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  1. Article ; Online: Is targeting Akt a viable option to treat advanced-stage COVID-19 patients?

    Somanath, Payaningal R

    American journal of physiology. Lung cellular and molecular physiology

    2020  Volume 319, Issue 1, Page(s) L45–L47

    MeSH term(s) Betacoronavirus ; Coronavirus Infections/drug therapy ; Humans ; Inflammation/drug therapy ; Pandemics ; Peptidyl-Dipeptidase A/drug effects ; Pneumonia, Viral/drug therapy ; Proto-Oncogene Proteins c-akt/drug effects
    Chemical Substances Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Peptidyl-Dipeptidase A (EC 3.4.15.1) ; angiotensin converting enzyme 2 (EC 3.4.17.-)
    Keywords covid19
    Language English
    Publishing date 2020-06-10
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 1013184-x
    ISSN 1522-1504 ; 1040-0605
    ISSN (online) 1522-1504
    ISSN 1040-0605
    DOI 10.1152/ajplung.00124.2020
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    Uc I Zs.89: Show issues Location:
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  2. Article: AKT Isoforms in the Immune Response in Cancer.

    Ahmad, Zayd / Somanath, Payaningal R

    Current topics in microbiology and immunology

    2022  Volume 436, Page(s) 349–366

    Abstract: AKT is a protein kinase that exists in three isoforms: AKT1, AKT2, and AKT3. Though similar in structure, these isoforms display different effects. AKT is activated downstream of PI3K, and together, this signaling pathway helps regulate cellular ... ...

    Abstract AKT is a protein kinase that exists in three isoforms: AKT1, AKT2, and AKT3. Though similar in structure, these isoforms display different effects. AKT is activated downstream of PI3K, and together, this signaling pathway helps regulate cellular processes including cell growth, proliferation, metabolism, survival, and apoptosis. Disruption in these pathways has been associated with disorders including cardiovascular diseases, developmental disorders, inflammatory responses, autoimmune diseases, neurologic disorders, type 2 diabetes, and several cancers. In cancer, deregulation in the PI3K/AKT pathway can be manifested as tumorigenesis, pathological angiogenesis, and metastasis. Increased activity has been correlated with tumor progression and resistance to cancer treatments. Recent studies have suggested that inhibition of the PI3K/AKT pathway plays a significant role in the development, expansion, and proliferation of cells of the immune system. Additionally, AKT has been found to play an important role in differentiating regulatory T cells, activating B cells, and augmenting tumor immunosurveillance. This emphasizes AKT as a potential target for inhibition in cancer therapy. This chapter reviews AKT structure and regulation, its different isoforms, its role in immune cells, and its modulation in oncotherapy.
    MeSH term(s) Diabetes Mellitus, Type 2 ; Humans ; Immunity ; Neoplasms ; Phosphatidylinositol 3-Kinases/genetics ; Protein Isoforms/genetics ; Protein Isoforms/metabolism ; Proto-Oncogene Proteins c-akt/genetics ; Proto-Oncogene Proteins c-akt/metabolism
    Chemical Substances Protein Isoforms ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
    Language English
    Publishing date 2022-10-15
    Publishing country Germany
    Document type Journal Article
    ISSN 0070-217X
    ISSN 0070-217X
    DOI 10.1007/978-3-031-06566-8_15
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    In stock of ZB MED Bonn / Germany

    Einzelsignatur: Show issues

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  4. Article ; Online: Secondary Analysis of Fluids and Catheters Treatment Trial (FACTT) data reveal poor clinical outcomes in acute respiratory distress syndrome patients with diabetes.

    Alanazi, Abdulaziz H / Almuntashiri, Sultan / Sikora, Andrea / Zhang, Duo / Somanath, Payaningal R

    Respiratory medicine

    2024  Volume 223, Page(s) 107540

    Abstract: Objectives: Conflicting reports exist about the link between diabetes mellitus (DM) and acute respiratory distress syndrome (ARDS). Our study examines the impact of pre-existing DM on ARDS patients within the Fluid and Catheter Treatment Trial (FACTT).!# ...

