimensional graphene sheets may provide an important approach to develop energy harvesting and conversion strategies. In this work, as a novel photoelectrode with a high photocurrent response performance based on a composite made with all carbon-based materials consisting of p-type graphene oxide (GO) and n-type nitrogen, sulfur co-doped carbon dot (NS-CD) has been prepared via the electrophoretic deposition approach. The photoelectrochemical measurement shows that the GO/NS-CD composite greatly suppresses the charge recombination and evidently enhances the photocurrent response activity. It is anticipated that this work may pave a valuable step for the further development of all carbon-based optoelectronic devices with excellent performance.