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Toll-like receptor signaling in hematopoietic homeostasis and the pathogenesis of hematologic diseases

Frontiers of medicine 2015年第3期9卷 288-303页

作者： Joseph Cannova Biochemistry and Molecular Biology Program Loyola University Chicago Maywood IL 60153 USA stritch school of medicine Loyo& University Chicago Maywood IL 60153 USA Oncology Institute Loyola University Chicago Maywood IL 60153 USA Department of Pathology Loyola University Chicago Maywood IL 60153 USA Department of Biology Loyola University Chicago Chicago IL 60660 USA Department of Molecular and Cellular Physiology Loyola University Chicago Maywood IL 60153 USA

Toll-like receptors （TLRs）, which are found in innate immune cells, are essential mediators of rapid inflammatory responses and appropriate T-cell activation in response to infection and tissue damage. Accumulating evidence suggests that TLR signaling is involved in normal hematopoiesis and specific hematologic pathologies. Particular TLRs and their downstream signaling mediators are expressed not only in terminally differentiated innate immune cells but also in early hematopoietic progenitors. Sterile activation of TLR signaling is required to generate early embryonic hematopoietic progenitor cells. In adult animals, TLR signaling directly or indirectly promotes differentiation of myeloid cells at the expense of that of lymphoid cells and the self renewal of hematopoietic stem cells during infection and tissue damage. Activating mutations of the MyD88 gene, which codes for a key adaptor involved in TLR signaling, are commonly detected in B-cell lymphomas and other B-cell hematopathologies. Dysregulated TLR signaling contributes to the pathogenesis of many hematopoietic disorders, including bone marrow failure, myelodysplastic syndrome, and acute myeloid leukemia. Complete elucidation of the molecular mechanisms by which TLR signaling mediates the regulation of both normal and pathogenic hematopoiesis will prove valuable to the development of targeted therapies and strategies for improved treatment of hematopoietic disorders.

关键词： TLR MyD88 hematopoiesis bone marrow failure leukemia myelodysplastic syndrome

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Novel oncogenes and tumor suppressor genes in hepatocellular carcinoma

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Liver Research 2021年第4期5卷 195-203页

作者： Fang Wang Peter Breslin S J Wei Qiu Department of Surgery and Cancer Biology Loyola University Chicago Stritch School of MedicineMaywoodILUSA Department of Molecular/Cellular Physiology Cancer BiologyCardinal Bernardin Cancer CenterLoyola University Medical Centerand BiologyLoyola University ChicagoChicagoILUSA

Hepatocellular carcinoma(HCC)is a very deadly *** initiation and progression involve multiple genetic events,including the activation of proto-oncogenes and disruption of the function of specific tumor suppressor *** of oncogenes stimulates cell growth and survival,while loss-of-function mutations of tumor suppressor genes result in unrestrained cell *** this review,we summarize the new findings that identified novel proto-oncogenes and tumor suppressors in HCC over the past five *** findings may inspire the development of novel therapeutic strategies to improve the outcome of HCC patients.

关键词： Hepatocellular carcinoma(HCC) Oncogene Tumor suppressor Activation Loss-of-function

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The size of Metastasis in the Sentinel Node Is a Predictor of Additional Non-Sentinel Node Positivity

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Journal of Cancer Therapy 2012年第5期3卷 712-717页

作者： Todd A. Baker Nitin Wadhwani Prabha Rajan Sharfi Sarker Gerard Aranha Margo Shoup Holly Mattix-Kramer Constantine Godellas Department of Pathology loyola university chicago Stritch School of Medicine Maywood USA Department of Preventative medicine and Epidemiology Loyola University Chicago Stritch School of Medicine Maywood USA Department of Surgery Loyola University Chicago Stritch School of Medicine Maywood USA

Background: The need for axillary lymph node dissection (ALND) when sentinel lymph nodes (SLN) contain micrometastasis is controversial. The purpose of this study was to determine if the size of tumor in the SLN corresponds with additional positive non-sentinel lymph nodes (non-SLN) in pT1 breast cancer. Methods: This retrospective review of 483 patients with pT1 breast cancer identified 96 patients with tumor positive SLN biopsies between June 1999 and February 2010. The size of SLN metastasis and the number of tumor positive non-SLN were recorded using AJCC criteria. Receiver operating characteristic analysis was used to discriminate the SLN size with the optimal sensitivity, specificity and likelihood ratios (LR) for additional positive non-SLN. Results: Among 96 patients with a tumor positive SLN, 41% (n = 39) had micrometastasis, and 59% (n = 57) had macrometastasis. A positive non-SLN was identified after ALND among 18% (n = 7 of 39) with micrometastasis compared with 39% (n = 22 of 57) with macrometastasis (p = 0.04). The size of the SLN metastasis and presence of additional tumor positive non-SLNs corresponds to a positive likelihood ratio of 1.1 for micrometastasis and 1.6 for macrometastasis (95%CI: 0.56 - 0.74). Conclusions: Increased size of tumor in SLN is associated with greater likelihood of non-SLN positivity and should be considered for more aggressive follow-up and therapy.

