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  1. Article ; Online: Cellular and molecular basis of liver development.

    Shin, Donghun / Monga, Satdarshan Pal Singh

    Comprehensive Physiology

    2013  Volume 3, Issue 2, Page(s) 799–815

    Abstract: Liver is a prime organ responsible for synthesis, metabolism, and detoxification. The organ is endodermal in origin and its development is regulated by temporal, complex, and finely balanced cellular and molecular interactions that dictate its origin, ... ...

    Abstract Liver is a prime organ responsible for synthesis, metabolism, and detoxification. The organ is endodermal in origin and its development is regulated by temporal, complex, and finely balanced cellular and molecular interactions that dictate its origin, growth, and maturation. We discuss the relevance of endoderm patterning, which truly is the first step toward mapping of domains that will give rise to specific organs. Once foregut patterning is completed, certain cells within the foregut endoderm gain competence in the form of expression of certain transcription factors that allow them to respond to certain inductive signals. Hepatic specification is then a result of such inductive signals, which often emanate from the surrounding mesenchyme. During hepatic specification bipotential hepatic stem cells or hepatoblasts become apparent and undergo expansion, which results in a visible liver primordium during the stage of hepatic morphogenesis. Hepatoblasts next differentiate into either hepatocytes or cholangiocytes. The expansion and differentiation is regulated by cellular and molecular interactions between hepatoblasts and mesenchymal cells including sinusoidal endothelial cells, stellate cells, and also innate hematopoietic elements. Further maturation of hepatocytes and cholangiocytes continues during late hepatic development as a function of various growth factors. At this time, liver gains architectural novelty in the form of zonality and at cellular level acquires polarity. A comprehensive elucidation of such finely tuned developmental cues have been the basis of transdifferentiation of various types of stem cells to hepatocyte-like cells for purposes of understanding health and disease and for therapeutic applications.
    MeSH term(s) Animals ; Cell Differentiation ; Endoderm/growth & development ; Hepatocytes/cytology ; Humans ; Liver/cytology ; Liver/growth & development ; Stem Cells/cytology
    Language English
    Publishing date 2013-05-29
    Publishing country United States
    Document type Journal Article ; Review
    ISSN 2040-4603
    ISSN (online) 2040-4603
    DOI 10.1002/cphy.c120022
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Role of Wnt/β-catenin signaling in liver metabolism and cancer.

    Monga, Satdarshan Pal Singh

    The international journal of biochemistry & cell biology

    2009  Volume 43, Issue 7, Page(s) 1021–1029

    Abstract: Wnt/β-catenin signaling is known for its role in embryogenesis as well as carcinogenesis. In the liver, it plays many critical roles during hepatic development and regeneration, and its dysregulation is evident in aberrant hepatic growth during various ... ...

    Abstract Wnt/β-catenin signaling is known for its role in embryogenesis as well as carcinogenesis. In the liver, it plays many critical roles during hepatic development and regeneration, and its dysregulation is evident in aberrant hepatic growth during various liver tumors. Its chief cellular roles in the liver include regulation of processes of cell proliferation, apoptosis, oxidative stress and differentiation, which in turn contributes to hepatic growth, zonation, xenobiotic metabolism and other metabolic processes inherent to the liver. Most of these functions of the Wnt/β-catenin signaling are dictated through the highly temporal and tissue-specific or non-specific transcriptional targets of the pathway. In addition, some of the critical functions such as cell-cell adhesion and perhaps maintenance of various junctions that are critical from an epithelial cell biology perspective are also a function of β-catenin, which is the central component of the canonical Wnt pathway. Various animal models and clinical studies have demonstrated the spectra of Wnt/β-catenin signaling in liver health and disease. Thus therapeutic modulation of this pathway for improved hepatic health is inevitable in the future. The current review discusses the advances in our understanding of the Wnt/β-catenin signaling in liver physiology and pathology especially in hepatic metabolism and various tumors in adult liver and goes on to extrapolate the pre-clinical significance and possible translational implications of such findings.
    MeSH term(s) Animals ; Cell Physiological Phenomena/physiology ; Focal Nodular Hyperplasia/metabolism ; Humans ; Liver/cytology ; Liver/embryology ; Liver/metabolism ; Liver Neoplasms/physiopathology ; Mice ; Mice, Transgenic ; Oxidative Stress/physiology ; Signal Transduction/physiology ; Wnt Proteins/metabolism ; beta Catenin/metabolism
    Chemical Substances Wnt Proteins ; beta Catenin
    Language English
    Publishing date 2009-09-09
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1228429-4
    ISSN 1878-5875 ; 1357-2725
    ISSN (online) 1878-5875
    ISSN 1357-2725
    DOI 10.1016/j.biocel.2009.09.001
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 431: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  3. Article ; Online: Impaired Bile Secretion Promotes Hepatobiliary Injury in Sickle Cell Disease.

