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1.
Limanjaya Anita Guo Nan Yin Soon-Sun Hong Ju-Hee Kang Yong Song Gho Jun-Kyu Suh Ji-Kan Ryu 《International journal of biological sciences》2022,18(9):3653
Diabetes mellitus is one of the main causes of erectile dysfunction (ED). Men with diabetic ED do not respond well to oral phosphodiesterase-5 inhibitors owing to neurovascular dysfunction. Pericyte-derived extracellular vesicle-mimetic nanovesicles (PC-NVs) are known to promote nerve regeneration in a mouse model of cavernous nerve injury. Here, we report that administration of PC-NVs effectively promoted penile angiogenesis and neural regeneration under diabetic conditions, thereby improving erectile function. Specifically, PC-NVs induced endothelial proliferation and migration and reduced cell apoptosis under diabetic conditions. In addition, PC-NVs induced neural regeneration in STZ-induced diabetic mice in dorsal root ganglion and major pelvic ganglion explants in vivo and ex vivo under high-glucose conditions. We found that lipocalin 2 (Lcn2) is a new target of PC-NVs in this process, demonstrating that PC-NVs exert their angiogenic and nerve-regeneration effects by activating MAP kinase and PI3K/Akt and suppressing P53 signaling pathway in an Lcn2-dependent manner. Our findings provide new conclusive evidence that PC-NVs can promote neurovascular regeneration and recovery of erectile function under diabetic conditions via an Lcn2-dependent mechanism. Thus, local administration of PC-NVs may be a promising treatment strategy for the treatment of diabetic ED. 相似文献
2.
Pustjens T. F. S. Streukens B. Vainer J. Gho B. Ruiters A. W. Stein M. Ilhan M. Veenstra L. Theunissen R. Bekkers S. C. A. M. van’t Hof A. W. J. Rasoul S. 《Netherlands heart journal》2020,28(2):75-80
Netherlands Heart Journal - To compare ischaemia-driven complete coronary revascularisation by percutaneous coronary intervention (PCI) with usual care in patients with non-ST-elevation myocardial... 相似文献
3.
Jung Ok Park Do‐Young Choi Dong‐Sic Choi Hee Joung Kim Jeong Won Kang Jae Hun Jung Jeong Hwa Lee Jayoung Kim Michael R. Freeman Kye Young Lee Yong Song Gho Kwang Pyo Kim 《Proteomics》2013,13(14):2125-2134
Microvesicles (MVs, also known as exosomes, ectosomes, microparticles) are released by various cancer cells, including lung, colorectal, and prostate carcinoma cells. MVs released from tumor cells and other sources accumulate in the circulation and in pleural effusion. Although recent studies have shown that MVs play multiple roles in tumor progression, the potential pathological roles of MV in pleural effusion, and their protein composition, are still unknown. In this study, we report the first global proteomic analysis of highly purified MVs derived from human nonsmall cell lung cancer (NSCLC) pleural effusion. Using nano‐LC–MS/MS following 1D SDS‐PAGE separation, we identified a total of 912 MV proteins with high confidence. Three independent experiments on three patients showed that MV proteins from PE were distinct from MV obtained from other malignancies. Bioinformatics analyses of the MS data identified pathologically relevant proteins and potential diagnostic makers for NSCLC, including lung‐enriched surface antigens and proteins related to epidermal growth factor receptor signaling. These findings provide new insight into the diverse functions of MVs in cancer progression and will aid in the development of novel diagnostic tools for NSCLC. 相似文献
4.
Ji Hyun Kim Yae Jin Yoon Jaewook Lee Eun-Jeong Choi Namwoo Yi Kyong-Su Park Jaesung Park Jan L?tvall Yoon-Keun Kim Yong Song Gho 《PloS one》2013,8(3)
Escherichia coli, as one of the gut microbiota, can evoke severe inflammatory diseases including peritonitis and sepsis. Gram-negative bacteria including E. coli constitutively release nano-sized outer membrane vesicles (OMVs). Although E. coli OMVs can induce the inflammatory responses without live bacteria, the effect of E. coli OMVs in vivo on endothelial cell function has not been previously elucidated. In this study, we show that bacteria-free OMVs increased the expression of endothelial intercellular adhesion molecule-1 (ICAM-1), E-selectin and vascular cell adhesion molecule-1, and enhanced the leukocyte binding on human microvascular endothelial cells in vitro. Inhibition of NF-κB and TLR4 reduced the expression of cell adhesion molecules in vitro. OMVs given intraperitoneally to the mice induced ICAM-1 expression and neutrophil sequestration in the lung endothelium, and the effects were reduced in ICAM-1-/- and TLR4-/- mice. When compared to free lipopolysaccharide, OMVs were more potent in inducing both ICAM-1 expression as well as leukocyte adhesion in vitro, and ICAM-1 expression and neutrophil sequestration in the lungs in vivo. This study shows that OMVs potently up-regulate functional cell adhesion molecules via NF-κB- and TLR4-dependent pathways, and that OMVs are more potent than free lipopolysaccharide. 相似文献
5.
