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  1. Article ; Online: Cell-Specific Actions of the Prostaglandin E-Prostanoid Receptor 4 Attenuating Hypertension: A Dominant Role for Kidney Epithelial Cells Compared With Macrophages.

    Yang, Ting / Song, Chengcheng / Ralph, Donna L / Andrews, Portia / Sparks, Matthew A / Koller, Beverly H / McDonough, Alicia A / Coffman, Thomas M

    Journal of the American Heart Association

    2022  Volume 11, Issue 19, Page(s) e026581

    Abstract: Background A beneficial role for prostanoids in hypertension is suggested by clinical studies showing nonsteroidal anti-inflammatory drugs, which block the production of all prostanoids, cause sodium retention and exacerbate hypertension. Among ... ...

    Abstract Background A beneficial role for prostanoids in hypertension is suggested by clinical studies showing nonsteroidal anti-inflammatory drugs, which block the production of all prostanoids, cause sodium retention and exacerbate hypertension. Among prostanoids, prostaglandin E2 and its E-prostanoid receptor 4 receptor (EP4R) have been implicated in blood pressure control. Our previous study found that conditional deletion of EP4R from all tissues in adult mice exacerbates angiotensin II-dependent hypertension, suggesting a powerful effect of EP4R to resist blood pressure elevation. We also found that elimination of EP4R from vascular smooth muscle cells did not affect the severity of hypertension, suggesting nonvascular targets of prostaglandin E mediate this antihypertensive effect. Methods and Results Here we generated mice with cell-specific deletion of EP4R from macrophage-specific EP4 receptor knockouts or kidney epithelial cells (KEKO) to assess the contributions of EP4R in these cells to hypertension pathogenesis. Macrophage-specific EP4 receptor knockouts showed similar blood pressure responses to alterations in dietary sodium or chronic angiotensin II infusion as Controls. By contrast, angiotensin II-dependent hypertension was significantly augmented in KEKOs (mean arterial pressure: 146±3 mm Hg) compared with Controls (137±4 mm Hg;
    MeSH term(s) Amiloride/therapeutic use ; Angiotensin II/metabolism ; Animals ; Anti-Inflammatory Agents/therapeutic use ; Antihypertensive Agents/therapeutic use ; Dinoprostone/metabolism ; Epithelial Cells ; Epithelial Sodium Channels/genetics ; Hypertension/drug therapy ; Kidney ; Macrophages/metabolism ; Mice ; Prostaglandins ; Receptors, Prostaglandin E, EP4 Subtype/genetics ; Receptors, Prostaglandin E, EP4 Subtype/metabolism ; Sodium/metabolism ; Sodium Chloride, Dietary/metabolism
    Chemical Substances Anti-Inflammatory Agents ; Antihypertensive Agents ; Epithelial Sodium Channels ; Prostaglandins ; Receptors, Prostaglandin E, EP4 Subtype ; Sodium Chloride, Dietary ; Angiotensin II (11128-99-7) ; Amiloride (7DZO8EB0Z3) ; Sodium (9NEZ333N27) ; Dinoprostone (K7Q1JQR04M)
    Language English
    Publishing date 2022-09-29
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2653953-6
    ISSN 2047-9980 ; 2047-9980
    ISSN (online) 2047-9980
    ISSN 2047-9980
    DOI 10.1161/JAHA.122.026581
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: A functional role for the cancer disparity-linked genes, CRYβB2 and CRYβB2P1, in the promotion of breast cancer.

    Barrow, Maya A / Martin, Megan E / Coffey, Alisha / Andrews, Portia L / Jones, Gieira S / Reaves, Denise K / Parker, Joel S / Troester, Melissa A / Fleming, Jodie M

    Breast cancer research : BCR

    2019  Volume 21, Issue 1, Page(s) 105

    Abstract: Background: In the USA, the breast cancer mortality rate is 41% higher for African-American women than non-Hispanic White women. While numerous gene expression studies have classified biological features that vary by race and may contribute to poorer ... ...

    Abstract Background: In the USA, the breast cancer mortality rate is 41% higher for African-American women than non-Hispanic White women. While numerous gene expression studies have classified biological features that vary by race and may contribute to poorer outcomes, few studies have experimentally tested these associations. CRYβB2 gene expression has drawn particular interest because of its association with overall survival and African-American ethnicity in multiple cancers. Several reports indicate that overexpression of the CRYβB2 pseudogene, CRYβB2P1, and not CRYβB2 is linked with race and poor outcome. It remains unclear whether either or both genes are linked to breast cancer outcomes. This study investigates CRYβB2 and CRYβB2P1 expression in human breast cancers and breast cancer cell line models, with the goal of elucidating the mechanistic contribution of CRYβB2 and CRYβB2P1 to racial disparities.
    Methods: Custom scripts for CRYβB2 or CRYβB2P1 were generated and used to identify reads that uniquely aligned to either gene. Gene expression according to race and tumor subtype were assessed using all available TCGA breast cancer RNA sequencing alignment samples (n = 1221). In addition, triple-negative breast cancer models engineered to have each gene overexpressed or knocked out were developed and evaluated by in vitro, biochemical, and in vivo assays to identify biological functions.
    Results: We provide evidence that CRYβB2P1 is expressed at higher levels in breast tumors compared to CRYβB2, but only CRYβB2P1 is significantly increased in African-American tumors relative to White American tumors. We show that independent of CRYβB2, CRYβB2P1 enhances tumorigenesis in vivo via promoting cell proliferation. Our data also reveal that CRYβB2P1 may function as a non-coding RNA to regulate CRYβB2 expression. A key observation is that the combined overexpression of both genes was found to suppress cell growth. CRYβB2 overexpression in triple-negative breast cancers increases invasive cellular behaviors, tumor growth, IL6 production, immune cell chemoattraction, and the expression of metastasis-associated genes. These data underscore that both CRYβB2 and CRYβB2P1 promote tumor growth, but their mechanisms for tumor promotion are likely distinct.
    Conclusions: Our findings provide novel data emphasizing the need to distinguish and study the biological effects of both CRYβB2 and CRYβB2P1 as both genes independently promote tumor progression. Our data demonstrate novel molecular mechanisms of two understudied, disparity-linked molecules.
    MeSH term(s) Animals ; Biomarkers, Tumor/genetics ; Biomarkers, Tumor/physiology ; Breast Neoplasms/ethnology ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Cell Transformation, Neoplastic ; Ethnic Groups/genetics ; Female ; Gene Expression ; Genetic Association Studies ; Genetic Predisposition to Disease/genetics ; Humans ; Interleukin-6/metabolism ; Mammary Neoplasms, Experimental ; Mice ; Mice, Nude ; Pseudogenes/genetics ; Pseudogenes/physiology ; Triple Negative Breast Neoplasms/ethnology ; Triple Negative Breast Neoplasms/genetics ; Triple Negative Breast Neoplasms/pathology ; beta-Crystallin B Chain/genetics ; beta-Crystallin B Chain/metabolism ; beta-Crystallin B Chain/physiology
    Chemical Substances Biomarkers, Tumor ; IL6 protein, human ; Interleukin-6 ; beta-Crystallin B Chain ; beta-crystallin B2
    Language English
    Publishing date 2019-09-11
    Publishing country England
    Document type Journal Article
    ZDB-ID 2015059-3
    ISSN 1465-542X ; 1465-5411
    ISSN (online) 1465-542X
    ISSN 1465-5411
    DOI 10.1186/s13058-019-1191-3
    Database MEDical Literature Analysis and Retrieval System OnLINE

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