{"id":{"repo_id":"uiuc","oai_identifier":"oai:www.ideals.illinois.edu:2142/19576"},"canonical_url":"https://search.dev.ndltd.org/etd/uiuc/oai:www.ideals.illinois.edu:2142/19576","repository":{"repo_id":"uiuc","name":"University of Illinois - Urbana-Champaign","base_url":"https://www.ideals.illinois.edu/oai-pmh"},"display":{"title":"Molecular interactions among insulin-like growth factor, its receptor and binding proteins on myeloid cells","abstract":"Atrophic thymus glands from old rats contained a greater population of CD4$\\sp-$CD8$\\sp-$ cells and a reduced percentage of CD4$\\sp+$CD8$\\sp+$ lymphocytes compared to those of young rats. These age-associated changes could be reversed by implanting the growth hormone (GH) secreting cells, GH$\\sb3$. To understand the molecular mechanism by which insulin-like growth factor-I (IGF-I), a mediator of GH's action, acts on cells of immune system, the expression of IGF-I, IGF-I receptor (IGF-IR) and IGF binding proteins (IGFBP) in myeloid cells were studied. Human myeloid cell lines expressed IGF-I mRNA and probably secreted IGF-I peptides as evidenced by suppression of basal proliferation by an antibody to IGF-IR. Expression of the IGF-IR on myeloid cells was required for enhanced proliferation caused by both exogenous IGF-I and IGF-II. IGFBP-3 also inhibited IGF-I-induced cell proliferation. Furthermore, thymus and spleen contained IGFBPs. Among leukocytes, IGFBPs were primarily expressed in myeloid cells and their expression increased as myeloid cells were differentiated into mature macrophages. IGFBP levels from activated macrophages were down-regulated by proteases from these cells. Affinity cross-linking and protein binding immunomobility-shift assays, as well as Northern blotting, identified the 25 kDa IGFBP as IGFBP-4 that was expressed in a thymic macrophage cell line (TMC). TMC cells secrete IGFBP-4 at approximately 373 ng/10$\\sp7$ cells/day as determined by ligand blot followed by PhosphorImager analysis. RT-PCR amplification of TMC mRNA with primers designed from rat and human IGFBP-4 sequences produced a 278 bp putative murine IGFBP-4 cDNA fragment which corresponded to 40% of the coding region. DNA sequencing revealed that this murine IGFBP-4 cDNA differed from the rat sequence at 6 residues (97% homology), but the deduced amino acid sequence was identical to that of the rat sequence. These results show that myeloid cells are the primary hematopoietic cells that synthesize and secrete IGFBP in leukocytes and that IGF-I together with IGFBP act in an autocrine fashion on these cells. Macrophage-derived IGFBP-4 may be a key regulator for the access of IGF-I to myeloid cells in thymic development and hematopoiesis.","abstract_html":"Atrophic thymus glands from old rats contained a greater population of CD4$\\sp-$CD8$\\sp-$ cells and a reduced percentage of CD4$\\sp+$CD8$\\sp+$ lymphocytes compared to those of young rats. These age-associated changes could be reversed by implanting the growth hormone (GH) secreting cells, GH$\\sb3$. To understand the molecular mechanism by which insulin-like growth factor-I (IGF-I), a mediator of GH's action, acts on cells of immune system, the expression of IGF-I, IGF-I receptor (IGF-IR) and IGF binding proteins (IGFBP) in myeloid cells were studied. Human myeloid cell lines expressed IGF-I mRNA and probably secreted IGF-I peptides as evidenced by suppression of basal proliferation by an antibody to IGF-IR. Expression of the IGF-IR on myeloid cells was required for enhanced proliferation caused by both exogenous IGF-I and IGF-II. IGFBP-3 also inhibited IGF-I-induced cell proliferation. Furthermore, thymus and spleen contained IGFBPs. Among leukocytes, IGFBPs were primarily expressed in myeloid cells and their expression increased as myeloid cells were differentiated into mature macrophages. IGFBP levels from activated macrophages were down-regulated by proteases from these cells. Affinity cross-linking and protein binding immunomobility-shift assays, as well as Northern blotting, identified the 25 kDa IGFBP as IGFBP-4 that was expressed in a thymic macrophage cell line (TMC). TMC cells secrete IGFBP-4 at approximately 373 ng/10$\\sp7$ cells/day as