    Abstract Objectives: Conflicting reports exist about the link between diabetes mellitus (DM) and acute respiratory distress syndrome (ARDS). Our study examines the impact of pre-existing DM on ARDS patients within the Fluid and Catheter Treatment Trial (FACTT).
    Design: Conducting a secondary analysis of FACTT data, we incorporated 967 participants with identified DM status (173 with DM, 794 without DM) and examined outcomes like 90-day mortality, hospital and ICU stays, and ventilator days until unassisted breathing. The primary outcome of hospital mortality at day 90 was evaluated through logistic regression using IBM SPSS software. Additionally, we assessed plasma cytokines and chemokines utilizing a human magnetic bead-based multiplex assay.
    Results: Patients with pre-existing DM exhibited a lower survival rate compared to non-DM patients (61.3 vs. 72.3 %, p = 0.006). Subjects with DM experienced significantly longer hospital lengths of stay (24.5 vs. 19.7 days; p = 0.008) and prolonged ICU stays (14.8 vs. 12.4 days; p = 0.029). No significant difference was found in ventilator days until unassisted breathing between the two groups (11.7 vs. 10; p = 0.1). Cytokine/chemokine analyses indicated a non-significant trend toward heightened levels of cytokines (TNF-α, IL-10, and IL-6) and chemokines (CRP, MCP-1) in DM patients compared to non-DM on both days 0 and 1. Notably, lipopolysaccharide-binding protein (LBP) exhibited significantly higher levels in DM compared to non-DM individuals.
    Conclusions: ARDS patients with DM suffered worse clinical outcomes compared to non-DM patients, indicating that DM may negatively affect the respiratory functions in these subjects. Further comprehensive clinical and pre-clinical studies will strengthen this relationship.
    MeSH term(s) Humans ; Diabetes Mellitus ; Respiratory Distress Syndrome/therapy ; Catheters ; Cytokines ; Chemokines
    Chemical Substances Cytokines ; Chemokines
    Language English
    Publishing date 2024-01-28
    Publishing country England
    Document type Journal Article
    ZDB-ID 1003348-8
    ISSN 1532-3064 ; 0954-6111
    ISSN (online) 1532-3064
    ISSN 0954-6111
    DOI 10.1016/j.rmed.2024.107540
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    Ui III Zs.19: Show issues Location:
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  5. Article ; Online: Distinct Mechanisms of Human Retinal Endothelial Barrier Modulation In Vitro by Mediators of Diabetes and Uveitis

    Madhuri Rudraraju / S. Priya Narayanan / Payaningal R. Somanath

    Life, Vol 12, Iss 33, p

    2022  Volume 33

    Abstract: Ocular diseases such as diabetic retinopathy (DR) and uveitis are associated with injury to the blood–retinal barrier (BRB). Whereas high glucose (HG) and advanced glycation end products (AGE) contribute to DR, bacterial infections causing uveitis are ... ...

    Abstract Ocular diseases such as diabetic retinopathy (DR) and uveitis are associated with injury to the blood–retinal barrier (BRB). Whereas high glucose (HG) and advanced glycation end products (AGE) contribute to DR, bacterial infections causing uveitis are triggered by endotoxins such as lipopolysaccharide (LPS). It is unclear how HG, AGE, and LPS affect human retinal endothelial cell (HREC) junctions. Moreover, tumor necrosis factor-α (TNFα) is elevated in both DR and ocular infections. In the current study, we determined the direct effects of HG, AGE, TNFα, and LPS on the expression and intracellular distribution of claudin-5, VE-cadherin, and β-catenin in HRECs and how these mediators affect Akt and P38 MAP kinase that have been implicated in ocular pathologies. In our results, whereas HG, AGE, and TNFα activated both Akt and P38 MAPK, LPS treatment suppressed Akt but increased P38 MAPK phosphorylation. Furthermore, while treatment with AGE and HG increased cell-junction protein expression in HRECs, LPS elicited a paradoxical effect. By contrast, when HG treatment increased HREC-barrier resistance, AGE and LPS stimulation compromised it, and TNFα had no effect. Together, our results demonstrated the differential effects of the mediators of diabetes and infection on HREC-barrier modulation leading to BRB injury.
    Keywords blood–brain barrier ; claudin-5 ; AGE ; TNFα ; hyperglycemia ; lipopolysaccharide ; Science ; Q
    Subject code 630
    Language English
    Publishing date 2022-12-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  6. Article ; Online: Endothelial Permeability Assays In Vitro.

    Adil, Mir S / Somanath, Payaningal R

    Methods in molecular biology (Clifton, N.J.)

    2020  Volume 2367, Page(s) 177–191

    Abstract: The endothelium is a thin layer of squamous cells that acts as a semipermeable barrier regulating vascular permeability to let molecules pass through it thereby maintaining tissue fluid homeostasis. Physiological increase in endothelial or vascular ... ...

