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 Concept Videos

You might also read

Related Articles

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

Sort by
Same author

Comparative efficacy of Gum Arabic (<i>Acacia senegal</i>) and <i>Tribulus terrestris</i> on male fertility.

Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society·2021
Same author

Annexin A7 Regulates Endometrial Receptivity.

Frontiers in cell and developmental biology·2020
Same author

Klotho Deficiency Induces Arteriolar Hyalinosis in a Trade-Off with Vascular Calcification.

The American journal of pathology·2019
Same author

Garcinol A Novel Inhibitor of Platelet Activation and Apoptosis.

Toxins·2019
Same author

Genetic deficiency of the tumor suppressor protein p53 influences erythrocyte survival.

Apoptosis : an international journal on programmed cell death·2018
Same author

Heterotrimeric G-protein subunit Gα<sub>i2</sub> contributes to agonist-sensitive apoptosis and degranulation in murine platelets.

Physiological reports·2018

Related Experiment Video

Updated: May 4, 2026

A Uniform Shear Assay for Human Platelet and Cell Surface Receptors via Cone-plate Viscometry
04:32

A Uniform Shear Assay for Human Platelet and Cell Surface Receptors via Cone-plate Viscometry

Published on: June 5, 2019

7.1K

Sgk1 sensitive pendrin expression in murine platelets.

Lisann Pelzl1, Hajar Fakhri, Anja T Umbach

  • 1Department of Physiology, University of Tübingen, Tübingen, Germany.

Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology
|January 17, 2014
PubMed
Summary

Pendrin (SLC26A4) is found in platelets and its expression is increased by mineralocorticoids, likely through the action of SGK1. This study reveals a new role for pendrin in platelet regulation.

More Related Videos

Megakaryocyte Differentiation and Platelet Formation from Human Cord Blood-derived CD34+ Cells
09:46

Megakaryocyte Differentiation and Platelet Formation from Human Cord Blood-derived CD34+ Cells

Published on: December 27, 2017

19.4K
Leukodepletion Filters-Derived CD34+ Cells As a Cell Source to Study Megakaryocyte Differentiation and Platelet Formation
06:57

Leukodepletion Filters-Derived CD34+ Cells As a Cell Source to Study Megakaryocyte Differentiation and Platelet Formation

Published on: May 20, 2021

3.6K

Related Experiment Videos

Last Updated: May 4, 2026

A Uniform Shear Assay for Human Platelet and Cell Surface Receptors via Cone-plate Viscometry
04:32

A Uniform Shear Assay for Human Platelet and Cell Surface Receptors via Cone-plate Viscometry

Published on: June 5, 2019

7.1K
Megakaryocyte Differentiation and Platelet Formation from Human Cord Blood-derived CD34+ Cells
09:46

Megakaryocyte Differentiation and Platelet Formation from Human Cord Blood-derived CD34+ Cells

Published on: December 27, 2017

19.4K
Leukodepletion Filters-Derived CD34+ Cells As a Cell Source to Study Megakaryocyte Differentiation and Platelet Formation
06:57

Leukodepletion Filters-Derived CD34+ Cells As a Cell Source to Study Megakaryocyte Differentiation and Platelet Formation

Published on: May 20, 2021

3.6K

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Physiology

Background:

  • Pendrin (SLC26A4) is a crucial anion exchanger involved in inner ear development, thyroid function, and epithelial transport.
  • Deficiency in SLC26A4 causes Pendred syndrome, characterized by hearing loss and thyroid abnormalities.
  • Mineralocorticoids like deoxycorticosterone (DOCA) up-regulate pendrin expression in various organs, but its role and regulation in platelets are unknown.

Purpose of the Study:

  • To investigate the expression and regulation of pendrin (SLC26A4) in murine platelets.
  • To determine the role of serum and glucocorticoid inducible kinase 1 (SGK1) in the mineralocorticoid-mediated regulation of platelet pendrin.

Main Methods:

  • Quantitative reverse transcription polymerase chain reaction (RT-qPCR) to measure Slc26a4 mRNA levels.
  • Western blotting to assess Slc26a4 protein abundance.
  • Experiments using gene-targeted mice lacking Sgk1 (sgk1(-/-)) and wild-type (sgk1(+/+)) mice, with and without DOCA treatment.

Main Results:

  • Pendrin (Slc26a4) is expressed in platelets.
  • Both in vitro and in vivo DOCA treatment increased Slc26a4 mRNA levels in wild-type platelets.
  • DOCA-induced upregulation of Slc26a4 mRNA and protein was dependent on the presence of Sgk1.
  • Sgk1 mRNA levels increased in parallel with Slc26a4 mRNA levels in wild-type platelets.

Conclusions:

  • Pendrin is expressed in platelets.
  • Platelet pendrin expression is regulated by mineralocorticoids (DOCA) in an SGK1-dependent manner.
  • These findings suggest a novel role for pendrin and SGK1 in platelet physiology.