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  1. Article ; Online: Chronic Obstructive Pulmonary Disease: Abandoning the "Streetlight Effect".

    Sidhaye, Venkataramana K / Biswal, Shyam

    American journal of respiratory and critical care medicine

    2018  Volume 198, Issue 6, Page(s) 697–698

    MeSH term(s) Forced Expiratory Volume ; Humans ; NF-E2-Related Factor 2 ; Phagocytosis ; Pulmonary Disease, Chronic Obstructive
    Chemical Substances NF-E2-Related Factor 2
    Language English
    Publishing date 2018-05-09
    Publishing country United States
    Document type Editorial ; Comment
    ZDB-ID 1180953-x
    ISSN 1535-4970 ; 0003-0805 ; 1073-449X
    ISSN (online) 1535-4970
    ISSN 0003-0805 ; 1073-449X
    DOI 10.1164/rccm.201803-0531ED
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  2. Article ; Online: Jumping on the Single-Cell RNA-Sequencing Bandwagon: Take Care Not to Put the Cart before the Horse.

    Sidhaye, Venkataramana K / Wu, Min / Tesfaigzi, Yohannes

    American journal of respiratory cell and molecular biology

    2020  Volume 62, Issue 2, Page(s) 267

    MeSH term(s) Humans ; Nerve Tissue Proteins/genetics ; RNA/genetics ; Sequence Analysis, RNA ; Single-Cell Analysis/methods
    Chemical Substances Nerve Tissue Proteins ; cocaine- and amphetamine-regulated transcript protein ; RNA (63231-63-0)
    Language English
    Publishing date 2020-01-18
    Publishing country United States
    Document type Letter
    ZDB-ID 1025960-0
    ISSN 1535-4989 ; 1044-1549
    ISSN (online) 1535-4989
    ISSN 1044-1549
    DOI 10.1165/rcmb.2019-0389LE
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  3. Article ; Online: Why new biology must be uncovered to advance therapeutic strategies for chronic obstructive pulmonary disease.

    Nguyen, Jennifer M K / Robinson, Douglas N / Sidhaye, Venkataramana K

    American journal of physiology. Lung cellular and molecular physiology

    2020  Volume 320, Issue 1, Page(s) L1–L11

    Abstract: Chronic obstructive pulmonary disease (COPD) is characterized by the destruction of alveolar tissue (in emphysema) and airway remodeling (leading to chronic bronchitis), which cause difficulties in breathing. It is a growing public health concern with ... ...

    Abstract Chronic obstructive pulmonary disease (COPD) is characterized by the destruction of alveolar tissue (in emphysema) and airway remodeling (leading to chronic bronchitis), which cause difficulties in breathing. It is a growing public health concern with few therapeutic options that can reverse disease progression or mortality. This is in part because current treatments mainly focus on ameliorating symptoms induced by inflammatory pathways as opposed to curing disease. Hence, emerging research focused on upstream pathways are likely to be beneficial in the development of efficient therapeutics to address the root causes of disease. Some of these pathways include mitochondrial function, cytoskeletal structure and maintenance, and airway hydration, which are all affected by toxins that contribute to COPD. Because of the complexity of COPD and unknown targets for disease onset, simpler model organisms have proved to be useful tools in identifying disease-relevant pathways and targets. This review summarizes COPD pathology, current treatments, and therapeutic discovery research, with a focus on the aforementioned pathways that can advance the therapeutic landscape of COPD.
    MeSH term(s) Animals ; Humans ; Pulmonary Disease, Chronic Obstructive/metabolism ; Pulmonary Disease, Chronic Obstructive/pathology ; Pulmonary Disease, Chronic Obstructive/therapy ; Signal Transduction
    Language English
    Publishing date 2020-11-11
    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.00367.2020
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  4. Article ; Online: Human microphysiological models of airway and alveolar epithelia.

    Lagowala, Dave Anuj / Kwon, Seoyoung / Sidhaye, Venkataramana K / Kim, Deok-Ho

    American journal of physiology. Lung cellular and molecular physiology

    2021  Volume 321, Issue 6, Page(s) L1072–L1088

    Abstract: Human organ-on-a-chip models are powerful tools for preclinical research that can be used to study the mechanisms of disease and evaluate new targets for therapeutic intervention. Lung-on-a-chip models have been one of the most well-characterized designs ...

