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  • 1
    Online Resource
    Online Resource
    Thromboxane Governs the Differentiation of Adipose-Derived Stromal Cells Toward Endothelial Cells In Vitro and In Vivo
    Ovid Technologies (Wolters Kluwer Health) ; 2016
    In:  Circulation Research Vol. 118, No. 8 ( 2016-04-15), p. 1194-1207
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 118, No. 8 ( 2016-04-15), p. 1194-1207
    Abstract: Autologous adipose-derived stromal cells (ASCs) offer great promise as angiogenic cell therapy for ischemic diseases. Because of their limited self-renewal capacity and pluripotentiality, the therapeutic efficacy of ASCs is still relatively low. Thromboxane has been shown to play an important role in the maintenance of vascular homeostasis. However, little is known about the effects of thromboxane on ASC-mediated angiogenesis. Objective: To explore the role of the thromboxane-prostanoid receptor (TP) in mediating the angiogenic capacity of ASCs in vivo. Methods and Results: ASCs were prepared from mouse epididymal fat pads and induced to differentiate into endothelial cells (ECs) by vascular endothelial growth factor. Cyclooxygenase-2 expression, thromboxane production, and TP expression were upregulated in ASCs on vascular endothelial growth factor treatment. Genetic deletion or pharmacological inhibition of TP in mouse or human ASCs accelerated EC differentiation and increased tube formation in vitro, enhanced angiogenesis in in vivo Matrigel plugs and ischemic mouse hindlimbs. TP deficiency resulted in a significant cellular accumulation of β-catenin by suppression of calpain-mediated degradation in ASCs. Knockdown of β-catenin completely abrogated the enhanced EC differentiation of TP-deficient ASCs, whereas inhibition of calpain reversed the suppressed angiogenic capacity of TP re-expressed ASCs. Moreover, TP was coupled with Gαq to induce calpain-mediated suppression of β-catenin signaling through calcium influx in ASCs. Conclusion: Thromboxane restrained EC differentiation of ASCs through TP-mediated repression of the calpain-dependent β-catenin signaling pathway. These results indicate that TP inhibition could be a promising strategy for therapy utilizing ASCs in the treatment of ischemic diseases.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/CIRCRESAHA.115.307853
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2016
    detail.hit.zdb_id: 1467838-X
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  • 2
    Online Resource
    Online Resource
    EP3 enhances adhesion and cytotoxicity of NK cells toward hepatic stellate cells in a murine liver fibrosis model
    Rockefeller University Press ; 2022
    In:  Journal of Experimental Medicine Vol. 219, No. 5 ( 2022-05-02)
    Details
    In: Journal of Experimental Medicine, Rockefeller University Press, Vol. 219, No. 5 ( 2022-05-02)
    Abstract: Natural killer (NK) cells exhibit antifibrotic properties in liver fibrosis (LF) by suppressing activated hepatic stellate cell (HSC) populations. Prostaglandin E2 (PGE2) plays a dual role in innate and adaptive immunity. Here, we found that E-prostanoid 3 receptor (EP3) was markedly downregulated in NK cells from liver fibrosis mice and patients with liver cirrhosis. NK cell–specific deletion of EP3 aggravated hepatic fibrogenesis in mouse models of LF. Loss of EP3 selectively reduced the cytotoxicity of the CD27+CD11b+ double positive (DP) NK subset against activated HSCs. Mechanistically, deletion of EP3 impaired the adhesion and cytotoxicity of DP NK cells toward HSCs through modulation of Itga4-VCAM1 binding. EP3 upregulated Itga4 expression in NK cells through promoting Spic nuclear translocation via PKC-mediated phosphorylation of Spic at T191. Activation of EP3 by sulprostone alleviated CCL4-induced liver fibrosis in mice. Thus, EP3 is required for adhesion and cytotoxicity of NK cells toward HSCs and may serve as a therapeutic target for the management of LF.
