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Lanthanum (La) is widely used in modern industry and agriculture because of its unique physicochemical properties and is broadly exposed in the population. Some studies have shown that La may have some effects on adipogenesis, but there is a lack of related in vivo evidence. In this study, the effects of La(NO3)3 on adipogenesis and its associated mechanism were studied using C57BL/6J mouse model. The results showed that La(NO3)3 exposure caused a decrease in body weight and the percentage of fat content in mice. In addition, the adipose marker molecules and specific adipogenic transcription factors decreased in both white adipose tissue (WAT) and brown adipose tissue (BAT). Detection of signaling pathway‐related molecules revealed that canonical wnt/β‐catenin pathway‐related molecules were upregulated in both adipose tissues. In summary, in vivo exposure to La(NO3)3 might inhibited adipogenesis in mice, possibly through upregulation of the canonical Wnt/β‐catenin signaling pathway. Lanthanum (La) is widely used in many aspects and might have some effects on adipogenesis. In this study, the effects of La(NO3)3 on adipogenesis and its associated mechanism were studied using C57BL/6J mouse model. The results showed that in vivo exposure to La(NO3)3 might inhibited adipogenesis in mice, possibly through upregulation of the canonical Wnt/β‐catenin signaling pathway. [ABSTRACT FROM AUTHOR]

Yttrium is a typical heavy rare earth element with widespread use in numerous sectors. Only one previous study has indicated that yttrium has the potential to cause developmental immunotoxicity (DIT). Therefore, there remains a paucity of evidence on the DIT of yttrium. This study aimed to explore the DIT of yttrium nitrate (YN) and the self‐recovery of YN‐induced DIT. Dams were treated with 0, 0.2, 2, and 20 mg/kg bw/day YN by gavage during gestation and lactation. No significant changes were found in innate immunity between the control and YN‐treated groups in offspring. In female offspring at postnatal day 21 (PND21), YN markedly inhibited humoral and cellular immune responses, the proliferative capacity of splenic T lymphocytes, and the expression of costimulatory molecules in splenic lymphocytes. Moreover, the inhibitory effect on cellular immunity in female offspring persisted to PND42. Unlike females, YN exposure did not change the adaptive immune responses in male offspring. Overall, maternal exposure to YN showed a strong DIT to offspring, with the lowest effective dose of 0.2 mg/kg in the current study. The toxicity of cellular immunity could persist throughout development into adulthood. There were sex‐specific differences in YN‐induced DIT, with females being more vulnerable. [ABSTRACT FROM AUTHOR]

Lanthanum (La) as a rare earth element is widely used in agriculture, industry, and medicine. It has been suggested in several studies that La might influence glycolipid metabolism in vivo. In this study, we used 3T3‐L1 preadipocytes as in vitro cell model to elucidate the effects of La(NO3)3 on adipogenesis and the underlying mechanisms. The results showed that La(NO3)3 could inhibit the adipogenic differentiation of 3T3‐L1 preadipocytes, which showed a decrease in lipid accumulation and the downregulation of specific adipogenic transcription factors. La(NO3)3 exerted its inhibitory effect mainly at the early differentiation stage. Furthermore, La(NO3)3 influenced the S‐phase entry and cell cycle process during the mitotic clonal expansion and regulated the phosphorylation of signal transducer and activator of transcription 3 (STAT3) and expressions of the proteins in phosphatidylinositol 3‐kinase (PI3K)/Akt pathway at the early stage of differentiation. Besides, La(NO3)3 upregulated the expressions of wnt10b mRNA and β‐catenin protein and promoted the nucleus translocation of β‐catenin. Additionally, we found that La(NO3)3 could promote the growth of 3T3‐L1 preadipocytes both with and without MDI (3‐isobutyl‐1‐methylxanthine [IBMX], dexamethasone [Dex], and insulin) stimulation. Collectively, these results indicated that La(NO3)3 could inhibit adipogenesis in 3T3‐L1 preadipocytes and influence cell proliferation. Lanthanum (La) as a rare earth element is widely used in many aspects and might influence glycolipid metabolism in vivo. In this study, we used 3T3‐L1 preadipocytes as in vitro cell model to elucidate the effects of La(NO3)3 on adipogenesis. The results showed that La(NO3)3 could inhibit the adipogenic differentiation of 3T3‐L1 preadipocytes and influence the cell cycle process during the mitotic clonal expansion. Also, the wnt/β‐catenin signaling pathway might be involved in the inhibitory effect of La(NO3)3. [ABSTRACT FROM AUTHOR]