Frizzled regulates localization of cell-fate determinants and mitotic spindle rotation during asymmetric cell division 总被引:1,自引:0,他引:1
Cell-fate diversity is generated in part by the unequal segregation of cell-fate determinants during asymmetric cell divisions. In the Drosophila pupa, the pI sense organ precursor cell is polarized along the anterior-posterior axis of the fly and divides asymmetrically to generate a posterior pIIa cell and an anterior pIIb cell. The anterior pIIb cell specifically inherits the determinant Numb and the adaptor protein Partner of Numb (Pon). By labelling both the Pon crescent and the microtubules in living pupae, we show that determinants localize at the anterior cortex before mitotic-spindle formation, and that the spindle forms with random orientation and rotates to line up with the Pon crescent. By imaging living frizzled (fz) mutant pupae we show that Fz regulates the orientation of the polarity axis of pI, the initiation of spindle rotation and the unequal partitioning of determinants. We conclude that Fz participates in establishing the polarity of pI. 相似文献
6.
Endostatin blocks vascular endothelial growth factor-mediated signaling via direct interaction with KDR/Flk-1 总被引:40,自引:0,他引:40
Kim YM Hwang S Kim YM Pyun BJ Kim TY Lee ST Gho YS Kwon YG 《The Journal of biological chemistry》2002,277(31):27872-27879
Endostatin, a fragment of collagen XVIII, is a potent anti-angiogenic protein, but the molecular mechanism of its action is not yet clear. We examined the effects of endostatin on the biological and biochemical activities of vascular endothelial growth factor (VEGF). Endostatin blocked VEGF-induced tyrosine phosphorylation of KDR/Flk-1 and activation of ERK, p38 MAPK, and p125(FAK) in human umbilical vein endothelial cells. Endostatin also inhibited the binding of VEGF(165) to both endothelial cells and purified extracellular domain of KDR/Flk-1. Moreover, the binding of VEGF(121) to KDR/Flk-1 and VEGF(121)-stimulated ERK activation were blocked by endostatin. The direct interaction between endostatin and KDR/Flk-1 was confirmed by affinity chromatography. However, endostatin did not bind to VEGF. Our findings suggest that a direct interaction of endostatin with KDR/Flk-1 may be involved in the inhibitory function of endostatin toward VEGF actions and responsible for its potent anti-angiogenic and anti-tumor activities in vivo. 相似文献
7.
Apoptosis plays a major role in vertebrate and invertebrate development. The adult Drosophila thoracic microchaete is a mechanosensory organ whose development has been extensively studied as a model of how cell division and cell determination intermingle. This sensory organ arises from a cell lineage that produces a glial cell and four other cells that form the organ. In this study, using an in vivo approach as well as fixed material, we show that the glial cell undergoes nucleus fragmentation shortly after birth. Fragmentation was blocked after overexpression of the caspase inhibitor p35 or removal of the pro-apoptotic genes reaper, hid and grim, showing that the glial cell undergoes apoptosis. Moreover, it seems that fragments are eliminated from the epithelium by mobile macrophages. Forcing survival of the glial cells induces precocious axonal outgrowth but does not affect final axonal patterning and connectivity. However, under these conditions, glial cells do not fragment but leave the epithelium by a mechanism that is reminiscent of cell competition. Finally, we present evidences showing that glial cells are committed to apoptosis independently of gcm and prospero expression. We suggest that apoptosis is triggered by a cell autonomous mechanism. 相似文献
8.
