| First Author | Komazaki S | Year | 1998 |
| Journal | Cell Tissue Res | Volume | 294 |
| Issue | 3 | Pages | 467-73 |
| PubMed ID | 9799464 | Mgi Jnum | J:113063 |
| Mgi Id | MGI:3664396 | Doi | 10.1007/s004410051198 |
| Citation | Komazaki S, et al. (1998) Morphological abnormalities of adrenal gland and hypertrophy of liver in mutant mice lacking ryanodine receptors. Cell Tissue Res 294(3):467-73 |
| abstractText | Ryanodine receptors (RyRs), which form Ca2+ channels in the membrane of the endoplasmic reticulum, consist of three subtypes (RyR1, RyR2, and RyR3). The RyRs release Ca2+ from the endoplasmic reticulum into the cytoplasm and thus play an important role, especially in the contraction of skeletal and cardiac muscle cells. The genes of these RyRs are also expressed in many non-muscle tissues, but the role played by RyRs in non-muscle cells is not fully understood. In the present study, we examined the morphological changes in such cells caused by a deficiency of RyRs genes using three mutant mice lacking RyR1, RyR3, or both RyR1 and RyR3. The results showed morphological abnormalities in the adrenal cortical cells in all three mutant mice. In addition, an excessive accumulation of glycogen granules in hepatic cells, and a hypertrophy of the liver were both present in those mutant mice lacking both RyR1 and RyR3. We discuss the relationship between the morphological abnormalities of the adrenal cortex and liver induced by a deficiency of RyRs, and the possible causes of these abnormalities. |
