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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]

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]

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]