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  • 1
    Online Resource
    Online Resource
    Adipocyte, Immune Cells, and miRNA Crosstalk: A Novel Regulator of Metabolic Dysfunction and Obesity
    MDPI AG ; 2021
    In:  Cells Vol. 10, No. 5 ( 2021-04-24), p. 1004-
    Details
    In: Cells, MDPI AG, Vol. 10, No. 5 ( 2021-04-24), p. 1004-
    Abstract: Obesity is characterized as a complex and multifactorial excess accretion of adipose tissue (AT) accompanied with alterations in the immune response that affects virtually all age and socioeconomic groups around the globe. The abnormal accumulation of AT leads to several metabolic diseases, including nonalcoholic fatty liver disorder (NAFLD), low-grade inflammation, type 2 diabetes mellitus (T2DM), cardiovascular disorders (CVDs), and cancer. AT is an endocrine organ composed of adipocytes and immune cells, including B-Cells, T-cells and macrophages. These immune cells secrete various cytokines and chemokines and crosstalk with adipokines to maintain metabolic homeostasis and low-grade chronic inflammation. A novel form of adipokines, microRNA (miRs), is expressed in many developing peripheral tissues, including ATs, T-cells, and macrophages, and modulates the immune response. miRs are essential for insulin resistance, maintaining the tumor microenvironment, and obesity-associated inflammation (OAI). The abnormal regulation of AT, T-cells, and macrophage miRs may change the function of different organs including the pancreas, heart, liver, and skeletal muscle. Since obesity and inflammation are closely associated, the dysregulated expression of miRs in inflammatory adipocytes, T-cells, and macrophages suggest the importance of miRs in OAI. Therefore, in this review article, we have elaborated the role of miRs as epigenetic regulators affecting adipocyte differentiation, immune response, AT browning, adipogenesis, lipid metabolism, insulin resistance (IR), glucose homeostasis, obesity, and metabolic disorders. Further, we will discuss a set of altered miRs as novel biomarkers for metabolic disease progression and therapeutic targets for obesity.
    Type of Medium: Online Resource
    ISSN: 2073-4409
    URL: Article
    DOI: 10.3390/cells10051004
    Language: English
    Publisher: MDPI AG
    Publication Date: 2021
    detail.hit.zdb_id: 2661518-6
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  • 2
    Online Resource
    Online Resource
    Reactive Oxygen Species in Regulating Lymphangiogenesis and Lymphatic Function
    MDPI AG ; 2022
    In:  Cells Vol. 11, No. 11 ( 2022-05-26), p. 1750-
    Details
    In: Cells, MDPI AG, Vol. 11, No. 11 ( 2022-05-26), p. 1750-
    Abstract: The lymphatic system is pivotal for immunosurveillance and the maintenance of tissue homeostasis. Lymphangiogenesis, the formation of new lymphatic vessels from pre-existing vessels, has both physiological and pathological roles. Recent advances in the molecular mechanisms regulating lymphangiogenesis have opened a new area of research on reparative lymphangiogenesis for the treatment of various pathological disorders comprising neurological disorders, cardiac repair, autoimmune disease, obesity, atherosclerosis, etc. Reactive oxygen species (ROS) produced by the various cell types serve as signaling molecules in several cellular mechanisms and regulate various aspects of growth-factor-mediated responses, including lymphangiogenesis. The ROS, including superoxide anion, hydrogen peroxide, and nitric oxide, play both beneficial and detrimental roles depending upon their levels and cellular microenvironment. Low ROS levels are essential for lymphangiogenesis. On the contrary, oxidative stress due to enhanced ROS generation and/or reduced levels of antioxidants suppresses lymphangiogenesis via promoting lymphatic endothelial cell apoptosis and death. In this review article, we provide an overview of types and sources of ROS, discuss the role of ROS in governing lymphangiogenesis and lymphatic function, and summarize the role of lymphatics in various diseases.
