First Author | Azouz A | Year | 2020 |
Journal | BMC Res Notes | Volume | 13 |
Issue | 1 | Pages | 301 |
PubMed ID | 32580758 | Mgi Jnum | J:290835 |
Mgi Id | MGI:6436994 | Doi | 10.1186/s13104-020-05130-1 |
Citation | Azouz A, et al. (2020) Post-developmental extracellular proteoglycan maintenance in attractin-deficient mice. BMC Res Notes 13(1):301 |
abstractText | OBJECTIVE: Neurodegeneration and hair pigmentation alterations in mice occur consequent to aberrations at the Atrn locus coding for the transmembrane form of attractin. Earlier results pointed to a possible involvement in intracellular trafficking/export of secretory vesicles containing proteoglycan. Here we examined kidney and liver, both heavily dependent upon proteoglycan, of attractin-deficient mice to determine whether abnormalities were observed in these tissues. RESULTS: Histological and histochemical analysis to detect glycosylated protein identified a severe loss in attractin-deficient mice of extracellular proteoglycan between kidney tubules in addition to a loss of glycosylated material within the intratubular brush border. In the liver, extracellular matrix material was significantly depleted between hepatocytes together with swollen sinuses and aberrations in the proteoglycan-dependent space of Disse. These results are consistent with a generalized defect in extracellular proteoglycan deposition in Atrn-mutant mice and support previous reports suggesting a role for attractin in the secretory vesicle pathway. |