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  1. Article ; Online: Epigenetic Alterations in Immune Cells of Systemic Lupus Erythematosus and Therapeutic Implications

    David E. Adams / Wen-Hai Shao

    Cells, Vol 11, Iss 506, p

    2022  Volume 506

    Abstract: Systemic lupus erythematosus (SLE) is an autoimmune disorder that is characterized by autoantibody production and dysregulated immune cell activation. Although the exact etiology of SLE remains unknown, genetic, hormonal, and complex environmental ... ...

    Abstract Systemic lupus erythematosus (SLE) is an autoimmune disorder that is characterized by autoantibody production and dysregulated immune cell activation. Although the exact etiology of SLE remains unknown, genetic, hormonal, and complex environmental factors are known to be critical for pathologic immune activation. In addition to the inherited genetic predisposition, epigenetic processes that do not change the genomic code, such as DNA methylation, histone modification, and noncoding RNAs are increasingly appreciated to play important roles in lupus pathogenesis. We herein focus on the up-to-date findings of lupus-associated epigenetic alterations and their pathophysiology in lupus development. We also summarize the therapeutic potential of the new findings. It is likely that advances in the epigenetic study will help to predict individual disease outcomes, promise diagnostic accuracy, and design new target-directed immunotherapies.
    Keywords epigenetics ; systemic lupus erythematosus ; therapeutics ; methylation ; acetylation ; Biology (General) ; QH301-705.5
    Subject code 610
    Language English
    Publishing date 2022-02-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: Axl Expression in Renal Mesangial Cells Is Regulated by Sp1, Ap1, MZF1, and Ep300, and the IL-6/miR-34a Pathway

    David E. Adams / Yuxuan Zhen / Xiaoyang Qi / Wen-Hai Shao

    Cells, Vol 11, Iss 1869, p

    2022  Volume 1869

    Abstract: Axl receptor tyrosine kinase expression in the kidney contributes to a variety of inflammatory renal disease by promoting glomerular proliferation. Axl expression in the kidney is negligible in healthy individuals but upregulated under inflammatory ... ...

    Abstract Axl receptor tyrosine kinase expression in the kidney contributes to a variety of inflammatory renal disease by promoting glomerular proliferation. Axl expression in the kidney is negligible in healthy individuals but upregulated under inflammatory conditions. Little is known about Axl transcriptional regulation. We analyzed the 4.4 kb mouse Axl promoter region and found that many transcription factor (TF)-binding sites and regulatory elements are located within a 600 bp fragment proximal to the translation start site. Among four TFs (Sp1, Ap1, MZF1, and Ep300) identified, Sp1 was the most potent TF that promotes Axl expression. Luciferase assays confirmed the siRNA results and revealed additional mechanisms that regulate Axl expression, including sequences encoding a 5′-UTR mini-intron and potential G-quadruplex forming regions. Deletion of the Axl 5′-UTR mini-intron resulted in a 3.2-fold increases in luciferase activity over the full-length UTR (4.4 kb Axl construct). The addition of TMPyP4, a G-quadruplex stabilizer, resulted in a significantly decreased luciferase activity. Further analysis of the mouse Axl 3′-UTR revealed a miRNA-34a binding site, which inversely regulates Axl expression. The inhibitory role of miRNA-34a in Axl expression was demonstrated in mesangial cells using miRNA-34a mimicry and in primary kidney cells with IL-6 stimulated STAT3 activation. Taken together, Axl expression in mouse kidney is synergistically regulated by multiple factors, including TFs and secondary structures, such as mini-intron and G-quadruplex. A unique IL6/STAT3/miRNA-34a pathway was revealed to be critical in inflammatory renal Axl expression.
    Keywords Axl ; mesangial cell ; transcription factor ; expression regulation ; Sp1 ; Ap1 ; Biology (General) ; QH301-705.5
    Subject code 570 ; 616
    Language English
    Publishing date 2022-06-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: Gas6/TAM Receptors in Systemic Lupus Erythematosus

    Philip L. Cohen / Wen-Hai Shao

    Disease Markers, Vol

    2019  Volume 2019

    Abstract: Systemic lupus erythematosus (SLE) is a multiorgan autoimmune disease associated with impaired immune system regulation. The exact mechanisms of SLE development remain to be elucidated. TAM receptor tyrosine kinases (RTKs) are important for apoptotic ... ...

    Abstract Systemic lupus erythematosus (SLE) is a multiorgan autoimmune disease associated with impaired immune system regulation. The exact mechanisms of SLE development remain to be elucidated. TAM receptor tyrosine kinases (RTKs) are important for apoptotic cell clearance, immune homeostasis, and resolution of immune responses. TAM deficiency leads to lupus-like autoimmune diseases. Activation of TAM receptors leads to proteolytic cleavage of the receptors, generating soluble forms of TAM. Circulating TAM receptors have an immunoregulatory function and may also serve as biomarkers for disease prognosis. Here, we review the biological function and signaling of TAM RTKs in the development and pathogenesis of lupus and lupus nephritis. Targeting Gas6/TAM pathways may be of therapeutic benefit. A discussion of potential TAM activation and inhibition in the treatment of lupus and lupus nephritis is included.
    Keywords Medicine (General) ; R5-920
    Language English
    Publishing date 2019-01-01T00:00:00Z
    Publisher Hindawi Limited
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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