Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

The human liver in extrahepatic cholestasis: ultrastructural morphometric data.

A M Jezequel, M L Librari, P G Mosca

    Liver
    |October 1, 1983
    PubMed
    Summary

    Extrahepatic cholestasis in humans does not cause smooth endoplasmic reticulum hypertrophy. Instead, increased mitochondrial cristae surface density is an early liver cell response to biliary pathway alterations.

    Related Concept Videos

    You might also read

    Related Articles

    Articles linked to this work by shared authors, journal, and citation graph.

    Sort by
    Same author

    The economic burden of pediatric growth hormone deficiency in Italy: a cost of illness study.

    Journal of endocrinological investigation·2024
    Same author

    Are severity and location of facial trauma risk factors for cervical spine injuries? 10-year analysis based on the use of the AO spine injury classification and the comprehensive facial injury (CFI) score.

    European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society·2023
    Same author

    Impact of the COVID-19 pandemic on surgery for thyroid cancer in Italy: nationwide retrospective study.

    The British journal of surgery·2021
    Same author

    LOX-1 and cancer: an indissoluble liaison.

    Cancer gene therapy·2021
    Same author

    TNFAIP3 Gene Polymorphisms in Three Common Autoimmune Diseases: Systemic Lupus Erythematosus, Rheumatoid Arthritis, and Primary Sjogren Syndrome-Association with Disease Susceptibility and Clinical Phenotypes in Italian Patients.

    Journal of immunology research·2019
    Same author

    Clusterin silencing restores myoblasts viability and down modulates the inflammatory process in osteoporotic disease.

    Journal of translational medicine·2019

    Area of Science:

    • Hepatology
    • Cell Biology
    • Pathology

    Background:

    • Extrahepatic cholestasis is a condition characterized by impaired bile flow.
    • Previous studies suggested smooth endoplasmic reticulum (SER) hypertrophy in cholestasis.
    • The role of cellular organelle changes in human cholestasis requires further elucidation.

    Purpose of the Study:

    • To quantitatively analyze ultrastructural changes in hepatocytes of jaundiced patients with extrahepatic cholestasis.
    • To investigate the surface density of the smooth endoplasmic reticulum (SER), rough endoplasmic reticulum (RER), peroxisomes, and mitochondrial cristae.
    • To determine if SER hypertrophy occurs in human hepatocytes during extrahepatic cholestasis.

    Main Methods:

    • Quantitative morphometric analysis of needle liver biopsies.

    Related Experiment Videos

  • Examination of five jaundiced patients with extrahepatic cholestasis.
  • Measurement of the surface density of various cellular organelles, including SER, RER, peroxisomes, and mitochondrial cristae.

    • Main Results:

    • The surface density of SER remained within the normal range in all patients, regardless of jaundice duration.
    • Elevated RER surface density was observed in three out of five patients.
    • An increased surface density of mitochondrial cristae was a consistent finding across all subjects, without changes to the outer mitochondrial membrane.

    Conclusions:

    • The study fails to provide evidence for SER hypertrophy in human hepatocytes during extrahepatic cholestasis.
    • Increased mitochondrial cristae surface density is an early and constant phenomenon in extrahepatic cholestasis.
    • This mitochondrial alteration may represent a fundamental liver cell response to disruptions in bile synthesis or excretion pathways.