关键词： Sentinel Node Axillary Lymph Node Dissection (ALND)

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SH-2-containing protein tyro-sine phosphatase 1 is required for IL-4-induced IL-4R expression in spleen cells

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Chinese Science Bulletin 2005年第14期50卷 1456-1461页

作者： CAO Xin HUANG Zan FAN Jingyi Department of Cell Biology and Medical Genetics Nanjing Medical University Nanjing 210029 China Molecular Biology Program Stritch School of Medicine Loyola University at Chicago Maywood IL 60153 USA Department of Organismal Biology and Anatomy University of Chicago Chicago IL 60637 USA

To investigate the role of SH-2-containing pro- tein tyrosine phosphatase 1, SHP-1, in IL-4-induced IL-4 receptor (IL-4R) expression, we examined IL-4 receptor α-chain (IL-4Rα) mRNA expression in Na3VO4-treated wild type (WT) spleen cells and measured IL-4R mRNA in IL-4-stimulated spleen cells of viable motheaten mice (mev/mev). It is found that IL-4-induced IL-4R mRNA ex- pression was impaired in Na3VO4-treated WT spleen cells and IL-4-stimulated mev/mev spleen cells. Here we show that the impaired IL-4-induced IL-4Rα mRNA expression was due to reduced expression of IL-4R that led to impaired STAT6 signaling. We further demonstrate that reduction of IL-4Rα protein expression in mev/mev spleen cells was due to alteration in cell compositions. In mev/mev spleen, the per- centages of CD4+, CD8+, and CD19+ cells expressing rela- tively high levels of IL-4R were reduced dramatically while the percentages of Mac-1+ and Gr-1+ cells with relative low levels of IL-4R increased greatly. Despite the profound effect of reduced expression of IL-4R protein, the IL-4Rα mRNA expression was comparable in spleen cells of littermate con- trol mice (+/?) and mev/mev mice and no differences were found in B cells, T cells, and macrophages, suggesting cell type-specific downregulation of IL-4R expression in macro- phages through a posttranscriptional mechanism. Our study suggests that SHP-1 is required for IL-4-meidated function and indirectly regulates IL-4-meidated function in spleen cells by affecting hematopoiesis.

关键词：蛋白质酪氨酸磷酸酶脾细胞

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Primary Intimal Sarcoma of the Pulmonary Vein with Extension into the Left Atrium: A Case Report

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Open Journal of Thoracic Surgery 2012年第2期2卷 25-28页

作者： Constantine D. Mavroudis Alfred Casillan Mark Rabbat Aileen Go Edward Melian Mamdouh Bakhos Christopher H. Wigfield Department of Cardiology Stritch School of Medicine Loyola University Chicago Maywood USA Department of Oncology Stritch School of Medicine Loyola University Chicago Maywood USA Department of Radiation Oncology Stritch School of Medicine Loyola University Chicago Maywood USA Department of Thoracic and Cardiovascular Surgery Stritch School of Medicine Loyola University Chicago Maywood USA

Sarcoma originating from the pulmonary veins represents one of the rarest subtypes of sarcoma. We report the case of a 52-year-old woman presenting with cough and scant hemoptysis and ultimately diagnosed with a primary intimal sarcoma of the left inferior pulmonary vein extending into the left lower lobe of the lung. To our knowledge, this is the first reported case of such pathology in the literature. We present the case and critically appraise the literature for sarcomas of the great vessels.