    Type of Medium: Online Resource
    ISSN: 2073-4409
    URL: Article
    DOI: 10.3390/cells11111750
    Language: English
    Publisher: MDPI AG
    Publication Date: 2022
    detail.hit.zdb_id: 2661518-6
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  • 3
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    Cannabinoid Receptor 2 (CB2) Inverse Agonist SMM-189 Induces Expression of Endogenous CB2 and Protein Kinase A That Differentially Modulates the Immune Response and Suppresses Experimental Colitis
    MDPI AG ; 2022
    In:  Pharmaceutics Vol. 14, No. 5 ( 2022-04-26), p. 936-
    Details
    In: Pharmaceutics, MDPI AG, Vol. 14, No. 5 ( 2022-04-26), p. 936-
    Abstract: The causes of Crohn’s disease (CD) and ulcerative colitis (UC), the two most common forms of inflammatory bowel disease (IBD), are multi-factorial and include dysregulation of immune cells in the intestine. Cannabinoids mediate protection against intestinal inflammation by binding to the G-protein coupled cannabinoid receptors 1 and 2 (CB1 and CB2). Here, we investigate the effects of the CB2 inverse agonist SMM-189 on dextran sodium sulfate (DSS)-induced experimental colitis. We observed that SMM-189 effectively attenuated the overall clinical score, reversed colitis-associated pathogenesis, and increased both body weight and colon length. Treatment with SMM-189 also increased the expression of CB2 and protein kinase A (PKA) in colon lamina propria lymphocytes (LPLs). We noticed alterations in the percentage of Th17, neutrophils, and natural killer T (NKT) cells in the spleen, mesenteric lymph nodes (MLNs), and LPLs of mice with DSS-induced colitis after treatment with SMM-189 relative to DSS alone. Further, myeloid-derived suppressor cells (MDSCs) during colitis progression increased with SMM-189 treatment as compared to DSS alone or with control cohorts. These findings suggest that SMM-189 may ameliorate experimental colitis by inducing the expression of endogenous CB2 and PKA in LPLs, increasing numbers of MDSCs in the spleen, and reducing numbers of Th17 cells and neutrophils in the spleen, MLNs, and LPLs. Taken together, these data support the idea that SMM-189 may be developed as a safe novel therapeutic target for IBD.
    Type of Medium: Online Resource
    ISSN: 1999-4923
    URL: Article
    DOI: 10.3390/pharmaceutics14050936
    Language: English
    Publisher: MDPI AG
    Publication Date: 2022
    detail.hit.zdb_id: 2527217-2
    SSG: 15,3
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  • 4
    Online Resource
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    Piceatannol induces regulatory T cells and modulates the inflammatory response and adipogenesis
    Elsevier BV ; 2023
    In:  Biomedicine & Pharmacotherapy Vol. 161 ( 2023-05), p. 114514-
    Details
    In: Biomedicine & Pharmacotherapy, Elsevier BV, Vol. 161 ( 2023-05), p. 114514-
    Type of Medium: Online Resource
    ISSN: 0753-3322
    URL: Article
    DOI: 10.1016/j.biopha.2023.114514
    RVK:
    XA 10000
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2023
    detail.hit.zdb_id: 1501510-5
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  • 5
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    High-fat diet-induced immune dysregulation in Th17/regulatory T cells promotes inflammation through protein kinase A (PKA) and PPAR-γ pathways
    The American Association of Immunologists ; 2022
    In:  The Journal of Immunology Vol. 208, No. 1_Supplement ( 2022-05-01), p. 105.03-105.03
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 208, No. 1_Supplement ( 2022-05-01), p. 105.03-105.03
    Abstract: Obesity is a hallmark around the globe, which is defined as a complex situation associated with various metabolic abnormalities and cardiovascular diseases. The increasing evidence suggests that type 1 inflammation-associated immune cells are dominant in adipose tissue and exert metabolically deleterious impacts. The precise mechanism of alteration of adipose tissue immune system and its effect on metabolic homeostasis is far from clear. We investigated how a high-fat diet (HFD) alters adipose tissue (AT) immune system and influences the inflammation. HFD consumption amends the metabolic parameters including body weight, glucose, and insulin levels. We noticed that there is increased infiltration of Th17 cells, dendritic cells, and macrophages in AT of mice fed HFD as compared to a normal diet (ND). In mice consuming HFD, we also find a reduction in regulatory T cells as compared to ND. We noticed a higher level of proinflammatory cytokines and chemokines in the HFD group as compared to ND. We also noticed an increase in IL-6 and KLF4 expression in the AT of HFD as compared to ND. Further, an increased level of AT protein kinase A in HFD fed and a decrease in PPAR-γ as compared to ND, suggesting acting as a negative regulator of Th17 cell differentiation. Taken together, these results suggest that HFD induces Th17, macrophage, dendritic cells, inflammatory cytokine and reduces Tregs and PPAR-γ to sustain AT inflammation. This study supports a key role of Th17/Tregs dysregulation and macrophages to induce AT inflammation through PKA and PPAR-γ pathways during obesity. (Supported by NIH grant R01 AI140405). Supported by NIH grant R01 AI140405.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.208.Supp.105.03