determined by ligand blot followed by PhosphorImager analysis. RT-PCR amplification of TMC mRNA with primers designed from rat and human IGFBP-4 sequences produced a 278 bp putative murine IGFBP-4 cDNA fragment which corresponded to 40% of the coding region. DNA sequencing revealed that this murine IGFBP-4 cDNA differed from the rat sequence at 6 residues (97% homology), but the deduced amino acid sequence was identical to that of the rat sequence. These results show that myeloid cells are the primary hematopoietic cells that synthesize and secrete IGFBP in leukocytes and that IGF-I together with IGFBP act in an autocrine fashion on these cells. Macrophage-derived IGFBP-4 may be a key regulator for the access of IGF-I to myeloid cells in thymic development and hematopoiesis.","abstract_has_math":true,"creators":["Li, Yongming"],"institution":"University of Illinois at Urbana-Champaign","degree_name":"Ph.D.","degree_level":"Dissertation","degree_discipline":"Animal Sciences","degree_department":null,"school":null,"contributors":["Kelley, Keith W."],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2011,"date_issued":"2011-05-07T12:11:56Z","date_published":"2011-05-07T12:11:56Z","updated_at":"2026-07-22T22:25:14Z","subjects":["Biology, Molecular","Biology, Animal Physiology","Health Sciences, Immunology"],"languages":["eng"],"rights":["Copyright 1994 Li, Yongming"],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["AAI9416393","(UMI)AAI9416393"],"render_values":[{"text":"AAI9416393","href":null,"code":true},{"text":"(UMI)AAI9416393","href":null,"code":true}]}]},"links":{"outbound_url":"http://hdl.handle.net/2142/19576","outbound_label":"Handle","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Kelley, Keith W."]},{"key":"dc:creator","label":"Author","values":["Li, Yongming"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2011-05-07T12:11:56Z","10000-01-01","1994"]},{"key":"dc:type","label":"Dc Type","values":["text"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Animal Sciences"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Dissertation"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Ph.D."]},{"key":"thesis:institution_name","label":"Thesis Institution Name","values":["University of Illinois at Urbana-Champaign"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Biology, Molecular","Biology, Animal Physiology","Health Sciences, Immunology"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["eng"]},{"key":"dc:rights","label":"Dc Rights","values":["Copyright 1994 Li, Yongming"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["AAI9416393","(UMI)AAI9416393","http://hdl.handle.net/2142/19576"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["Atrophic thymus glands from old rats contained a greater population of CD4$\\sp-$CD8$\\sp-$ cells and a reduced percentage of CD4$\\sp+$CD8$\\sp+$ lymphocytes compared to those of young rats. These age-associated changes could be reversed by implanting the growth hormone (GH) secreting cells, GH$\\sb3$. To understand the molecular mechanism by which insulin-like growth factor-I (IGF-I), a mediator of GH's action, acts on cells of immune system, the expression of IGF-I, IGF-I receptor (IGF-IR) and IGF binding proteins (IGFBP) in myeloid cells were studied. Human myeloid cell lines expressed IGF-I mRNA and probably secreted IGF-I peptides as evidenced by suppression of basal proliferation by an antibody to IGF-IR. Expression of the IGF-IR on myeloid cells was required for enhanced proliferation caused by both exogenous IGF-I and IGF-II. IGFBP-3 also inhibited IGF-I-induced cell proliferation. Furthermore, thymus and spleen contained IGFBPs. Among leukocytes, IGFBPs were primarily expressed in myeloid cells and their expression increased as myeloid cells were differentiated into mature macrophages. IGFBP levels from activated macrophages were down-regulated by proteases from these cells. Affinity cross-linking and protein binding immunomobility-shift assays, as well as Northern blotting, identified the 25 kDa IGFBP as IGFBP-4 that was expressed in a thymic macrophage cell line (TMC). TMC cells secrete IGFBP-4 at approximately 373 ng/10$\\sp7$ cells/day as determined by ligand