Loutit J F, Sansom J M
Calcif Tissue Res. 1976 Jun 14;20(3):251-9. doi: 10.1007/BF02546413.
The recessive genes mi and gl in the homozygous state determine, among other phenotypic effects, osteopetrosis in the house mouse. From a stock carrying mi derived from Grüneberg (1963) the mi gene was bred into the standard CBA/H inbred strain. Microphthalmic mice of these two stocks and their hybrids were treated as newborn by intraperitoneal injection and at weaning or maturity by intravenous injection of cell suspensions containing hematopoietic stem cells from phenotypically normal mice. Resolution of much of the osteopetrosis but not the other phenotypic effects occurred within a few months in the majority of cases, provided syngeneic or H-2 compatible allogeneic cells were given: it did not occur spontaneously or on giving H-2 incompatible cells or on giving compatible material by an inappropriate route. The results accord with hypotheses that (1) osteoclasis of scaffoldtype woven bone is impaired in mi mi, (2) that osteoclastic cells are derived through circulating monocytes from hematopoietic stem cells, and (3) in mi mi this defect can be overcome by a transplant of normal hemopoietic stem cells.
纯合状态下的隐性基因mi和gl，除了其他表型效应外，还决定家鼠的骨质石化症。从源自格伦贝格（1963年）的携带mi的品系中，将mi基因培育到标准CBA/H近交系中。这两个品系的小眼小鼠及其杂种在新生时通过腹腔注射进行处理，在断奶或成熟时通过静脉注射含有来自表型正常小鼠的造血干细胞的细胞悬液进行处理。在大多数情况下，只要给予同基因或H-2相容的异基因细胞，大部分骨质石化症会在几个月内得到缓解，但其他表型效应不会缓解：骨质石化症不会自发缓解，给予H-2不相容的细胞或通过不适当途径给予相容材料时也不会缓解。这些结果符合以下假设：（1）在mi mi中，支架型编织骨的破骨作用受损；（2）破骨细胞通过循环单核细胞源自造血干细胞；（3）在mi mi中，这种缺陷可以通过移植正常造血干细胞来克服。