关键词： Sarcoma Pulmonary Vein

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STAT1 signaling is required for optimal Th1 cell differentiation in mice

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Chinese Science Bulletin 2010年第11期55卷 1032-1040页

作者： MA Da HUANG Hua HUANG Zan The Key Laboratory of Developmental Genes and Human Disease of Education Ministry School of Basic Medical Science Southeast University Nanjing 210009 China Department of Cell Biology Neurology and Anatomy Stritch School of Medicine Loyola University Chicago Maywood IL 60153 USA

Although IFN-γ alone does not prime type I T helper cell (Th1) differentiation, the loss of IFN-γ signaling leads to impaired Th1 phenotype: IFN-γ receptor-deficient (Ifngr-/-) Th1 cells fail to permanently repress IL-4 expression. They can differentiate into IL-4-producing cells under Th2-inducing conditions. These observations suggest that IFN-γ signaling plays a critical role in si- lencing Il4 gene in Th1 cells and stabilizing Th1 phenotype. IFN-γ signaling has been further shown to inhibit IL-4 expression by inhibiting STAT6 phosphorylation. This work aims to study the mechanism by which STAT1, the downstream molecule that transduces IFN-γ signaling, may mediate suppression of IL-4 expression in Th1 cells. The results show that STAT1-deficient naive CD4+ T cells express a reduced level of IFN-γ as well as an elevated level of IL-4. These cells exhibit bias to differentiate into Th2 cells under unpolarized conditions. Under Th1-inducing conditions, STAT1-deficient naive CD4+ T cells show impaired Th1 differentiation: Stat1-/- Th1 cells express reduced levels of IFN-γ and T-bet. These cells also fail to repress the expression of IL-4 and GATA-3 and retain STAT6 signaling. More importantly, Stat1-/- Th1 cells can be effectively induced to differentiate into IL-4-producing cells under Th2-inducing conditions. Ectopic expression of T-bet in Stat1-/- Th1 cells dramatically represses their ability to do so and drastically restores IFN-γ expression, suggesting that STAT1 may inhibit IL-4 expression through T-bet. Finally, histone H3 acetylation (H3AC) and histone H3 K4 dimethylation (H3K4dim) were observed in two enhancer regions of Il4 gene locus in Stat1-/- Th1 cells, suggesting a permissive status of Il4 gene locus in these cells. Thus, this study reveals new mechanisms by which STAT1 signaling may mediate repression of Il4 gene in Th1 cells: upregulating T-bet that subsequently represses GATA3 and IL-4 expression, antagonizing STAT6 signaling, and inhibiting epigen

关键词： STAT1 Th1/Th2 房间 T 赌注 STAT6 信号 transduction

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Baroreflex Control of Heart Rate in Mice Overexpressing Human SOD1: Functional Changes in Central and Vagal Efferent Components

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Neuroscience Bulletin 2019年第1期35卷 91-97页

作者： Jin Chen He Gu Robert D.Wurster Zixi Cheng Division of Neuroscience and Division of Metabolic and Cardiovascular Sciences Burnett School of Biomedical SciencesCollege of MedicineUniversity of Central FloridaOrlandoFL 32816USA Department of Cellular and Molecular Physiology Stritch School of MedicineLoyola UniversityMaywoodIL 60153USA

Excessive reactive oxygen species(ROS)(such as the superoxide radical) are commonly associated with cardiac autonomic dysfunctions. Though superoxide dismutase 1(SOD1) overexpression may protect against ROS damage to the autonomic nervous system, superoxide radical reduction may change normal physiological functions. Previously, we demonstrated that human SOD1(hSOD1) overexpression does not change baroreflex bradycardia and tachycardia but rather increases aortic depressor nerve activity in response to arterial pressure changes in C57 B6 SJL-Tg(SOD1)2 Gur/J mice. Since the baroreflex arc includes afferent, central, and efferent components, the objective of this study was to determine whether hSOD1 overexpression alters the central and vagal efferent mediation of heart rate(HR) responses. Our data indicate that SOD1 overexpression decreased the HR responses to vagal efferent nerve stimulation but did not change the HR responses to aortic depressor nerve(ADN)stimulation. Along with the previous study, we suggest that SOD1 overexpression preserves normal baroreflex function but may differentially alter the functions of the ADN, vagal efferents, and central components. While SOD1 overexpression likely enhanced ADN function and the central mediation of bradycardia, it decreased vagal efferent control of HR.

关键词： SOD1 Parasympathetic Baroreflex

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The role of ginseng as an anti-asthmatic agent

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Acupuncture and Herbal medicine 2024年第3期4卷 358-366页

作者： Kailynn J.Yang Liana Y.A.Bautista Danielle G.Iben Dana H.Tran loyola university of chicago stritch school of medicine MaywoodILUSA

Introduction Asthma is an inflammatory obstructive respiratory lung disease characterized by limited *** is estimated that more than 300 million people worldwide are affected by asthma,and this number is expected to increase over the next few years[1].Uncontrolled asthma is associated with a severely impaired quality of life and increased mortality rates[2].Other adverse effects of poorly controlled asthma include obesity,pneumonia.