    Type of Medium: Online Resource
    ISSN: 0022-1007 , 1540-9538
    URL: Article
    DOI: 10.1084/jem.20212414
    RVK:
    XA 10000
    Language: English
    Publisher: Rockefeller University Press
    Publication Date: 2022
    detail.hit.zdb_id: 1477240-1
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  • 3
    Online Resource
    Online Resource
    Mycoplasma hyopneumoniae Inhibits Porcine Beta-Defensin 2 Production by Blocking the Unfolded Protein Response To Facilitate Epithelial Adhesion and Infection
    American Society for Microbiology ; 2020
    In:  Infection and Immunity Vol. 88, No. 7 ( 2020-06-22)
    Details
    In: Infection and Immunity, American Society for Microbiology, Vol. 88, No. 7 ( 2020-06-22)
    Abstract: Mycoplasma hyopneumoniae causes the disease porcine enzootic pneumonia, a highly contagious and chronic disease affecting pigs. Understanding the molecular mechanisms of its pathogenicity is critical for developing effective interventions to control this swine respiratory disease. Here, we describe a novel virulence mechanism by which M. hyopneumoniae interferes with the host unfolded protein response (UPR) and eventually facilitates bacterial adhesion and infection. We observed that M. hyopneumoniae infection suppressed the UPR target molecules GRP78 and CHOP by reducing PKR-like endoplasmic reticulum kinase/eukaryotic initiation factor 2 alpha (PERK/eIF2α) phosphorylation, ATF6 cleavage, and X-box binding protein 1 (XBP1) splicing. Interestingly, further analyses revealed that host UPR inhibition subsequently suppressed the NF‐κB pathway, leading to the reduced production of porcine beta-defensin 2 (PBD-2), thus facilitating M. hyopneumoniae adherence and infection. This study provides new insights into the molecular pathogenesis of M. hyopneumoniae and sheds light upon its interactions with the host.
    Type of Medium: Online Resource
    ISSN: 0019-9567 , 1098-5522
    URL: Article
    DOI: 10.1128/IAI.00164-20
    RVK:
    XA 10000
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2020
    detail.hit.zdb_id: 1483247-1
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  • 4
    Online Resource
    Online Resource
    VisuMax Flap 2.0: a flap plus technique to reduce incidence of an opaque bubble layer in femtosecond laser–assisted LASIK
    Springer Science and Business Media LLC ; 2023
    In:  Graefe's Archive for Clinical and Experimental Ophthalmology Vol. 261, No. 4 ( 2023-04), p. 1187-1194
    Details
    In: Graefe's Archive for Clinical and Experimental Ophthalmology, Springer Science and Business Media LLC, Vol. 261, No. 4 ( 2023-04), p. 1187-1194
    Abstract: To evaluate the incidence of an opaque bubble layer (OBL) in femtosecond laser–assisted in situ keratomileusis (FS-LASIK) flaps created with VisuMax Flap 2.0 as a result of a modification in the parameters of the flap programming. Methods This retrospective study was comprised of 1400 eyes of 715 patients who received FS-LASIK surgery. OBLs were measured and reported as a percentage of the flap area to identify the incidence and extent. Flap creation, which is a modification technique, was performed with 8.1-mm flap diameters plus 0.3-mm enlarged interlamellar photodisruption (group Flap 2.0). The same flap diameters without extra photodisruption as the previous standard setting were also implemented (group Flap 1.0). The preoperative measurements, including sphere, cylinder, keratometry, and intraoperative characteristics such as flap size and thickness, were documented. Possible risk factors for the occurrence of OBLs were investigated in this study. Results The incidence of an OBL was reduced when using the Flap 2.0 program (31.4%) compared to the Flap 1.0 program (63.7%). The area of hard and soft OBLs created by the Flap 2.0 program is smaller than those created by the Flap 1.0 program ( P  = 0.007 and P   〈  0.001). Multivariate logistic regression indicated that a thinner flap ( P  = 0.038) and a higher sphere ( P  = 0.001) affected the chance of hard OBLs occurring. Conclusion The VisuMax Flap 2.0 program promotes gas venting by enlarging the interlamellar photodisruption size. The incidence and extent of OBLs appear to be reduced significantly when the Flap 2.0 program is applied.