    Abstract The endothelium is a thin layer of squamous cells that acts as a semipermeable barrier regulating vascular permeability to let molecules pass through it thereby maintaining tissue fluid homeostasis. Physiological increase in endothelial or vascular permeability is transient, transpired by post-tissue injury during the initial phases of healing, whereas pathological permeability is persistent commonly witnessed in conditions such as atherosclerosis, chronic inflammation, tumor growth, and diabetic retinopathy. The in vivo or in situ use of animal models in the assessment of permeability not only raises inevitable ethical concerns but also confers difficulty to apply to high-throughput screening. Therefore, there is an ever-increasing dependency on in vitro studies to assess drug permeability, and various research programs have suffered to develop appropriate in vitro assays for measurement and prediction. In vitro models that both mimic in vivo microvascular endothelium and can be utilized to record changes in endothelial permeability are vital in delineating the mechanisms involved in the prevention and treatment of disorders related to vascular permeability. The Transwell
    MeSH term(s) Animals ; Biological Assay ; Capillary Permeability ; Cells, Cultured ; Electric Impedance ; Endothelium ; Endothelium, Vascular/metabolism ; Permeability
    Keywords covid19
    Language English
    Publishing date 2020-04-28
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/7651_2020_309
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  7. Article ; Online: Vascular Permeability Assays In Vivo.

    Adil, Mir S / Somanath, Payaningal R

    Methods in molecular biology (Clifton, N.J.)

    2020  Volume 2367, Page(s) 165–175

    Abstract: Whereas physiological vascular permeability (VP) mediates selective transport of plasma, electrolytes, proteins, and cells across an intact endothelial barrier, pathological VP results in the loss of endothelial barrier integrity. Whereas physiological ... ...

    Abstract Whereas physiological vascular permeability (VP) mediates selective transport of plasma, electrolytes, proteins, and cells across an intact endothelial barrier, pathological VP results in the loss of endothelial barrier integrity. Whereas physiological VP is a feature of regular host defense and tissue repair, compromised barrier function may lead to aberrant vascular leakage, concurrent tissue edema, and inflammation eventually causing life-threatening conditions such as acute lung injury or acute respiratory distress syndrome, cancer, kidney injury, etc. Measurement of VP helps to identify, design, and optimize anti-leak therapies. Further, it can define the effect of a stimulus or a gene modulation in endothelial-barrier regulation. The degree of VP can be of importance to determine the stage of cancer and disease prognosis. This chapter discusses Miles assay, which is a well-established, relatively simple, and a reliable in vivo technique to assess VP as a surrogate measurement. Although a reliable technique, Miles assay is time-consuming, and the technique does not consider the compounding factors that may increase VP independently of endothelial-barrier regulation, such as blood pressure or blood flow. As an alternative, we describe fluorescein isothiocyanate-dextran lung permeability assay, a method that can also be adapted to measure VP and edema in other organs such as the brain and kidney.
    MeSH term(s) Acute Lung Injury ; Brain ; Capillary Permeability ; Humans ; Inflammation ; Permeability
    Keywords covid19
    Language English
    Publishing date 2020-08-31
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/7651_2020_310
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  8. Article ; Online: Spermine oxidase inhibitor, MDL 72527, reduced neovascularization, vascular permeability, and acrolein-conjugated proteins in a mouse model of ischemic retinopathy.

    Alhumaid, Abdullah / Liu, Fang / Shan, Shengshuai / Jafari, Eissa / Nourin, Nadia / Somanath, Payaningal R / Narayanan, S Priya

    Tissue barriers

    2024  , Page(s) 2347070

    Abstract: Disruptions in polyamine metabolism have been identified as contributing factors to various central nervous system disorders. Our laboratory has previously highlighted the crucial role of polyamine oxidation in retinal disease models, specifically noting ...

    Abstract Disruptions in polyamine metabolism have been identified as contributing factors to various central nervous system disorders. Our laboratory has previously highlighted the crucial role of polyamine oxidation in retinal disease models, specifically noting elevated levels of spermine oxidase (SMOX) in inner retinal neurons. Our prior research demonstrated that inhibiting SMOX with MDL 72527 protected against vascular injury and microglial activation induced by hyperoxia in the retina. However, the effects of SMOX inhibition on retinal neovascularization and vascular permeability, along with the underlying molecular mechanisms of vascular protection, remain incompletely understood. In this study, we utilized the oxygen-induced retinopathy (OIR) model to explore the impact of SMOX inhibition on retinal neovascularization, vascular permeability, and the molecular mechanisms underlying MDL 72527-mediated vasoprotection in the OIR retina. Our findings indicate that inhibiting SMOX with MDL 72527 mitigated vaso-obliteration and neovascularization in the OIR retina. Additionally, it reduced OIR-induced vascular permeability and Claudin-5 expression, suppressed acrolein-conjugated protein levels, and downregulated P38/ERK1/2/STAT3 signaling. Furthermore, our results revealed that treatment with BSA-Acrolein conjugates significantly decreased the viability of human retinal endothelial cells (HRECs) and activated P38 signaling. These observations contribute valuable insights into the potential therapeutic benefits of SMOX inhibition by MDL 72527 in ischemic retinopathy.
    Language English
    Publishing date 2024-04-29
    Publishing country United States
    Document type Journal Article
    ISSN 2168-8370
    ISSN (online) 2168-8370
    DOI 10.1080/21688370.2024.2347070
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  9. Article ; Online: MMP3 in Severe COVID-19: A Biomarker or Therapeutic Target?

