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Post-developmental extracellular proteoglycan maintenance in attractin-deficient mice
Abdallah Azouz1, Jonathan S Duke-Cohan2,3
1Department of Pathology, Regional One Health, University of Tennessee Health Science Center, Memphis, TN, USA.
BMC Research Notes
|June 26, 2020
Summary
Attractin deficiency in mice causes significant loss of extracellular proteoglycans in the kidney and liver. This study supports attractin's role in proteoglycan transport and deposition.
Area of Science:
- Molecular Biology
- Cell Biology
- Genetics
Background:
- Aberrations at the attractin (Atrn) locus cause neurodegeneration and hair pigmentation changes in mice.
- Attractin is a transmembrane protein potentially involved in intracellular trafficking of secretory vesicles containing proteoglycans.
Purpose of the Study:
- To investigate the role of attractin in proteoglycan deposition.
- To examine kidney and liver tissues of attractin-deficient mice for abnormalities.
Main Methods:
- Histological analysis of kidney and liver tissues.
- Histochemical staining to detect glycosylated proteins and proteoglycans.
Main Results:
- Attractin-deficient mice showed a severe loss of extracellular proteoglycans between kidney tubules.
- A reduction in glycosylated material was observed in the kidney's intratubular brush border.
- The liver exhibited depleted extracellular matrix material between hepatocytes, swollen sinuses, and aberrations in the space of Disse.
Conclusions:
- Attractin deficiency leads to a generalized defect in extracellular proteoglycan deposition.
- These findings support attractin's involvement in the secretory vesicle pathway and proteoglycan transport.
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