    Abstract Human organ-on-a-chip models are powerful tools for preclinical research that can be used to study the mechanisms of disease and evaluate new targets for therapeutic intervention. Lung-on-a-chip models have been one of the most well-characterized designs in this field and can be altered to evaluate various types of respiratory disease and to assess treatment candidates prior to clinical testing. These systems are capable of overcoming the flaws of conventional two-dimensional (2-D) cell culture and in vivo animal testing due to their ability to accurately recapitulate the in vivo microenvironment of human tissue with tunable material properties, microfluidic integration, delivery of precise mechanical and biochemical cues, and designs with organ-specific architecture. In this review, we first describe an overview of currently available lung-on-a-chip designs. We then present how recent innovations in human stem cell biology, tissue engineering, and microfabrication can be used to create more predictive human lung-on-a-chip models for studying respiratory disease. Finally, we discuss the current challenges and future directions of lung-on-a-chip designs for in vitro disease modeling with a particular focus on immune and multiorgan interactions.
    MeSH term(s) Alveolar Epithelial Cells/cytology ; Alveolar Epithelial Cells/physiology ; Animals ; Drug Evaluation, Preclinical ; Humans ; Lab-On-A-Chip Devices ; Models, Biological ; Respiratory Mucosa/cytology ; Respiratory Mucosa/physiology ; Respiratory Tract Diseases/physiopathology ; Tissue Engineering
    Language English
    Publishing date 2021-10-06
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1013184-x
    ISSN 1522-1504 ; 1040-0605
    ISSN (online) 1522-1504
    ISSN 1040-0605
    DOI 10.1152/ajplung.00103.2021
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  5. Article ; Online: Cigarette smoke-induced injury induces distinct sex-specific transcriptional signatures in mice tracheal epithelial cells.

    Ghosh, Baishakhi / Chengala, Pratulya Pragadaraju / Shah, Sonya / Chen, Daniel / Karnam, Vaishnavi / Wilmsen, Kai / Yeung-Luk, Bonnie / Sidhaye, Venkataramana K

    American journal of physiology. Lung cellular and molecular physiology

    2023  Volume 325, Issue 4, Page(s) L467–L476

    Abstract: The airway epithelial barrier is crucial for defending against respiratory insults and diseases. Disruption of epithelial integrity contributes to respiratory diseases, and sex-specific differences in susceptibility and severity have been observed. ... ...

    Abstract The airway epithelial barrier is crucial for defending against respiratory insults and diseases. Disruption of epithelial integrity contributes to respiratory diseases, and sex-specific differences in susceptibility and severity have been observed. However, sex-specific differences in the context of respiratory diseases are often overlooked, especially in murine models. In this study, we investigated the in vitro transcriptomics of male and female murine tracheal epithelial cells (mTECs) in response to chronic cigarette smoke (CS) exposure using an International Organization for Standardization (ISO) puff regimen. Our findings reveal sex-specific differences in the baseline characteristics of airway epithelial cells. Female mTECs demonstrated stronger barrier function and higher ciliary function compared with males. The barrier function was disrupted in both males and females following chronic CS, but the difference was more significant in females due to their higher baseline. Female mice exhibited transcriptional signatures suggesting dedifferentiation with increased basal cells and markers of cellular senescence. Pathway analysis indicated potential protective roles of planar cell polarity (PCP) in preventing dedifferentiation in male mice exposed to CS. We also observed sex-specific differences in the DNA damage response and antioxidant levels, suggesting distinct mechanisms underlying cellular stress. Understanding these sex-specific mechanisms could facilitate the development of targeted therapeutic strategies for lung diseases associated with environmental insults. Recognizing sex-based differences in disease susceptibility and treatment response can lead to personalized care and improved outcomes. Clinical trials should consider sex as a biological variable to develop effective interventions that address the unique differences between men and women in respiratory diseases.
    MeSH term(s) Humans ; Mice ; Male ; Animals ; Female ; Lung/metabolism ; Cigarette Smoking ; Disease Susceptibility ; Epithelial Cells/metabolism ; Pulmonary Disease, Chronic Obstructive/metabolism
    Language English
    Publishing date 2023-08-22
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1013184-x
    ISSN 1522-1504 ; 1040-0605
    ISSN (online) 1522-1504
    ISSN 1040-0605
    DOI 10.1152/ajplung.00104.2023
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  6. Article ; Online: Precision medicine in COPD: where are we and where do we need to go?

    Sidhaye, Venkataramana K / Nishida, Kristine / Martinez, Fernando J

    European respiratory review : an official journal of the European Respiratory Society

    2018  Volume 27, Issue 149

    Abstract: Chronic obstructive pulmonary disease (COPD) was the fourth leading cause of death worldwide in 2015. Current treatments for patients ease discomfort and help decrease disease progression; however, none improve lung function or change mortality. COPD is ... ...