    Almuntashiri, Sultan / Zhang, Duo / Somanath, Payaningal R / Sikora, Andrea

    Infectious disorders drug targets

    2022  Volume 23, Issue 1, Page(s) e190622206159

    Abstract: Identifying novel therapies is a critical need in the treatment of coronavirus disease-19 (COVID-19) and acute respiratory distress syndrome (ARDS). Stromelysin-1, also known as matrixmetalloproteinase 3 (MMP3), has been investigated as a diagnostic ... ...

    Abstract Identifying novel therapies is a critical need in the treatment of coronavirus disease-19 (COVID-19) and acute respiratory distress syndrome (ARDS). Stromelysin-1, also known as matrixmetalloproteinase 3 (MMP3), has been investigated as a diagnostic biomarker and a potential pharmacological target. Here, we discuss the recent findings of Gelzo et al. in the context of additional MMP3 investigations to delineate its exact role in diagnosis, prognostication, and phenotyping, in addition to its promising role as a therapeutic target in COVID-19-associated respiratory failure.
    MeSH term(s) Humans ; COVID-19 ; Matrix Metalloproteinase 3/therapeutic use ; Respiratory Distress Syndrome/diagnosis ; Respiratory Distress Syndrome/drug therapy ; COVID-19 Drug Treatment ; Biomarkers
    Chemical Substances Matrix Metalloproteinase 3 (EC 3.4.24.17) ; Biomarkers ; MMP3 protein, human (EC 3.4.24.17)
    Language English
    Publishing date 2022-06-22
    Publishing country United Arab Emirates
    Document type Journal Article
    ZDB-ID 2234298-9
    ISSN 2212-3989 ; 1871-5265
    ISSN (online) 2212-3989
    ISSN 1871-5265
    DOI 10.2174/1871526522666220619121539
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    Zs.A 5598: Show issues Location:
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  10. Article: Targeting P21-Activated Kinase-1 for Metastatic Prostate Cancer.

    Somanath, Payaningal R / Chernoff, Jonathan / Cummings, Brian S / Prasad, Sandip M / Homan, Harvey D

    Cancers

    2023  Volume 15, Issue 8

    Abstract: Metastatic prostate cancer (mPCa) has limited therapeutic options and a high mortality rate. The p21-activated kinase (PAK) family of proteins is important in cell survival, proliferation, and motility in physiology, and pathologies such as infectious, ... ...

    Abstract Metastatic prostate cancer (mPCa) has limited therapeutic options and a high mortality rate. The p21-activated kinase (PAK) family of proteins is important in cell survival, proliferation, and motility in physiology, and pathologies such as infectious, inflammatory, vascular, and neurological diseases as well as cancers. Group-I PAKs (PAK1, PAK2, and PAK3) are involved in the regulation of actin dynamics and thus are integral for cell morphology, adhesion to the extracellular matrix, and cell motility. They also play prominent roles in cell survival and proliferation. These properties make group-I PAKs a potentially important target for cancer therapy. In contrast to normal prostate and prostatic epithelial cells, group-I PAKs are highly expressed in mPCA and PCa tissue. Importantly, the expression of group-I PAKs is proportional to the Gleason score of the patients. While several compounds have been identified that target group-I PAKs and these are active in cells and mice, and while some inhibitors have entered human trials, as of yet, none have been FDA-approved. Probable reasons for this lack of translation include issues related to selectivity, specificity, stability, and efficacy resulting in side effects and/or lack of efficacy. In the current review, we describe the pathophysiology and current treatment guidelines of PCa, present group-I PAKs as a potential druggable target to treat mPCa patients, and discuss the various ATP-competitive and allosteric inhibitors of PAKs. We also discuss the development and testing of a nanotechnology-based therapeutic formulation of group-I PAK inhibitors and its significant potential advantages as a novel, selective, stable, and efficacious mPCa therapeutic over other PCa therapeutics in the pipeline.
    Language English
    Publishing date 2023-04-11
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers15082236
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