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           Search results for: Monoclonal Anti c kit SCF Receptor produced in mouse    

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Distinct stages of melanocyte differentiation revealed by anlaysis of nonuniform pigmentation patterns.

The injection of an antagonistic anti-murine c-kit monoclonal antibody ACK2 during mouse embryonic development produced three distinctive pigmentation patterns on the coat of the offspring. Pattern 1 consisted of pigmentation in craniofacial and caudal regions and was induced by an ACK2 injection between 9.5 and 11.5 days post coitum (dpc). In pattern 2, the entire coat was unpigmented and was induced by the injection at around 13.0 dpc. Pattern 3 consisted of pigmented patches spreading ventrolaterally from the dorsoanterior trunk regions towards the anterior and posterior directions and it was induced by ACK2 administered at 14.5-15.0 dpc. We investigated the embryological basis of these nonuniform pigmentation patterns to elucidate the process of melanoblast differentiation between lineage commitment and colonization into developing hair follicles. The results showed the following. (1) Melanocyte differentiation at the embryonic stage from 10.5 to 12.5 dpc progresses in a spatially nonuniform fashion, being faster in the craniofacial and caudal regions than in the trunk; pattern 1 reflects this. (2) Melanoblasts are activated to proliferate synchronously upon entering into the epidermis; pattern 2 correlates with this process. (3) c-kit functions as a survival signal for proliferating melanoblasts in the epidermis. (4) The melanoblasts that enter developing hair follicles can survive without a c-kit signal; pattern 3 essentially represents the hair follicles colonized by these cells. Analysis of the melanoblast distribution of ls/ls embryos that bear a loss-of-function mutation in the endothelin 3 gene suggested that endothelin 3 is required for early melanoblast differentiation before entering into the epidermis, whereas proliferation in the epidermis takes place without this molecule. Based on these data, we propose 4 distinct steps of embryonic melanocyte differentiation: (1) migration in the dermis, which requires both c-kit and endothelin 3; (2) a state before epidermal entry that is resistant to anti-c-kit mAb; (3) cell proliferation after entering the epidermal layer, which requires c-kit and endothelin receptor B but not endothelin 3 and (4) integration into developing hair follicles, which renders melanoblasts resistant to anti-c-kit mAb. Thus, melanoblast differentiation proceeds by alternately repeating c-kit -dependent and c-kit-independent stages and c-kit functions as a survival factor for the proliferating melanoblasts.

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Ofloxacin CAS Number [824 Epidermal Growth Factor ( Mesenchymal Stem Cell Ost Rabbit Anti-IEX1 Differen Rabbit Anti-IEX1 Differen Prostate cancer tissue ar Human Growth and Differen Rabbit Anti-IEX1 Differen Rabbit Anti-IEX1 Differen Goat Anti- T-cell differe Growth Differentiation Fa Rabbit Anti-IEX1 Differen

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Functional hierarchy of c-kit and c-fms in intramarrow production of CFU-M.

Whereas the molecular natures of M-CSF/CSF-1 and its receptor c-fms are well characterized, its actual role in the intramarrow hematopoiesis remains obscure. This is because disruption of this signaling pathway results in the osteopetrosis mouse that lacks the bone cavity for hematopoiesis. To elucidate the role of c-fms in intramarrow hematopoiesis, we produced an antagonistic monoclonal antibody to murine c-fms and investigated its expression and function in the normal bone marrow. c-fms+ cells were detected both in mature and immature hematopoietic cells. Morphologically, c-kit+c-fms-, c-kit+c-fms+ and c-kit-c-fms+ cells were medium sized blasts, large promyelocytes with azurophilic granules and mature monocytes respectively. CFU-M was 10-fold more enriched in the c-kit+c-fms- than c-kit+c-fms+ fraction. Moreover, injection of the anti c-fms antibody had no effect on the production of CFU-M in the bone marrow, while anti-c-kit mAb could deplete them. As c-kit+c-fms+ cells were readily generated in the culture of c-kit+c-fms- cells, most of the CFU-M in the bone marrow are, in fact, c-fms- cells that differentiate into c-fms+ upon culture. These observations indicate a clear functional hierarchy of c-kit and c-fms in the bone marrow. Namely, c-kit plays the primary role in the production and maintenance of CFU-M, while c-fms, though it co-expressed with c-kit and functions as the growth receptor for M-CSF in the culture, has only a minimum role in the proliferation of c-fms+ cells in the bone marrow.

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Effects of monoclonal anti-c-kit antibody (ACK2) on melanocytes in newborn mice.