    Abstract Chronic obstructive pulmonary disease (COPD) was the fourth leading cause of death worldwide in 2015. Current treatments for patients ease discomfort and help decrease disease progression; however, none improve lung function or change mortality. COPD is heterogeneous in its molecular and clinical presentation, making it difficult to understand disease aetiology and define robust therapeutic strategies. Given the complexity of the disease we propose a precision medicine approach to understanding and better treating COPD. It is possible that multiOMICs can be used as a tool to integrate data from multiple fields. Moreover, analysis of electronic medical records could aid in the treatment of patients and in the predictions of outcomes. The Precision Medicine Initiative created in 2015 has made precision medicine approaches to treat disease a reality; one of these diseases being COPD.
    MeSH term(s) Clinical Decision-Making ; Early Diagnosis ; Genetic Markers ; Genetic Predisposition to Disease ; Humans ; Lung/drug effects ; Lung/physiopathology ; Phenotype ; Precision Medicine ; Predictive Value of Tests ; Pulmonary Disease, Chronic Obstructive/drug therapy ; Pulmonary Disease, Chronic Obstructive/genetics ; Pulmonary Disease, Chronic Obstructive/metabolism ; Pulmonary Disease, Chronic Obstructive/physiopathology ; Treatment Outcome
    Chemical Substances Genetic Markers
    Language English
    Publishing date 2018-08-01
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 1077620-5
    ISSN 1600-0617 ; 0905-9180
    ISSN (online) 1600-0617
    ISSN 0905-9180
    DOI 10.1183/16000617.0022-2018
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  7. Article ; Online: Aqp5

    Al-Samir, Samer / Yildirim, Ali Önder / Sidhaye, Venkataramana K / King, Landon S / Breves, Gerhard / Conlon, Thomas M / Stoeger, Claudia / Gailus-Durner, Valerie / Fuchs, Helmut / Hrabé de Angelis, Martin / Gros, Gerolf / Endeward, Volker

    American journal of physiology. Regulatory, integrative and comparative physiology

    2022  Volume 324, Issue 1, Page(s) R109–R119

    Abstract: The fundamental body functions that determine maximal ... ...

    Abstract The fundamental body functions that determine maximal O
    MeSH term(s) Animals ; Mice ; Pulmonary Gas Exchange ; Adipose Tissue, Brown/metabolism ; Thermogenesis/physiology ; Lung ; Oxygen Consumption ; Cold Temperature
    Language English
    Publishing date 2022-11-21
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 603839-6
    ISSN 1522-1490 ; 0363-6119
    ISSN (online) 1522-1490
    ISSN 0363-6119
    DOI 10.1152/ajpregu.00130.2022
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  8. Article: Validation of SeptiCyte RAPID to Discriminate Sepsis from Non-Infectious Systemic Inflammation.

    Balk, Robert / Esper, Annette M / Martin, Greg S / Miller, Russell R / Lopansri, Bert K / Burke, John P / Levy, Mitchell / Opal, Steven / Rothman, Richard E / D'Alessio, Franco R / Sidhaye, Venkataramana K / Aggarwal, Neil R / Greenberg, Jared A / Yoder, Mark / Patel, Gourang / Gilbert, Emily / Parada, Jorge P / Afshar, Majid / Kempker, Jordan A /
    van der Poll, Tom / Schultz, Marcus J / Scicluna, Brendon P / Klein Klouwenberg, Peter M C / Liebler, Janice / Blodget, Emily / Kumar, Santhi / Navalkar, Krupa / Yager, Thomas D / Sampson, Dayle / Kirk, James T / Cermelli, Silvia / Davis, Roy F / Brandon, Richard B

    Journal of clinical medicine

    2024  Volume 13, Issue 5

    Abstract: 1) ...

    Abstract (1)
    Language English
    Publishing date 2024-02-20
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2662592-1
    ISSN 2077-0383
    ISSN 2077-0383
    DOI 10.3390/jcm13051194
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  9. Article ; Online: Disruption of Sinonasal Epithelial Nrf2 Enhances Susceptibility to Rhinosinusitis in a Mouse Model.