    Vats, Ravi / Liu, Silvia / Zhu, Junjie / Mukhi, Dhanunjay / Tutuncuoglu, Egemen / Cardenes, Nayra / Singh, Sucha / Brzoska, Tomasz / Kosar, Karis / Bamne, Mikhil / Jonassaint, Jude / Adebayo Michael, Adeola / Watkins, Simon C / Hillery, Cheryl / Ma, Xiaochao / Nejak-Bowen, Kari / Rojas, Mauricio / Gladwin, Mark T / Kato, Gregory J /
    Ramakrishnan, Sadeesh / Sundd, Prithu / Monga, Satdarshan Pal / Pradhan-Sundd, Tirthadipa

    Hepatology (Baltimore, Md.)

    2020  Volume 72, Issue 6, Page(s) 2165–2181

    Abstract: Background and aims: Hepatic crisis is an emergent complication affecting patients with sickle cell disease (SCD); however, the molecular mechanism of sickle cell hepatobiliary injury remains poorly understood. Using the knock-in humanized mouse model ... ...

    Abstract Background and aims: Hepatic crisis is an emergent complication affecting patients with sickle cell disease (SCD); however, the molecular mechanism of sickle cell hepatobiliary injury remains poorly understood. Using the knock-in humanized mouse model of SCD and SCD patient blood, we sought to mechanistically characterize SCD-associated hepato-pathophysiology applying our recently developed quantitative liver intravital imaging, RNA sequence analysis, and biochemical approaches.
    Approach and results: SCD mice manifested sinusoidal ischemia, progressive hepatomegaly, liver injury, hyperbilirubinemia, and increased ductular reaction under basal conditions. Nuclear factor kappa B (NF-κB) activation in the liver of SCD mice inhibited farnesoid X receptor (FXR) signaling and its downstream targets, leading to loss of canalicular bile transport and altered bile acid pool. Intravital imaging revealed impaired bile secretion into the bile canaliculi, which was secondary to loss of canalicular bile transport and bile acid metabolism, leading to intrahepatic bile accumulation in SCD mouse liver. Blocking NF-κB activation rescued FXR signaling and partially ameliorated liver injury and sinusoidal ischemia in SCD mice.
    Conclusions: These findings identify that NF-κB/FXR-dependent impaired bile secretion promotes intrahepatic bile accumulation, which contributes to hepatobiliary injury of SCD. Improved understanding of these processes could potentially benefit the development of therapies to treat sickle cell hepatic crisis.
    MeSH term(s) Adolescent ; Adult ; Anemia, Sickle Cell/blood ; Anemia, Sickle Cell/complications ; Anemia, Sickle Cell/drug therapy ; Anemia, Sickle Cell/genetics ; Animals ; Bile/metabolism ; Bile Ducts, Intrahepatic/diagnostic imaging ; Bile Ducts, Intrahepatic/pathology ; Cholestasis/etiology ; Cholestasis/pathology ; Cholestasis/prevention & control ; Disease Models, Animal ; Female ; Gene Knock-In Techniques ; Hemoglobin, Sickle/genetics ; Hepatic Insufficiency/etiology ; Hepatic Insufficiency/pathology ; Hepatic Insufficiency/prevention & control ; Humans ; Intravital Microscopy ; Liver/diagnostic imaging ; Liver/pathology ; Male ; Mice ; Middle Aged ; NF-kappa B/antagonists & inhibitors ; NF-kappa B/drug effects ; NF-kappa B/metabolism ; Receptors, Cytoplasmic and Nuclear/metabolism ; Signal Transduction/drug effects ; Young Adult
    Chemical Substances Hemoglobin, Sickle ; NF-kappa B ; Receptors, Cytoplasmic and Nuclear ; farnesoid X-activated receptor (0C5V0MRU6P)
    Language English
    Publishing date 2020-11-13
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Video-Audio Media
    ZDB-ID 604603-4
    ISSN 1527-3350 ; 0270-9139
    ISSN (online) 1527-3350
    ISSN 0270-9139
    DOI 10.1002/hep.31239
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1660: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  4. Article ; Online: Dual catenin loss in murine liver causes tight junctional deregulation and progressive intrahepatic cholestasis.