Previous studies indicate that c-Kit is required for postnatal melanocyte development. To understand the precise mechanisms of c-Kit dependence, we studied melanocyte development in newborn C57BL/6 mice by means of peritoneal injection of a monoclonal anti-c-Kit antibody (ACK2), which blocks c-Kit functions. The mice were injected once or more with ACK2 at various intervals after birth. In experiment 1, skin samples were examined on day 10 post-partum and in experiment 2 they were examined daily until day 10 post-partum. We studied melanocytes in the hair follicles, epidermis, and dermis by light and electron microscopy with dopa reactions and immunohistochemistry. Epidermal melanocytes in untreated mice were dopa negative and c-Kit positive on day 0 post-partum but became dopa positive soon thereafter. In ACK2-treated mice, the earlier the mice received ACK2 injections after birth, the fewer melanocytes they had, not only in the epidermis, but also in follicles. In these mice, melanocytes that had undergone apoptosis in the dermis and the follicles were detected ultrastructurally. Some appeared to have produced tyrosinase, because they had dopa-positive melanosomes. These results suggest that melanocytes in newborn mice are c-Kit dependent and undergo apoptosis when c-Kit receptors are blocked by ACK2 in the early days after birth. During this c-Kit-dependent period, melanocytes differentiate from dopa negative to positive and migrate from the epidermis to hair follicles.

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Characterization of chicken kit tyrosine kinase receptor in Cos cell transfectants and in chicken brain.

The Kit tyrosine kinase (Kit) encoded by the c-kit proto-oncogene is a receptor for stem cell factor (SCF). Kit proteins of mice and humans are expressed in various kinds of hematopoietic progenitor cells and are essential for the growth of these cells. Wild-type chKit (chKit+) and a mutant chKit (chKit42) that contained an amino acid change from Asp777 to Asn corresponding to that in Kit of the W42 mutant mice were produced in Cos-1 cells transfected with expression plasmids containing the chicken c-kit cDNA, and characterized using two kinds of anti-chKit antisera. The W42 mutant Kit has previously been shown to be defective for kinase activity. The chKit+ of 145 kilodalton (kDa) and 130 kDa with varying degrees of N-linked glycosylation were detected. Western blot analysis using an anti-phosphotyrosine monoclonal antibody showed that autophosphorylation of chKit+ was greatly enhanced upon chicken SCF induction. The chKit+ did not respond to mouse SCF. The kinase activity of chKit42 was abolished by the amino acid substitution, indicating the Asp777 residue was essential for the activity. In addition, 145 kDa chKit conjugated with sialic acid residue(s) was detected in chicken brain by immunoprecipitation using the antisera. An in vitro kinase assay showed the kinase activity of this protein. These structural and functional similarities of chKit to mammalian Kit proteins shown in this study implicate a possible role of chKit in chicken hematopoietic system.

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A murine stromal cell line promotes the proliferation of the human factor-dependent leukemic cell line UT-7.

In long-term human bone marrow cultures, stromal cells of human origin are usually used on the assumption that human primitive progenitor cells do not respond to cytokines produced by stromal cells from other species. There is accumulating evidence, however, that murine stromal cells also promote maintenance and differentiation of very primitive human stem cells, which suggests the existence of novel stromal activities that cross species barriers. In this study, we show that a murine bone marrow-derived stromal cell line, MS-5, allows the proliferation of the human leukemic cell line UT-7. The long-term growth of UT-7 is usually supported only by human interleukin-3 (IL-3), granulocyte-macrophage colony-stimulating factor (GM-CSF), or erythropoietin (Epo). None of these three cytokines was involved in the observed effect, since murine GM-CSF and IL-3 do not act on human cells and MS-5 cells do not produce Epo. Soluble stem cell factor (SCF) induced UT-7 cell proliferation. However, S1/S1 mutant fibroblasts also supported UT-7 cell growth and anti-c-kit antibodies only partially abolished UT-7 cell proliferative response to MS-5 cells. These observations excluded a major role of SCF in this system. MS-5-derived growth-promoting activity was diffusible, but attempts to grow UT-7 cells in high levels of known soluble murine stromal-derived cytokines active on human cells showed no or minimal response, suggesting that MS-5's proliferative effect was not mediated by known cytokines. Finally, involvement of an autocrine loop of activation induced by MS-5 was excluded: RT-PCR analysis did not detect increased transcripts for GM-CSF, IL-3, IL-6, SCF, or Epo in UT-7 cells cocultured for 2 to 6 days with MS-5. In addition, UT-7 cell proliferation on MS-5 was not inhibited by neutralizing antibodies against the human GM-CSF receptor or the human IL-6 receptor alpha chain. Whether UT-7 cell proliferation triggered by MS-5 reflects the existence of novel stromal cytokines or results from synergistic interactions on the MS-5 cell surface between extracellular matrix proteins and cytokines will require further investigation.

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