    Ramanathan, Murugappan / Tharakan, Anuj / Sidhaye, Venkataramana K / Lane, Andrew P / Biswal, Shyam / London, Nyall R

    The Laryngoscope

    2020  Volume 131, Issue 4, Page(s) 713–719

    Abstract: Objectives/hypothesis: Oxidative stress has been postulated to play an important role in chronic rhinosinusitis. Nrf2 is a transcription factor that is involved in the regulation of multiple antioxidant genes, and its function has been previously shown ... ...

    Abstract Objectives/hypothesis: Oxidative stress has been postulated to play an important role in chronic rhinosinusitis. Nrf2 is a transcription factor that is involved in the regulation of multiple antioxidant genes, and its function has been previously shown to be important in sinonasal inflammation. Although the sinonasal implications of whole body Nrf2
    Study design: Basic science.
    Methods: An epithelial-specific Nrf2 knockout mouse was generated by crossing Krt5-cre(K5) with Nrf2
    Results: Papain-sensitized mice lacking epithelial-specific Nrf2 demonstrate increased goblet cell hyperplasia, significant tissue eosinophilia, and statistically significant increase in mucosal IL-13 when compared to Nrf2 wild-type mice. Lastly, mucosal T cells were identified as the cellular source of IL-13.
    Conclusions: We demonstrate enhanced severity of eosinophilic sinonasal inflammation from disruption of the epithelial-specific Nrf2 pathway. The responsiveness of Nrf2-directed antioxidant pathways may act as a major determinant of susceptibility to eosinophilic inflammation and may have potential as a therapeutic target for chronic rhinosinusitis.
    Level of evidence: NA Laryngoscope, 131:713-719, 2021.
    MeSH term(s) Animals ; Disease Models, Animal ; Disease Susceptibility ; Inflammation ; Mice ; Mice, Knockout ; NF-E2-Related Factor 2/metabolism ; Oxidative Stress ; Papain ; Rhinitis/metabolism ; Sinusitis/metabolism
    Chemical Substances NF-E2-Related Factor 2 ; Nfe2l2 protein, mouse ; Papain (EC 3.4.22.2)
    Language English
    Publishing date 2020-07-06
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 80180-x
    ISSN 1531-4995 ; 0023-852X
    ISSN (online) 1531-4995
    ISSN 0023-852X
    DOI 10.1002/lary.28884
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  10. Article ; Online: Epithelial plasticity in COPD results in cellular unjamming due to an increase in polymerized actin.

    Ghosh, Baishakhi / Nishida, Kristine / Chandrala, Lakshmana / Mahmud, Saborny / Thapa, Shreeti / Swaby, Carter / Chen, Si / Khosla, Atulya Aman / Katz, Joseph / Sidhaye, Venkataramana K

    Journal of cell science

    2022  Volume 135, Issue 4

    Abstract: The airway epithelium is subjected to insults such as cigarette smoke (CS), a primary cause of chronic obstructive pulmonary disease (COPD) and serves as an excellent model to study cell plasticity. Here, we show that both CS-exposed and COPD-patient ... ...

    Abstract The airway epithelium is subjected to insults such as cigarette smoke (CS), a primary cause of chronic obstructive pulmonary disease (COPD) and serves as an excellent model to study cell plasticity. Here, we show that both CS-exposed and COPD-patient derived epithelia (CHBE) display quantitative evidence of cellular plasticity, with loss of specialized apical features and a transcriptional profile suggestive of partial epithelial-to-mesenchymal transition (pEMT), albeit with distinct cell motion indicative of cellular unjamming. These injured/diseased cells have an increased fraction of polymerized actin, due to loss of the actin-severing protein cofilin-1. We observed that decreasing polymerized actin restores the jammed state in both CHBE and CS-exposed epithelia, indicating that the fraction of polymerized actin is critical in unjamming the epithelia. Our kinetic energy spectral analysis suggests that loss of cofilin-1 results in unjamming, similar to that seen with both CS exposure and in CHBE cells. The findings suggest that in response to chronic injury, although epithelial cells display evidence of pEMT, their movement is more consistent with cellular unjamming. Inhibitors of actin polymerization rectify the unjamming features of the monolayer. This article has an associated First Person interview with the first author of the paper.
    MeSH term(s) Actins/metabolism ; Epithelial Cells/metabolism ; Epithelial-Mesenchymal Transition/physiology ; Humans ; Pulmonary Disease, Chronic Obstructive/metabolism ; Smoke/adverse effects
    Chemical Substances Actins ; Smoke
    Language English
    Publishing date 2022-02-24
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2993-2
    ISSN 1477-9137 ; 0021-9533
    ISSN (online) 1477-9137
    ISSN 0021-9533
    DOI 10.1242/jcs.258513
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