Leading with purpose: Unraveling the impact of responsible leadership on employee green behavior in the workplace.

Although sustainability has been a priority for organizations, there is still a lack of research on how leaders with a stakeholder perspective can motivate employees to adopt green behavior for sustainability in a complex and changing environment. This paper introduced social cognitive theory to describe two mechanisms by which responsible leadership predicts employee green behavior. Our research considers felt obligation for constructive change and stakeholder value as mediations with cognitive perspective in this process. Additionally, we consider the moderating effects of positive emotion and the superior-subordinate relationship. Our model received support from the investigation and research. By emphasizing the significance of perceived responsible leadership and proposing a new way of perceiving employee green behavior that ensures guidance from responsible leadership along the cognition perspective, the present research contributes to our understanding of the incentive effect of responsible leadership on employee green behavior.

Vascular Endothelial Growth Factor Inhibits Phagocytosis of Apoptotic Cells by Airway Epithelial Cells.

Professional phagocytes such as dendritic cells and macrophages can ingest particles larger than 0.5 µm in diameter. Epithelial cells are nonprofessional phagocytes that cannot ingest pathogenic microorganisms, but they can ingest apoptotic cells. Inhibition of the engulfment of apoptotic cells by the airway epithelium can cause severe airway inflammation. Vascular endothelial growth factor (VEGF) is an angiogenesis-promoting factor that can mediate allergic airway inflammation and can promote airway epithelial cells (AECs) proliferation, but it is not clear whether it affects the engulfment of apoptotic cells by AECs. In the present study, VEGF inhibited engulfment of apoptotic cells by AECs via binding to VEGF receptor(R)2. This inhibitory effect of VEGF was not influenced by masking of phosphatidylserine (PS) on the surface of apoptotic cells and was partially mediated by the PI3K-Akt signaling pathway. VEGF inhibition of phagocytosis involved polymerization of actin and downregulation of the expression of the phagocytic-associated protein Beclin-1 in AECs. Since engulfment of apoptotic cells by AECs is an important mechanism for airway inflammation regression, VEGF inhibition of the engulfment of apoptotic cells by airway epithelial cells may be important for mediating allergic airway inflammation.

Yes-associated protein upregulates filopodia formation to promote alveolar epithelial-cell phagocytosis.

Cells engulf particles larger than 0.5 µm in diameter by phagocytosis, which is driven by cytoskeletal rearrangements. Phagocytosis by alveolar epithelial cells (AECs) helps to maintain the alveolar homeostasis. Yes-associated protein (YAP), a transcriptional coactivator of the Hippo pathway, affects proliferation, differentiation, and cytoskeletal rearrangement of AECs, but it is not clear whether YAP regulates phagocytosis. In this study, interference with YAP expression inhibited phagocytosis in MLE-12 cells and in primary cultures of AEC. Filopodia formation promoted phagocytosis in AECs, and YAP enhanced filopodia formation in AECs. Blocking PI3K signaling resulted in reduced YAP protein expression and inhibition of phagocytosis. The results indicate that YAP expression was regulated by PI3K signaling and promoted phagocytosis in AECs by upregulating filopodia formation.

[Phagocytosis of alveolar macrophages is suppressed in a mouse model of lipopolysaccharide-induced acute lung injury].

OBJECTIVE: To investigate the changes in phagocytic function of alveolar macrophages (AMs) in mice with lipopolysaccharide (LPS)-induced acute lung injury (ALI) and explore the possible mechanism. METHODS: Kunming mice were randomly divided into normal control group and ALI (induced by LPS instillation in the airway) model group. AMs were obtained from bronchoalveolar lavage fluid in both groups, and phagocytosis of the AMs was observed using flow cytometry and fluorescence microscopy. Western blotting and ELISA were used to detect the expression and secretion of IL-33 in the lung tissue of the mice. We also detected the secretion of IL-33 by an alveolar epithelial cell line MLE-12 in response to stimulation with different concentrations of LPS. The AMs from the normal control mice were treated with different concentrations of LPS and IL-33, and the changes in the phagocytic activity of the cells were observed. RESULTS: Compared with those in normal control group, the percentage of AMs phagocytosing fluorescent microspheres was significantly decreased, and the expression of IL-33 in lung tissue and IL-33 level in the bronchoalveolar lavage fluid were significantly increased in ALI mice (P < 0.01). LPS (100-1000 ng/mL) obviously promoted the secretion of IL-33 in cultured MLE-12 cells (P < 0.01). Both LPS (10-500 ng/mL) and IL-33 (100 ng/mL) significantly inhibited the phagocytic activity of the AMs from normal control mice (P < 0.01). CONCLUSIONS: The phagocytic activity of AMs is weakened in ALI mice possibly due to direct LPS stimulation and the inhibitory effect of the alarmin IL-33 produced by LPS-stimulated alveolar epithelial cells.

