Enhanced High Thermal Conductivity Cellulose Filaments via Hydrodynamic Focusing.

Nanocellulose is regarded as a green and renewable nanomaterial that has attracted increased attention. In this study, we demonstrate that nanocellulose materials can exhibit high thermal conductivity when their nanofibrils are highly aligned and bonded in the form of filaments. The thermal conductivity of individual filaments, consisting of highly aligned cellulose nanofibrils, fabricated by the flow-focusing method is measured in dried condition using a T-type measurement technique. The maximum thermal conductivity of the nanocellulose filaments obtained is 14.5 W/m-K, which is approximately five times higher than those of cellulose nanopaper and cellulose nanocrystals. Structural investigations suggest that the crystallinity of the filament remarkably influence their thermal conductivity. Smaller diameter filaments with higher crystallinity, that is, more internanofibril hydrogen bonds and less intrananofibril disorder, tend to have higher thermal conductivity. Temperature-dependence measurements also reveal that the filaments exhibit phonon transport at effective dimension between 2D and 3D.

DGCR5 induces osteogenic differentiation by up-regulating Runx2 through miR-30d-5p.

BACKGROUND: Postmenopausal osteoporosis (PMOP) is a metabolic bone disease caused by unbalance between osteoblast bone formation and osteoclast bone resorption. In this study, the moderating effect of DGCR5 on osteogenic differentiation and its role in PMOP was assessed. METHODS: The expression levels of DGCR5, miR-30d-5p, and Runt-related transcription factor 2 (Runx2) mRNA and protein were determined by qRT-PCR and western blot, separately. The bone marrow human mesenchymal stem cells (hMSCs) were isolated from bone marrow of patients with PMOP or the healthy control. ALP activity and bone mineral density (BMD) were detected to reflect the osteogenic differentiation status. RIP and RNA pull-down assay were performed to explore the combination and interaction between DGCR5 and miR-30d-5p. RESULTS: Compared with the healthy control group (n = 20), DGCR5 was down-regulated in hMSCs from patients with PMOP (n = 20). Overexpression of DGCR5 induced osteogenic differentiation of hMSCs. DGCR5 up-regulated the expression of Runx2 through miR-30d-5p. DGCR5 up-regulated the expression of Runx2 through miR-30d-5p to induce osteogenic differentiation of hMSCs. CONCLUSION: DGCR5 negatively regulates miR-30d-5p, and it up-regulates Runx2 through miR-30d-5p, thereby inducing osteogenic differentiation of hMSCs, which may help to delay PMOP development.

LncRNA RAD51-AS1 Regulates Human Bone Marrow Mesenchymal Stem Cells via Interaction with YBX1 to Ameliorate Osteoporosis.

Long noncoding RNA (lncRNA) is a new key regulatory molecule in the occurrence of osteoporosis, but its research is still in the primary stage. In order to study the role and mechanism of lncRNA in the occurrence of osteoporosis, we reannotated the GSE35956 datasets, compared and analyzed the differential expression profiles of lncRNAs between bone marrow mesenchymal stem cells (hBMSCs) from healthy and osteoporotic patients, and then screened a lncRNA RAD51-AS1 with low expression in hBMSCs from osteoporotic patients, and its role in the occurrence of osteoporosis has not been studied. We confirmed that the expression level of lncRNA RAD51-AS1 in hBMSCs from patients with osteoporosis was significantly lower than those from healthy donors. A nuclear cytoplasmic separation experiment and RNA fluorescence in situ hybridization showed that RAD51-AS1 was mainly located in the nucleus. RAD51-AS1 knockdown significantly inhibited the proliferation and osteogenic differentiation of hBMSCs and significantly increased their apoptosis, while RAD51-AS1 overexpression significantly promoted the proliferation, osteogenic differentiation, and ectopic bone formation of hBMSCs. Mechanistically, we found that RAD51-AS1 banded to YBX1 and then activated the TGF-ß signal pathway by binding to Smad7 and Smurf2 mRNA to inhibit their translation and transcription up-regulated PCNA and SIVA1 by binding to their promoter regions. In conclusion, RAD51-AS1 promoted the proliferation and osteogenic differentiation of hBMSCs by binding YBX1, inhibiting the translation of Smad7 and Smurf2, and transcriptionally up-regulated PCNA and SIVA1.

