CD45 antigen (leukocyte common antigen), a unique and ubiquitous membrane glycoprotein with a molecular mass of about 200 kDa, is expressed on almost all hematopoietic cells except for mature erythrocytes. However, the biological function of this glycoprotein still remains to be resolved. In order to clarify the role of CD45 antigen in hematopoietic cell differentiation and function, its expression on human leukemia lymphoma cell lines was studied by membrane immunofluorescence. Thirty eight established cell lines were analyzed using T29–33, a monoclonal antibody (MoAb) that recognizes the common epitopes of this glycoprotein molecule. Conventional cell marker studies were also carried out on these cell lines to compare their CD45 expression. It was shown that CD45 expression varies among B lineage cells depending on cell differentiation, in contrast to its stable expression on leukemic T cell (6/6, positive) and myeloid (5/5, positive) lineage cell lines. On the other hand, only two out of six histiomonocytoid lineage cell lines were positive. Human T cell leukemia lymphoma virus type I (HTLV‐I) associated T cell lines derived from peripheral blood leukocytes of patients with adult T cell leukernia/ lymphoma (ATL/L) in Japan did not express CD45 on their cell surface. Taken together, these observations suggest that CD45 has a functional role in hematopoietic cell activation and differentiation. Acta Pathol Jpn 40: 107–115, 1990.
In this study, we established a unique cell line, HPB-AML-I (AML-I), from peripheral blood mononuclear cells collected from a patient with acute myeloid leukemia (AML: M1). Morphological and phenotypical analyses of the established AML-I cells demonstrated that they belong to a preadipocyte cell line as indicated by their storage of lipid droplets and expression of surface antigens similar to those found on bone marrow stromal cells (MSC). Through cell culture under adipogenic conditions, effective differentiation of AML-I cells into adipocytes was induced by an adipogenesis inducing cocktail (INC) made up of a mixture of methylisobutylxanthine, hydrocortisone, and indomethacin. By contrast, activation of peroxisome proliferator-activated receptor (PPARgamma), which plays a key role in lipids metabolism and is highly expressed in AML-I cells, decreased the number of lipid droplets in AML-I cells. Here we report the establishment of a unique human derived-preadipocyte cell line, AML-I, and its bi-directional adipogenic response to different type stimulation, i.e., one is a refractory response to troglitazone, a well-known adipogenic stimulator, and a positive response to INC, an adipogenesis induction cocktail. These results suggest that, based on the adipogenic response, there might be some distinct lineages in human adipocytes and that the unique differentiation of AML-I cells should be useful for analyzing both the differentiation and regulation of human preadipocytes.
We describe a novel genetic variant mouse that exhibited ataxia and male sterility, named the AMS mouse. It arose in autoimmune-prone MRL/lpr strain and putative ams mutation showed an autosomal recessive inheritance pattern. Clinical symptoms were first discernible at approximately 21 days of age and consisting of subtle sway of the trunk followed by failure to maintain still posture and appearance of abnormal walk, but no further worsening was noted with advancement of age. The abnormal motor coordination was ascribed to almost complete loss of Purkinje cells of the cerebellum. The cell loss in the Purkinje cell layer began before onset of ataxia and rapidly progressed towards near-complete loss by 6 weeks of age. Another symptom was male sterility due to severe oligozoospermia associated with cellular degeneration during spermatic differentiation in the seminiferous tubules. Thus, the effects of the genetic variation were apparent in two different organs after the development of their basic histological structures, and degeneration and loss of particular cell types in these two tissues produced overt clinical symptoms. Genetic pleiotropism, provided that the nature of genetic variation is of a single gene mutation, is discussed.
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