Black carbon (BC) correlates with the occurrence and progression of atherosclerosis and other cardiovascular diseases. Increasing evidence has demonstrated that BC could impair vascular endothelial cells, but the underlying mechanisms remain obscure. It is known that IL‐33 exerts a significant biological role in cardiovascular disease, but little is known about the molecular regulation of IL‐33 expression at present. We first found that BC significantly increased IL‐33 mRNA in EA.hy926 cells in a concentration and time‐dependent manner, and we conducted this study to explore its underlying mechanism. We identified that BC induced mitochondrial damage and suppressed autophagy function in EA.hy926 cells, as evidenced by elevation of the aspartate aminotransferase (GOT2), reactive oxygen species (ROS) and p62, and the reduction of mitochondrial membrane potential (ΔΨm). However, ROS cannot induce IL‐33 mRNA‐production in BC‐exposed EA.hy926 cells. Further, experiments revealed that BC could promote IL‐33 mRNA production through the PI3K/Akt/AP‐1 and p38/AP‐1 signaling pathways. It is concluded that BC could induce oxidative stress and suppress autophagy function in endothelial cells. This study also provided evidence that the pro‐cardiovascular‐diseases properties of BC may be due to its ability to stimulate the PI3K/AKT/AP‐1 and p38/AP‐1 pathway, further activate IL‐33 and ultimately result in a local vascular inflammation. [ABSTRACT FROM AUTHOR]

Obesogens are a subset of endocrine disruptor chemicals (EDCs) that cause obesity. The typical EDC 4‐nonylphenol (4‐NP) has been identified as an obesogen. However, the in vitro effects of 4‐NP on adipogenesis remain unclear. In this study, 3T3‐L1 preadipocytes and C3H/10T1/2 mesenchymal stem cells (MSCs) were used to investigate the influence of 4‐NP on adipogenesis. The differentiation protocols for 3T3‐L1 preadipocytes and C3H/10T1/2 MSCs took 8 and 12 days, respectively, beginning at Day 0. In differentiated 3T3‐L1 preadipocytes, 20 μM 4‐NP decreased cell viability on Days 4 and 8. Exposure to 4‐NP inhibited triglyceride (TG) accumulation and adipogenic marker expression on Days 0–8, but the inhibitory effects were weaker on Days 2–8. The protein expression of pSTAT3 or STAT3 decreased on Days 0–8 and 2–8. Conversely, 4‐NP promoted TG accumulation and the adipogenic marker expression in C3H/10T1/2 adipocytes. The opposing effects were attributed to physiological differences between the two cell lines. The 3T3‐L1 preadipocytes are dependent on mitotic clonal expansion (MCE) to drive differentiation, while C3H/10T1/2MSCs and human preadipocytes are not. Additionally, 4‐NP downregulated β‐catenin expression in C3H/10T1/2 adipocytes. Accordingly, we hypothesized that 4‐NP promotes adipogenesis. The role of the canonical Wnt pathway in the promotion of adipogenesis by 4‐NP requires further validation. This study provides new insights into the mechanisms and appropriate risk management of 4‐NP. This study aimed to investigate the effects of 4‐nonylphenol (4‐NP) on adipogenesis in vitro. The results showed that 4‐NP inhibited 3T3‐L1 preadipocyte differentiation but promoted C3H/10T1/2 mesenchymal stem cell (MSC) adipogenesis. The opposing effects were likely due to physiological differences between the two cell lines. The 3T3‐L1 preadipocytes are dependent on MCE to drive differentiation, whereas C3H/10T1/2 MSCs are not. We found that 4‐NP promoted adipogenesis, and new insights into the mechanisms have been provided. [ABSTRACT FROM AUTHOR]