    Pradhan-Sundd, Tirthadipa / Zhou, Lili / Vats, Ravi / Jiang, An / Molina, Laura / Singh, Sucha / Poddar, Minakshi / Russell, Jacquelyn / Stolz, Donna B / Oertel, Michael / Apte, Udayan / Watkins, Simon / Ranganathan, Sarangarajan / Nejak-Bowen, Kari N / Sundd, Prithu / Monga, Satdarshan Pal

    Hepatology (Baltimore, Md.)

    2018  Volume 67, Issue 6, Page(s) 2320–2337

    Abstract: β-Catenin, the downstream effector of the Wnt signaling, plays important roles in hepatic development, regeneration, and tumorigenesis. However, its role at hepatocyte adherens junctions (AJ) is relatively poorly understood, chiefly due to spontaneous ... ...

    Abstract β-Catenin, the downstream effector of the Wnt signaling, plays important roles in hepatic development, regeneration, and tumorigenesis. However, its role at hepatocyte adherens junctions (AJ) is relatively poorly understood, chiefly due to spontaneous compensation by γ-catenin. We simultaneously ablated β- and γ-catenin expression in mouse liver by interbreeding β-catenin-γ-catenin double-floxed mice and Alb-Cre transgenic mice. Double knockout mice show failure to thrive, impaired hepatocyte differentiation, cholemia, ductular reaction, progressive cholestasis, inflammation, fibrosis, and tumorigenesis, which was associated with deregulation of tight junctions (TJ) and bile acid transporters, leading to early morbidity and mortality, a phenotype reminiscent of progressive familial intrahepatic cholestasis (PFIC). To address the mechanism, we specifically and temporally eliminated both catenins from hepatocytes using adeno-associated virus 8 carrying Cre-recombinase under the thyroid-binding globulin promoter (AAV8-TBG-Cre). This led to a time-dependent breach of the blood-biliary barrier associated with sequential disruption of AJ and TJ verified by ultrastructural imaging and intravital microscopy, which revealed unique paracellular leaks around individual hepatocytes, allowing mixing of blood and bile and leakage of blood from one sinusoid to another. Molecular analysis identified sequential losses of E-cadherin, occludin, claudin-3, and claudin-5 due to enhanced proteasomal degradation, and of claudin-2, a β-catenin transcriptional target, which was also validated in vitro.
    Conclusion: We report partially redundant function of catenins at AJ in regulating TJ and contributing to the blood-biliary barrier. Furthermore, concomitant hepatic loss of β- and γ-catenin disrupts structural and functional integrity of AJ and TJ via transcriptional and posttranslational mechanisms. Mice with dual catenin loss develop progressive intrahepatic cholestasis, providing a unique model to study diseases such as PFIC. (Hepatology 2018;67:2320-2337).
    MeSH term(s) Adherens Junctions ; Animals ; Cholestasis, Intrahepatic/etiology ; Female ; Hepatocytes ; Male ; Mice ; Mice, Knockout ; Tight Junctions ; beta Catenin/genetics ; beta Catenin/physiology ; gamma Catenin/genetics ; gamma Catenin/physiology
    Chemical Substances beta Catenin ; gamma Catenin
    Language English
    Publishing date 2018-04-19
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 604603-4
    ISSN 1527-3350 ; 0270-9139
    ISSN (online) 1527-3350
    ISSN 0270-9139
    DOI 10.1002/hep.29585
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1660: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  5. Article: Selective targeting of α

    Gupta, Biki / Rai, Ravi Prakash / Pal, Pabitra B / Chaudhary, Sudrishti / Chiaro, Anna / Seaman, Shannon / Singhi, Aatur D / Monga, Satdarshan P / Iyer, Smita S / Raeman, Reben

    bioRxiv : the preprint server for biology

    2023  

    Abstract: ... Integrin ... ...

    Abstract Integrin α
    Language English
    Publishing date 2023-05-31
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.02.20.528201
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: Western diet dampens T regulatory cell function to fuel hepatic inflammation in nonalcoholic fatty liver disease.

    Chaudhary, Sudrishti / Rai, Ravi / Pal, Pabitra B / Tedesco, Dana / Singhi, Aatur D / Monga, Satdarshan P / Grakoui, Arash / Iyer, Smita S / Raeman, Reben

    bioRxiv : the preprint server for biology

    2023  

    Abstract: Background and aims: The immunosuppressive T regulatory cells (Tregs) regulate immune responses and maintain immune homeostasis, yet their functions in nonalcoholic fatty liver disease (NAFLD) pathogenesis remains controversial.: Methods: Mice were ... ...