SCF promotes the production of IL-13 via the MEK-ERK-CREB signaling pathway in mast cells.

Mast cells serve a key role in the occurrence and development of allergy. As an important growth factor of mast cells, stem cell factor (SCF) has an effect on the apoptosis, chemotaxis, adhesion, degranulation and other biological characteristics of mast cells. However, there are few studies regarding the effect of SCF signal on the production of cytokines from mast cells, particularly Th2 type cytokines. In the present study, the expression and secretion of IL-13 in P815 cells stimulated by SCF were detected by fluorescence quantitative PCR and ELISA, and western blotting and EMSA were used to detect ERK phosphorylation and activation of CREB in stimulated P815 cells. The results demonstrated that the production of IL-13 was significantly increased in P815 cells stimulated by SCF (1-100 ng/ml; P<0.01). There was an obvious phosphorylation of ERK and CREB activation in P815 cells stimulated by SCF (50 ng/ml). Compared with the SCF single stimulation group, the production of IL-13 was significantly reduced in P815 cells stimulated with U0126 (ERK-MEK/pathway inhibitor) or H-89 (CREB inhibitor) combined with SCF stimulation group (P<0.01). However, JSI-124 (JAK/STAT3 pathway inhibitor), Wortmannin (PI3K/Akt pathway inhibitor) and PDTC (NF-κB inhibitor) had no effect on the role of SCF promoting the P815 cells producing IL-13. Therefore, SCF signaling promotes mast cell P815 to produce IL-13, and this effect is associated with the MEK-ERK-CREB signaling pathway.

miR­20b negatively regulates VEGF expression by targeting STAT3 in H22 hepatocellular carcinoma cells.

Vascular endothelial growth factor (VEGF) promotes angiogenesis during tumor growth, and its expression involves multiple signaling pathways and transcription factors. In the present study, transforming growth factor (TGF)­ß1 promoted upregulation of VEGF and downregulation of microRNA (miR)­20b expression in mouse H22 hepatocellular carcinoma cells. miR­20b negatively regulated both constitutive VEGF expression and TGF­ß1­induced VEGF expression. The miRanda algorithm predicted that a binding site of the miR­20b GCAAUCUGGGCACUUU sequence was present in the signal transducer and activator of transcription (STAT)3 3'­untranslated region. Following transfection of miR­20b mimics into H22 cells, expression of STAT3 protein was downregulated. A dual­luciferase activity assay revealed that miR­20b directly targeted STAT3 to regulate its expression, and that interference with STAT3 expression significantly downregulated VEGF mRNA and protein expression. Interference with STAT3 expression resulted in increased VEGF expression in H22 cells overexpressing miR­20b, but expression was lower than that in quiescent H22 cells. This indicated that STAT3 was involved in the negative regulation of VEGF expression in H22 cells by miR­20b. The data demonstrated that miR­20b negatively regulated VEGF expression by directly targeting STAT3 in H22 cells.

[SCF/c-Kit signaling promotes invasion of T24 cells via PI3K pathway].

OBJECTIVE: To explore the role of SCF/c-Kit signaling in the invasion of bladder cancer T24 cells. METHODS: Western blotting was used to detect the expression of c-Kit and PI3K pathway activation stimulated by stem cell factor (SCF) in T24 cells. The invasiveness of T24 cells before and after SCF stimulation and Wortmannin (aspecific PI3K inhibitor) treatment was evaluated using Transwell invasion assay (direct and indirect counting methods). RESULTS: T24 cells expressed c-Kit protein and showed obvious Akt phosphorylation after stimulation with SCF (1 ng/ml) for 24 h. Compared to the control group, SCF stimulation (1 ng/ml) caused a greater number of T24 cells to migrate through the polycarbonate film (P<0.01), and this effect was blocked by the application of Wortmannin before the stimulation. CONCLUSION: SCF/c-Kit signaling promotes the invasiveness of T24 cells, and this effect is mediated by the PI3K pathway.