Pablo M. Vergara Cecilia Smith Cristian A. Delpiano Ignacio Orellana Dafne Gho Inao Vazquez 《Oecologia》2010,164(4):981-991
Habitat degradation and fragmentation are expected to reduce seed dispersal rates by reducing fruit availability as well as
the movement and abundance of frugivores. These deleterious impacts may also interact with each other at different spatial
scales, leading to nonlinear effects of fruit abundance on seed dispersal. In this study we assessed whether the degradation
and fragmentation of southern Chilean forests had the potential to restrict seed dispersal the lingue (Persea lingue) tree, a fleshy-fruited tree species. Of five frugivore bird species, the austral thrush (Turdus falcklandii) and the fire-eyed diucon (Xolmis pyrope) were the only legitimate seed dispersers as well as being the most abundant species visiting lingue trees. The results showed
little or no direct effect of habitat fragmentation on seed dispersal estimates, possibly because the assemblage of frugivore
birds was comprised habitat-generalist species. Instead, the number of fruits removed per focal tree exhibited an enhanced
response to crop size, but only in the more connected fragments. In the fruit-richer fragment networks, there was an increased
fragment-size effect on the proportion of fruits removed in comparison to fruit-poor networks in which the fragment size effect
was spurious. We suggest that such nonlinear effects are widespread in fragmented forest regions, resulting from the link
between the spatial scales over which frugivores sample resources and the spatial heterogeneity in fruiting resources caused
by habitat fragmentation and degradation. 相似文献
9.
Kim YK Oh SY Jeon SG Park HW Lee SY Chun EY Bang B Lee HS Oh MH Kim YS Kim JH Gho YS Cho SH Min KU Kim YY Zhu Z 《Journal of immunology (Baltimore, Md. : 1950)》2007,178(8):5375-5382
Allergic asthma is characterized by airway inflammation initiated by adaptive immune responses to aeroallergens. Recent data suggest that severe asthma may be a different form of asthma rather than an increase in asthma symptoms and that innate immune responses to LPS can modulate adaptive immune responses to allergens. In this study, we evaluated the hypothesis that airway exposure to different doses of LPS induces different form of asthma. Our study showed that neutrophilic inflammation and IFN-gamma expression were higher in induced sputum from severe asthma patients than from mild to moderate asthmatics. Animal experiments indicated that allergen sensitization with low-dose LPS (0.1 microg) induced type 2 asthma phenotypes, i.e., airway hyperresponsiveness, eosinophilic inflammation, and allergen-specific IgE up-regulation. In contrast, allergen sensitization with high-dose LPS (10 microg) induced asthma phenotypes, i.e., airway hyperresponsiveness and noneosinophilic inflammation that were not developed in IFN-gamma-deficient mice, but unaffected in the absence of IL-4. During the allergen sensitization period, TNF-alpha expression was found to be enhanced by both low- and high-dose LPS, whereas IL-12 expression was only enhanced by high-dose LPS. Interestingly, the asthma phenotypes induced by low-dose LPS, but not by high-dose LPS, were completely inhibited in TNF-alpha receptor-deficient mice, whereas the asthma phenotypes induced by high-dose LPS were abolished in the homozygous null mutation of the STAT4 gene. These findings suggest that airway exposure levels of LPS induces different forms of asthma that are type 1 and type 2 asthma phenotypes by high and low LPS levels, respectively. 相似文献
10.
Choi DS Lee JM Park GW Lim HW Bang JY Kim YK Kwon KH Kwon HJ Kim KP Gho YS 《Journal of proteome research》2007,6(12):4646-4655
Microvesicles (MV) are membrane vesicles secreted from the plasma and endosomal membrane compartment by various cell types such as hematopoietic, epithelial, and tumor cells. Actively growing tumor cells shed MV, and the rate of shedding increases in malignant tumors. Although recent progress in this area has revealed that tumor-derived MV play multiple roles in tumor growth and metastasis via immune escape, tumor invasion, and angiogenesis, the mechanism of vesicle formation and the biological roles of tumor-derived MV are not understood. Here, we report the first global proteomic analysis of highly purified MV from human colorectal cancer cells. Using 1D SDS gel electrophoresis and nano-LC-MS/MS analyses, we identified a total of 547 microvesicular proteins from three independent experiments with high confidence; 416 proteins were identified at least in two trials, including 181 as yet unreported proteins. We identified 49 proteins involved in the biogenesis of MV, including annexins, ADP-ribosylation factors, and Rab proteins. We also identified 28 proteins that may function in tumorigenesis via promotion of migration, invasion, and growth of tumor cells, immune modulation, metastasis, and angiogenesis. Taken together with previously reported results, our observations suggest that tumor-derived MV may act as communicasomes, that is, extracellular organelles that play diverse roles in intercellular communication. This information will help elucidate the biogenesis and functions of tumor-derived MV, and aid in the development of effective vaccines for various cancers, including colorectal cancer. 相似文献