Bisphenol A (BPA) is widely used as the raw material for the production of plastics and paper products. People can be exposed to BPA through dermal contact, particularly for cashiers in contact with thermal paper every day. BPA is a known endocrine disruptor that has been shown to be carcinogenic. Many tumors show weak gap junctional intercellular communication (GJIC) function. The aim of this study was to investigate the effects and possible mechanisms of BPA's action on GJIC of human HaCaT skin cells. The results showed that BPA increased cell proliferation rates, prolonged GJIC photobleaching fluorescence recovery times and reduced overall fluorescence recovery rates at 0.01, 0.1 and 1 μm. BPA downregulated connexin (Cx)26 mRNA level at 0.1 μm. Estrogen receptor (ER) antagonist ICI 182 780 at 5 nm partially blocked the above effects of BPA indicating involvement of the ER pathway with BPA exposure. However, BPA did not influence Cx43 mRNA and protein levels. Our immunofluorescence data showed that Cx26 was expressed in the cytoplasm and plasma membrane, and was involved in the formation of gap junctions between adjacent cells, while Cx43 was expressed only in the cytoplasm. Therefore, our data indicate that Cx26 gap junctions may be involved in the GJIC inhibition caused by BPA. In conclusion, our results indicate that BPA can promote human skin cell proliferation, inhibit skin cell GJIC function but not formation and downregulate Cx26 mRNA levels partially through the ER pathway. We hypothesize that BPA can exhibit carcinogenicity by inhibiting GJIC. The aim of this study was to investigate the effects and possible mechanisms of BPA's action on gap junctional intercellular communication (GJIC) of human normal keratinocytes, HaCaT cells. The results reveal that BPA can promote human skin cell proliferation, inhibit skin cell GJIC function but not formation and downregulate connexin 26 mRNA levels partially through the estrogen receptor pathway. We hypothesize that BPA can exhibit carcinogenicity by inhibiting GJIC. [ABSTRACT FROM AUTHOR]

ABSTRACT: In fracture treatment, biological bone union generally depends on the bone's natural fracture healing capacity, even in surgically treated cases. Hydroxyapatite/collagen composite (HAp/Col) has high osteoconductivity and stimulates osteogenic progenitors. Furthermore, it has the potent capacity to adsorb bone morphogenetic proteins (BMPs). In this study, we prepared an injectable HAp/Col paste and evaluated its augmentation of bone union. Furthermore, the effect of HAp/Col paste combined with BMP‐2 was also evaluated. We used a rat femur osteotomy model with a defect size of 1 mm. Male Wistar rats were assigned to one of the following four groups; a control group without any implant, a HAp/Col implant group, a group that received an absorbable collagen sponge (ACS) implant impregnated with BMP‐2 (1 μg), and a group that received a HAp/Col implant impregnated with BMP‐2 implant. Micro‐CT analysis, three‐point bending tests, and histological evaluation were performed. Bone union was achieved in two of eight cases in the HAp/Col group, five of eight cases in the ACS + BMP‐2 group, and all cases in the HAp/Col + BMP‐2 group at 8 weeks post‐surgery. The control group did not achieve bone union. In addition, in the HAp/Col + BMP‐2 group, the biomechanical strength of the fused femurs was comparable to that of the contralateral intact femur; the ratio of the mechanical load at the breaking point of the osteotomy side relative to that of the contralateral side was 1.00 ± 0.151 (SD). These results indicate that HAp/Col paste with or without BMP‐2 augments bone union. © 2017 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 36:129–137, 2018. [ABSTRACT FROM AUTHOR]

Articular cartilage has a limited capacity for spontaneous repair, and an effective method to repair damaged articular cartilage has not yet been established. The purpose of this study was to evaluate the effect of transplantation of porous hydroxyapatite collagen ( HAp/ Col) impregnated with bone morphogenetic protein-2 ( BMP-2). To evaluate the characteristics of porous HAp/ Col as a drug delivery carrier of recombinant human BMP-2 ( rhBMP-2), the rhBMP-2 adsorption capacity and release kinetics of porous HAp/ Col were analyzed. Porous HAp/ Col impregnated with different amounts of rhBMP-2 (0, 5, and 25 μg) was implanted into osteochondral defects generated in the patellar groove of Japanese white rabbits to evaluate the effect on osteochondral defect regeneration. At 3, 6, 12, and 24 weeks after operation, samples were harvested and subjected to micro-computed tomography analysis and histological evaluation of articular cartilage and subchondral bone repair. The adsorption capacity was 329.4 μg of rhBMP-2 per cm3 of porous HAp/ Col. Although 36% of rhBMP-2 was released within 24 h, more than 50% of the rhBMP-2 was retained in the porous HAp/ Col through the course of the experiment. Defects treated with 5 μg of rhBMP-2 showed the most extensive subchondral bone repair and the highest histological regeneration score, and differences against the untreated defect group were significant. The histological regeneration score of defects treated with 25 μg of rhBMP-2 increased up to 6 weeks after implantation, but then decreased. Porous HAp/ Col, therefore, is an appropriate carrier for rhBMP-2. Implantation of porous HAp/ Col impregnated with rhBMP-2 is effective for rigid subchondral bone repair, which is important for the repair of the smooth articular surface. [ABSTRACT FROM AUTHOR]