    Abstract Background and aims: The immunosuppressive T regulatory cells (Tregs) regulate immune responses and maintain immune homeostasis, yet their functions in nonalcoholic fatty liver disease (NAFLD) pathogenesis remains controversial.
    Methods: Mice were fed a normal diet (ND) or a western diet (WD) for 16 weeks to induce NAFLD. Diphtheria toxin injection to deplete Tregs in Foxp3
    Results: WD triggered accumulation of adaptive immune cells, including Tregs and effector T cells, within the liver parenchyma. This pattern was also observed in NASH patients, where an increase in intrahepatic Tregs was noted. In the absence of adaptive immune cells in Rag1 KO mice, WD promoted accumulation of intrahepatic neutrophils and macrophages and exacerbated hepatic inflammation and fibrosis. Similarly, targeted Treg depletion exacerbated WD-induced hepatic inflammation and fibrosis. In Treg-depleted mice, hepatic injury was associated with increased accumulation of neutrophils, macrophages, and activated T cells within the liver. Conversely, induction of Tregs using recombinant IL2/αIL2 mAb cocktail reduced hepatic steatosis, inflammation, and fibrosis in WD-fed mice. Analysis of intrahepatic Tregs from WD-fed mice revealed a phenotypic signature of impaired Treg function in NAFLD.
    Conclusions: Our findings indicate that the liver microenvironment in NAFLD impairs ability of Tregs to suppress effector immune cell activation, thus perpetuating chronic inflammation and driving NAFLD progression. These data suggest that targeted approaches aimed at restoring Treg function may represent a potential therapeutic strategy for treating NAFLD.
    Lay summary: In this study, we elucidate the mechanisms contributing to the perpetuation of chronic hepatic inflammation in nonalcoholic fatty liver disease (NAFLD). We show that dietary sugar and fatty acids promote chronic hepatic inflammation in NAFLD by impairing immunosuppressive function of regulatory T cells. Finally, our preclinical data suggest that targeted approaches aimed at restoring T regulatory cell function have the potential to treat NAFLD.
    Language English
    Publishing date 2023-03-25
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.03.23.533977
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article: Role of Wnt/β-catenin signaling in liver metabolism and cancer

    Monga, Satdarshan Pal Singh

    international journal of biochemistry & cell biology

    Volume v. 43,, Issue no. 7

    Abstract: Wnt/β-catenin signaling is known for its role in embryogenesis as well as carcinogenesis. In the liver, it plays many critical roles during hepatic development and regeneration, and its dysregulation is evident in aberrant hepatic growth during various ... ...

    Abstract Wnt/β-catenin signaling is known for its role in embryogenesis as well as carcinogenesis. In the liver, it plays many critical roles during hepatic development and regeneration, and its dysregulation is evident in aberrant hepatic growth during various liver tumors. Its chief cellular roles in the liver include regulation of processes of cell proliferation, apoptosis, oxidative stress and differentiation, which in turn contributes to hepatic growth, zonation, xenobiotic metabolism and other metabolic processes inherent to the liver. Most of these functions of the Wnt/β-catenin signaling are dictated through the highly temporal and tissue-specific or non-specific transcriptional targets of the pathway. In addition, some of the critical functions such as cell–cell adhesion and perhaps maintenance of various junctions that are critical from an epithelial cell biology perspective are also a function of β-catenin, which is the central component of the canonical Wnt pathway. Various animal models and clinical studies have demonstrated the spectra of Wnt/β-catenin signaling in liver health and disease. Thus therapeutic modulation of this pathway for improved hepatic health is inevitable in the future. The current review discusses the advances in our understanding of the Wnt/β-catenin signaling in liver physiology and pathology especially in hepatic metabolism and various tumors in adult liver and goes on to extrapolate the pre-clinical significance and possible translational implications of such findings.
    Keywords apoptosis ; metabolism ; animal models ; clinical trials ; transcription (genetics) ; oxidative stress ; embryogenesis ; translation (genetics) ; cell proliferation ; carcinogenesis ; liver neoplasms ; adults ; liver ; cell adhesion ; epithelial cells
    Language English
    Document type Article
    ISSN 1357-2725
    Database AGRIS - International Information System for the Agricultural Sciences and Technology

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