    Type of Medium: Online Resource
    ISSN: 0721-832X , 1435-702X
    URL: Article
    DOI: 10.1007/s00417-022-05894-1
    RVK:
    XA 10000
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2023
    detail.hit.zdb_id: 1459159-5
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  • 5
    Online Resource
    Online Resource
    T-Cell Mineralocorticoid Receptor Controls Blood Pressure by Regulating Interferon-Gamma
    Ovid Technologies (Wolters Kluwer Health) ; 2017
    In:  Circulation Research Vol. 120, No. 10 ( 2017-05-12), p. 1584-1597
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 120, No. 10 ( 2017-05-12), p. 1584-1597
    Abstract: Hypertension remains to be a global public health burden and demands novel intervention strategies such as targeting T cells and T-cell–derived cytokines. Mineralocorticoid receptor (MR) antagonists have been clinically used to treat hypertension. However, the function of T-cell MR in blood pressure (BP) regulation has not been elucidated. Objective: We aim to determine the role of T-cell MR in BP regulation and to explore the mechanism. Methods and Results: Using T-cell MR knockout mouse in combination with angiotensin II–induced hypertensive mouse model, we demonstrated that MR deficiency in T cells strikingly decreased both systolic and diastolic BP and attenuated renal and vascular damage. Flow cytometric analysis showed that T-cell MR knockout mitigated angiotensin II–induced accumulation of interferon-gamma (IFN-γ)–producing T cells, particularly CD8 + population, in both kidneys and aortas. Similarly, eplerenone attenuated angiotensin II–induced elevation of BP and accumulation of IFN-γ–producing T cells in wild-type mice. In cultured CD8 + T cells, T-cell MR knockout suppressed IFN-γ expression whereas T-cell MR overexpression and aldosterone both enhanced IFN-γ expression. At the molecular level, MR interacted with NFAT1 (nuclear factor of activated T-cells 1) and activator protein-1 in T cells. Finally, T-cell MR overexpressing mice manifested more elevated BP compared with control mice after angiotensin II infusion and such difference was abolished by IFN-γ–neutralizing antibodies. Conclusions: MR may interact with NFAT1 and activator protein-1 to control IFN-γ in T cells and to regulate target organ damage and ultimately BP. Targeting MR in T cells specifically may be an effective novel approach for hypertension treatment.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/CIRCRESAHA.116.310480
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2017
    detail.hit.zdb_id: 1467838-X
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  • 6
    Online Resource
    Online Resource
    Effects of Metoprolol on Sympathetic Remodeling and Electrical Remodeling at Infarcted Border Zone after Myocardial Infarction in Rabbits
    S. Karger AG ; 2007
    In:  Cardiology Vol. 108, No. 3 ( 2007), p. 176-182
    Details
    In: Cardiology, S. Karger AG, Vol. 108, No. 3 ( 2007), p. 176-182
    Abstract: 〈 i 〉 Background: 〈 /i 〉 The findings of sympathetic remodeling and its electrophysiological implications force us to rerecognize the drugs presently used. The aim of this study was toinvestigate the effects of metoprolol on sympathetic remodeling and electrical remodeling at the infarcted border zone (IBZ) after myocardial infarction (MI). 〈 i 〉 Methods: 〈 /i 〉 Forty rabbits were randomly assigned into two groups: MI group (n = 20), ligation of the anterior descending coronary; Metoprolol group (n = 20), ligation of the anterior descending coronary and administration of oral metoprolol 5 mg/kg/day. Eight weeks after surgery, transmural dispersion of repolarization (TDR) at baseline, TDR and difference of TDR (ΔTDR) during sympathetic nerve stimulation were measured at the IBZ. The distribution and densities of growth associated protein 43 and tyrosine hydroxylase positive nerves at the IBZ were detected with immunohistochemical techniques. 〈 i 〉 Results: 〈 /i 〉 The study was completed in the 36 surviving animals (18 rabbits in each group). The densities of growth associated protein 43 and tyrosine hydroxylase positive nerves in the Metoprolol group (2,550 ± 554 and 1,779 ± 458 µm 〈 sup 〉 2 〈 /sup 〉 /mm 〈 sup 〉 2 〈 /sup 〉 , respectively) were lower than in the MI group (3,217 ± 589 and 2,616 ± 528 µm 〈 sup 〉 2 〈 /sup 〉 /mm 〈 sup 〉 2 〈 /sup 〉 , respectively; both p 〈 0.01). TDR at baseline, TDR and ΔTDR during sympathetic nerve stimulation were shorter in the Metoprolol group than in the MI group (p 〈 0.01 for all). 〈 i 〉 Conclusion: 〈 /i 〉 Metoprolol can inhibit sympathetic remodeling and electrical remodeling at the IBZ after MI. The association of metoprolol with improved electrical remodeling may be partly related to the inhibition of sympathetic remodeling.