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2022
    detail.hit.zdb_id: 1475085-5
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  • 6
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    Inverse-agonist (SMM-189) suppresses colitis by inducing endogenous cannabinoids and attenuating Th17, neutrophils, natural killer cells
    The American Association of Immunologists ; 2022
    In:  The Journal of Immunology Vol. 208, No. 1_Supplement ( 2022-05-01), p. 113.01-113.01
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 208, No. 1_Supplement ( 2022-05-01), p. 113.01-113.01
    Abstract: The cause of inflammatory bowel disease (IBD), including Crohn’s disease (CD) and ulcerative colitis (UC), are multi-factorial and include activated immune cells, chronic inflammation, genetics, and environmental exposure. It is well known that endocannabinoids mediate protection against intestinal inflammation and other autoimmune diseases. However, the effect of cannabinoid receptors induction by inverse-agonist during experimental colitis has not been investigated. Here, we investigate the activation of the cannabinoid receptor-2 (CB2) by SMM-189, a potent CB2 inverse agonist, on the inhibition of dextran sodium sulfate (DSS) induced colitis. In the present study, we found that SMM-189 effectively attenuated the overall clinical score, reversed colitis-associated pathogenesis, increased body weight and colon length while increasing the expression of CB2 receptors and protein kinase A (PKA) in the colon lamina propria (LPs). We also measured a decrease in the percentage and number of Th17 cells in the spleen, mesenteric lymph nodes (MLNs), and LPs treated with SMM-189 compared to DSS controls. Similarly, the percentage and number of natural killer T (NKT) cells and neutrophils are decreased after SMM-189 treatment. SMM-189 also induces the myeloid-derived suppressor cells (MDSCs) during chronic colitis progression as compared to DSS alone. These findings suggest that SMM-189 ameliorates experimental colitis by inducing CB2 receptors and PKA in the LPs, MDSCs and reduces Th17, NKT cells, and neutrophils from the spleen and LPs. Taken together, these data support the idea that the CB2 inverse agonists, such as SMM-189, may be developed as a novel therapeutic target for IBD. Supported by NIH grant R01 AI140405
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.208.Supp.113.01
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2022
    detail.hit.zdb_id: 1475085-5
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  • 7
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    Differential Expression of microRNAs Correlates With the Severity of Experimental Autoimmune Cystitis
    Frontiers Media SA ; 2021
    In:  Frontiers in Immunology Vol. 12 ( 2021-7-14)
    Details
    In: Frontiers in Immunology, Frontiers Media SA, Vol. 12 ( 2021-7-14)
    Abstract: Interstitial cystitis (IC)/bladder pain syndrome (BPS) primarily affects women. It varies in its severity and currently has no effective treatment. The symptoms of IC include pelvic pain, urgency and frequency of urination, and discomfort or pain in the bladder and lower abdomen. The bladders of IC patients exhibit infiltration by immune cells, which lends credence to the hypothesis that immune mechanisms also play a role in the etiology and pathophysiology of IC. The Differentially expressed microRNAs (miRs) in immune cells may serve as crucial immunoregulators in the IC. Therefore, we sought to determine whether miRs might play a regulatory role in the progression and pathogenesis of IC, using experimental autoimmune cystitis (EAC) model. In the present study, we observed differential expression of a specific subset of miRs in iliac lymph nodes (ILNs) and urinary bladders (UB) of IC mice compared to that in control mice. Microarray analysis of 96 miRs from the bladder and 135 miRs from ILNs allowed us to identify 50 that exhibited at least a 1.5-fold greater difference in expression in EAC mice compared to control mice. Hierarchical cluster analysis of the microarray data was used to search available databases to predict molecular pathways with which the miRs might interact. Four miRs from each organ that exhibited altered expression in EAC mice and that were predicted to have roles in inflammation (miR-146a, -181, -1931, and -5112) were selected for further analysis by reverse transcription-polymerase chain reaction (RT-PCR). All were confirmed to be elevated in EAC mice. Histological inflammatory scores, systemic chemokines, and cytokines expressed by T helper type 1 (Th1) lymphocytes were also elevated in EAC mice as compared to control animals. We hypothesize that the mechanism of EAC induction might involve the modulation of specific miRs that increase local and systemic levels of chemokines and cytokines. The present study identifies novel miRs expressed in UB and ILNs that will allow us to highlight mechanisms of EAC pathogenesis and may provide potential biomarkers and/or serve as the basis of new therapies for the treatment of IC.