Long non-coding RNA DUXAP10 exerts oncogenic properties in osteosarcoma by recruiting HuR to enhance SOX18 mRNA stability.

Recent studies have demonstrated that several long non-coding RNAs (lncRNAs) play an important role in the occurrence and development of osteosarcoma (OS). However, more lncRNAs and their mechanisms in regulating growth and migration of OS cells remain to be investigated. In this study, we identified an lncRNA called DUXAP10 by analysis of GEO data, which was significantly up-regulated in OS tissues and cell lines. Experiments in vitro revealed that lncRNA DUXAP10 promoted proliferation, migration, and invasion of OS cells and inhibited their apoptosis. We also demonstrated that DUXAP10 promoted the formation and growth of OS by tumor formation assay. Furthermore, SOX18 was identified as a critical downstream target of DUXAP10 by transcriptome RNA-seq. Mechanistically, DUXAP10 mainly localized in cytoplasm and could specifically bind to HuR to increase the stability of SOX18 mRNA. Meanwhile, SOX18 knockdown largely reversed increased proliferation of OS cells induced by DUXAP10 overexpression. Findings from this study indicate that lncRNA DUXAP10 can act as an oncogene in osteosarcoma by binding HuR to up-regulate the expression of SOX18 at a post-transcriptional level, which may provide a new target for OS clinical diagnosis and treatment.

Suppression effect of N-acetylcysteine on bone loss in ovariectomized mice.

Oxidative stress can trigger DNA damage response and activation of cellular senescence. Accumulating studies have demonstrated that senescent cells can produce senescence-associated secretory phenotype that leads to increased bone resorption and decreased bone formation. And elimination of senescent cells or inhibition of SASP secretion has been shown to prevent bone loss in mice. N-acetylcysteine (NAC) is a strong antioxidant. However, it is unclear whether reversed estrogen deficiency-induced bone loss by antioxidant NAC was associated with the inhibition of oxidative stress, DNA damage, osteocyte senescence and SASP. In this study, OVX mice were supplemented with/without E2 or NAC, and were compared with each other. Our results showed that oxidative stress, DNA damage, osteocyte senescence and the secretion of senescence-associated inflammatory cytokines were increased in OVX mice compared with sham-operated mice. However, these parameters were obviously rescued in OVX mice supplemented with E2 or NAC. Data from this study suggest that NAC can prevent OVX-induced bone loss by inhibiting oxidative stress, DNA damage, cell senescence and the secretion of the senescence-associated secretory phenotype.

N-acetylcysteine prevents orchiectomy-induced osteoporosis by inhibiting oxidative stress and osteocyte senescence.

Oxidative stress is associated with many diseases and has been found to induce DNA damage and cellular senescence. Numerous evidences support the detrimental effects of oxidative stress or cellular senescence on skeletal homeostasis. N-acetylcysteine (NAC) is a powerful antioxidant. However, it is unclear whether NAC can suppress orchiectomy (ORX)-induced osteoporosis by inhibiting oxidative stress and osteocyte senescence. In this study, ORX mice were supplemented with/without NAC, and were compared with each other and with sham-operated mice. Our results showed that NAC could prevent ORX-induced osteoporosis by inhibiting oxidative stress, DNA damage, osteocyte senescence and senescence-associated secretory phenotype (SASP), subsequently stimulating osteoblastic bone formation and inhibiting osteoclastic bone resorption. The results from this study suggest that NAC could be considered as a potential therapeutic agent for prevention and treatment of osteoporosis caused by testosterone deficiency.