关键词： asthma impaired mortality

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Alcohol-induced Wnt signaling inhibition during bone fracture healing is normalized by intermittent parathyroid hormone treatment

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Animal Models and Experimental medicine 2020年第2期3卷 200-207页

作者： Esha M.Kapania Taylor JReif Aaron Tsumura Jonathan M。Eby John J.Callaci Internal medicine-Pediatric Resident Rush University Medical CenterChicagoILUSA Limb Lengthening and Complex Reconstruction Fellowship Hospital for Special SurgeryNew YorkNYUSA Department of Orthopaedic Surgery and Rehabilitation Loyola University Medical CenterMaywoodILUSA Alcohol Research Program(ARP) Loyola University Chicago Stritch School of MedicineMaywoodILUSA

Nearly half of orthopaedic trauma patients are intoxicated at the time of injury, and excess alcohol consumption increases the risk for fracture nonunion. Previous studies show alcohol disrupts fracture associated Wnt signaling required for normal bone fracture repair. Intermittent parathyroid hormone(PTH) promotes bone growth through canonical Wnt signaling, however, no studies have investigated the effect of PTH on alcohol-inhibited bone fracture repair. Male C57 BL/6 mice received two-3 day alcohol binges separated by 4 days before receiving a mid-shaft tibia fracture. Postoperatively, mice received PTH daily until euthanasia. Wnt/β-catenin signaling was analyzed at 9 days post-fracture. As previously observed, acute alcohol exposure resulted in a >2-fold decrease in total and the active form of β-catenin and a 2-fold increase in inactive β-catenin within the fracture callus. Intermittent PTH abrogated the effect of alcohol on β-catenin within the fracture callus. Upstream of β-catenin, alcohol-treated animals had a 2-fold decrease in total LRP6, the Wnt co-receptor, which was restored with PTH treatment. Alcohol nor PTH had any significant effect on GSK-3β. These data show that intermittent PTH following a tibia fracture restores normal expression of Wnt signaling proteins within the fracture callus of alcohol-treated mice.

关键词： ethanol fracture callus parathyroid hormone Wnt signaling pathway

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Adjuvant radiotherapy for pathologically advanced prostate cancer improves biochemical recurrence free survival compared to salvage radiotherapy

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World Journal of Clinical Urology 2016年第1期5卷 45-52页

作者： Robert H Blackwell William Gange Alexander M Kandabarow Matthew M Harkenrider Gopal N Gupta Marcus L Quek Robert C Flanigan Department of Urology Loyola University Medical Center stritch school of medicine Loyola University Chicago Department of Radiation Oncology Loyola University Medical Center

AIM: To evaluate the long-term outcomes of patients receiving adjuvant and salvage radiotherapy following prostatectomy with adverse pathologic features and an undetectable prostate specific antigen(PSA).METHODS: A retrospective review was performed of patients who received post-prostatectomy radiation at loyola university Medical Center between 1992 and 2013. Adverse pathologic features(Gleason score ≥ 8, seminal vesicle invasion, extracapsular extension, pathologic T4 disease, and/or positive surgical margins) and an undetectable PSA following prostatectomy were required for inclusion. Adjuvant patients received therapy with an undetectable PSA, salvage patients following biochemical recurrence(BCR). Post-radiation BCR, overall survival, bone metastases, and initiation of hormonal therapy were assessed. Kaplan-Meier time-to-event analyses and stepwise Cox proportional hazards regression(HR) were performed. RESULTS: Post-prostatectomy patients(n = 134) received either adjuvant(n = 47) or salvage(n = 87) radiation. Median age at radiotherapy(RT) was 63 years, and median follow-up was 53 mo. Five-year post-radiation BCR-free survival was 78% for adjuvant vs 50% salvage radiotherapy(SRT)(Logrank P = 0.001). Patients with radiation administered following a detectable PSA had an increased risk of BCR compared to undetectable: PSA > 0.0-0.2: HR = 4.1(95%CI: 1.5-11.2; P = 0.005); PSA > 0.2-1.0: HR = 4.4(95%CI: 1.6-11.9; P = 0.003); and PSA > 1.0: HR = 52(95%CI: 12.9-210; P < 0.001). There was no demonstrable difference in rates of overall survival, bone metastases or utilization of hormonal therapy between adjuvant and SRT patients. CONCLUSION: Adjuvant RT improves BCR-free survival compared to SRT in patients with adverse pathologic features and an undetectable post-prostatectomy PSA.

关键词： Radiotherapy Adjuvant Radiotherapy Salvage therapy Recurrence Prostatic neoplasms

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