    Type of Medium: Online Resource
    ISSN: 1664-3224
    URL: Article
    DOI: 10.3389/fimmu.2021.716564
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2021
    detail.hit.zdb_id: 2606827-8
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  • 8
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    High Fat Diet-Induced CD8+ T Cells in Adipose Tissue Mediate Macrophages to Sustain Low-Grade Chronic Inflammation
    Frontiers Media SA ; 2021
    In:  Frontiers in Immunology Vol. 12 ( 2021-6-23)
    Details
    In: Frontiers in Immunology, Frontiers Media SA, Vol. 12 ( 2021-6-23)
    Abstract: Obesity in the United States and worldwide reached epidemic proportions within the last 20 years. Obesity is a very powerful health determinant or indicator that facilitates the development and progression of several metabolic diseases, insulin resistance, and low-grade chronic inflammation. Low-grade chronic inflammation in adipose tissue (AT) is marked by the accumulation of T cells, macrophages, and other immune cells and increased production of proinflammatory cytokines. During the onset of obesity but before the influx of macrophages, the AT is infiltrated by T cells that are strongly implicated in the initiation of obesity-associated inflammation. In comparing mice fed a high-fat diet (HFD) with those fed a normal diet (ND), we observed in HFD epididymal AT induction and infiltration of activated T cells, an accumulation and polarization of macrophages, and an increase in populations of activated CD4 + T cells and CD8 + T cells that express CXCR3 or killer cell lectin-like receptor subfamily G member 1 (KLRG1). Levels of inflammatory cytokines and leptin and the results of in vitro co-culture experiments revealed interactions among HFD- and ND-induced CD8 + T cells, macrophages, and adipocytes. Our findings suggest that obese tissues activate and induce both CD4 + and CD8 + CD69 + T cells and augment the expression of CXCR3 receptors, which promotes the recruitment and numbers of pro-inflammatory M1 macrophages to maintain low-grade chronic inflammation. The results support the hypothesis that CXCR3-expressing CD8 + T cells play an essential role in the initiation and maintenance of adipose tissue inflammation.
    Type of Medium: Online Resource
    ISSN: 1664-3224
    URL: Article
    DOI: 10.3389/fimmu.2021.680944
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2021
    detail.hit.zdb_id: 2606827-8
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  • 9
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    Ablation of Siglec-E enhances adipose tissue inflammation through CXCR3 activation and induces monocytic myeloid-derived suppressor cells
    The American Association of Immunologists ; 2023
    In:  The Journal of Immunology Vol. 210, No. 1_Supplement ( 2023-05-01), p. 163.03-163.03
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 210, No. 1_Supplement ( 2023-05-01), p. 163.03-163.03
    Abstract: Obesity is a worldwide epidemic associated with dysregulated metabolism and chronic low-grade inflammation in adipose tissue (AT). AT infiltrates with several immune cells, which secrete proinflammatory cytokines that mediate the severity of AT inflammation during obesity. During our ongoing studies, we observed the downregulation of various genes, particularly sialic acid-binding Ig-like lectin E (Siglec-E) by RNA-seq analysis in AT immune cells isolated from high-fat diet (HFD) fed mice as compared to normal diet (ND) mice. Siglec-E is mainly expressed in the cells of myeloid lineages, including macrophages, dendritic cells (DCs), and neutrophils. We confirmed the RNA-seq data of downregulation of Siglec-E in AT derived from HFD-fed mice by RT-PCR analysis. To determine the role of Siglec-E in mediating AT inflammation, we fed ND and HFD to wild-type (WT) and Siglec-E knockout mice (Siglec-E −/−), respectively. HFD consumption increased the body weight and blood glucose levels in Siglec-E −/−mice as compared to WT mice. Further, we observed increased infiltration of macrophages and decreased frequency of DCs in HFD-fed Siglec-E −/−mice AT compared to WT HFD-fed mice. We also noticed an increase in the frequency of CD8 +CXCR3 +cells and monocytic myeloid-derived suppressor cells (M-MDSCs) in AT of HFD-fed Siglec-E −/−mice as compared to WT HFD-fed mice. We also noticed the increased expression of AKT, and TNF receptor-associated factor 3 (TRAF3) in HFD-fed Siglec-E −/−mice. These results suggest that Siglec-E deletion plays a role in AT inflammation and obesity through the activation of CXCR3 and M-MDSCs. This study supports the notion that modulating Siglec-E pathways protect from AT inflammation and metabolic disorders. This research is supported by NIH grant R01 AI140405
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.210.Supp.163.03
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2023
    detail.hit.zdb_id: 1475085-5
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  • 10
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    Inhibition of microRNA-34c reduces detrusor ROCK2 expression and urinary bladder inflammation in experimental cystitis
    Elsevier BV ; 2024
    In:  Life Sciences Vol. 336 ( 2024-01), p. 122317-
    Details
    In: Life Sciences, Elsevier BV, Vol. 336 ( 2024-01), p. 122317-
    Type of Medium: Online Resource
    ISSN: 0024-3205
    URL: Article
    DOI: 10.1016/j.lfs.2023.122317
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2024
    detail.hit.zdb_id: 2013911-1
    SSG: 12
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