    Type of Medium: Online Resource
    ISSN: 0008-6312 , 1421-9751
    URL: Article
    DOI: 10.1159/000096647
    RVK:
    XA 36200
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2007
    detail.hit.zdb_id: 1482041-9
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  • 7
    Online Resource
    Online Resource
    Inhibition of CRTH2-mediated Th2 activation attenuates pulmonary hypertension in mice
    Rockefeller University Press ; 2018
    In:  Journal of Experimental Medicine Vol. 215, No. 8 ( 2018-08-06), p. 2175-2195
    Details
    In: Journal of Experimental Medicine, Rockefeller University Press, Vol. 215, No. 8 ( 2018-08-06), p. 2175-2195
    Abstract: Pulmonary arterial hypertension (PAH) is a life-threatening disease characterized by progressive pulmonary artery (PA) remodeling. T helper 2 cell (Th2) immune response is involved in PA remodeling during PAH progression. Here, we found that CRTH2 (chemoattractant receptor homologous molecule expressed on Th2 cell) expression was up-regulated in circulating CD3+CD4+ T cells in patients with idiopathic PAH and in rodent PAH models. CRTH2 disruption dramatically ameliorated PA remodeling and pulmonary hypertension in different PAH mouse models. CRTH2 deficiency suppressed Th2 activation, including IL-4 and IL-13 secretion. Both CRTH2+/+ bone marrow reconstitution and CRTH2+/+ CD4+ T cell adoptive transfer deteriorated hypoxia + ovalbumin–induced PAH in CRTH2−/− mice, which was reversed by dual neutralization of IL-4 and IL-13. CRTH2 inhibition alleviated established PAH in mice by repressing Th2 activity. In culture, CRTH2 activation in Th2 cells promoted pulmonary arterial smooth muscle cell proliferation through activation of STAT6. These results demonstrate the critical role of CRTH2-mediated Th2 response in PAH pathogenesis and highlight the CRTH2 receptor as a potential therapeutic target for PAH.
    Type of Medium: Online Resource
    ISSN: 0022-1007 , 1540-9538
    URL: Article
    DOI: 10.1084/jem.20171767
    RVK:
    XA 10000
    Language: English
    Publisher: Rockefeller University Press
    Publication Date: 2018
    detail.hit.zdb_id: 1477240-1
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  • 8
    Online Resource
    Online Resource
    Evaluation of Tear Protein Markers in Dry Eye Disease with Different Lymphotoxin-Alpha Expression Levels
    Elsevier BV ; 2020
    In:  American Journal of Ophthalmology Vol. 217 ( 2020-09), p. 198-211
    Details
    In: American Journal of Ophthalmology, Elsevier BV, Vol. 217 ( 2020-09), p. 198-211
    Type of Medium: Online Resource
    ISSN: 0002-9394
    URL: Article
    DOI: 10.1016/j.ajo.2020.03.013
    RVK:
    XA 19500
    RVK:
    XA 10000
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2020
    detail.hit.zdb_id: 2019600-3
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  • 9
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    Online Resource
    PKA regulatory IIα subunit is essential for PGD2-mediated resolution of inflammation
    Rockefeller University Press ; 2016
    In:  Journal of Experimental Medicine Vol. 213, No. 10 ( 2016-09-19), p. 2209-2226
    Details
    In: Journal of Experimental Medicine, Rockefeller University Press, Vol. 213, No. 10 ( 2016-09-19), p. 2209-2226
    Abstract: The kinetic participation of macrophages is critical for inflammatory resolution and recovery from myocardial infarction (MI), particularly with respect to the transition from the M1 to the M2 phenotype; however, the underlying mechanisms are poorly understood. In this study, we found that the deletion of prostaglandin (PG) D2 receptor subtype 1 (DP1) in macrophages retarded M2 polarization, antiinflammatory cytokine production, and resolution in different inflammatory models, including the MI model. DP1 deletion up-regulated proinflammatory genes expression via JAK2/STAT1 signaling in macrophages, whereas its activation facilitated binding of the separated PKA regulatory IIα subunit (PRKAR2A) to the transmembrane domain of IFN-γ receptor, suppressed JAK2–STAT1 axis–mediated M1 polarization, and promoted resolution. PRKAR2A deficiency attenuated DP1 activation–mediated M2 polarization and resolution of inflammation. Collectively, PGD2–DP1 axis–induced M2 polarization facilitates resolution of inflammation through the PRKAR2A-mediated suppression of JAK2/STAT1 signaling. These observations indicate that macrophage DP1 activation represents a promising strategy in the management of inflammation-associated diseases, including post-MI healing.
    Type of Medium: Online Resource
    ISSN: 0022-1007 , 1540-9538
    URL: Article
    DOI: 10.1084/jem.20160459
    RVK:
    XA 10000
    Language: English
    Publisher: Rockefeller University Press
    Publication Date: 2016
    detail.hit.zdb_id: 1477240-1
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