blot followed by PhosphorImager analysis. RT-PCR amplification of TMC mRNA with primers designed from rat and human IGFBP-4 sequences produced a 278 bp putative murine IGFBP-4 cDNA fragment which corresponded to 40% of the coding region. DNA sequencing revealed that this murine IGFBP-4 cDNA differed from the rat sequence at 6 residues (97% homology), but the deduced amino acid sequence was identical to that of the rat sequence. These results show that myeloid cells are the primary hematopoietic cells that synthesize and secrete IGFBP in leukocytes and that IGF-I together with IGFBP act in an autocrine fashion on these cells. Macrophage-derived IGFBP-4 may be a key regulator for the access of IGF-I to myeloid cells in thymic development and hematopoiesis.","Made available in DSpace on 2011-05-07T12:11:56Z (GMT). No. of bitstreams: 2 license.txt: 4922 bytes, checksum: 910b249b4beec47e7ab768910c8f966f (MD5) 9416393.pdf: 7589285 bytes, checksum: 184010db30b2902501966017dc56d8da (MD5) Previous issue date: 1994","Item marked as restricted to the 'UIUC Users [automated]' Group (id=2) by Howard Ding (hding2@illinois.edu) on 2011-05-07T14:37:59Z Item is restricted indefinitely.","Restriction data tranferred 2014-07-01T11:15:42-05:00 Original Data Group with Access UIUC Users [automated] Release Date: none Reason: ETDs are only available to UIUC Users without author permission","ETDs are only available to UIUC Users without author permission","U of I Only"]},{"key":"dc:title","label":"Title","values":["Molecular interactions among insulin-like growth factor, its receptor and binding proteins on myeloid cells"]}]}],"canonical_facts":{"dc:contributor":["Kelley, Keith W."],"dc:creator":["Li, Yongming"],"dc:date":["2011-05-07T12:11:56Z","10000-01-01","1994"],"dc:description":["Atrophic thymus glands from old rats contained a greater population of CD4$\\sp-$CD8$\\sp-$ cells and a reduced percentage of CD4$\\sp+$CD8$\\sp+$ lymphocytes compared to those of young rats. These age-associated changes could be reversed by implanting the growth hormone (GH) secreting cells, GH$\\sb3$. To understand the molecular mechanism by which insulin-like growth factor-I (IGF-I), a mediator of GH's action, acts on cells of immune system, the expression of IGF-I, IGF-I receptor (IGF-IR) and IGF binding proteins (IGFBP) in myeloid cells were studied. Human myeloid cell lines expressed IGF-I mRNA and probably secreted IGF-I peptides as evidenced by suppression of basal proliferation by an antibody to IGF-IR. Expression of the IGF-IR on myeloid cells was required for enhanced proliferation caused by both exogenous IGF-I and IGF-II. IGFBP-3 also inhibited IGF-I-induced cell proliferation. Furthermore, thymus and spleen contained IGFBPs. Among leukocytes, IGFBPs were primarily expressed in myeloid cells and their expression increased as myeloid cells were differentiated into mature macrophages. IGFBP levels from activated macrophages were down-regulated by proteases from these cells. Affinity cross-linking and protein binding immunomobility-shift assays, as well as Northern blotting, identified the 25 kDa IGFBP as IGFBP-4 that was expressed in a thymic macrophage cell line (TMC). TMC cells secrete IGFBP-4 at approximately 373 ng/10$\\sp7$ cells/day as determined by ligand blot followed by PhosphorImager analysis. RT-PCR amplification of TMC mRNA with primers designed from rat and human IGFBP-4 sequences produced a 278 bp putative murine IGFBP-4 cDNA fragment which corresponded to 40% of the coding region. DNA sequencing revealed that this murine IGFBP-4 cDNA differed from the rat sequence at 6 residues (97% homology), but the deduced amino acid sequence was identical to that of the rat sequence. These results show that myeloid cells are the primary hematopoietic cells that synthesize and secrete IGFBP in leukocytes and that IGF-I together with IGFBP act in an autocrine fashion on these cells. Macrophage-derived IGFBP-4 may be a key regulator for the access of IGF-I to myeloid cells in thymic development and hematopoiesis.","Made available in DSpace on 2011-05-07T12:11:56Z (GMT). No. of bitstreams: 2 license.txt: 4922 bytes, checksum: 910b249b4beec47e7ab768910c8f966f (MD5) 9416393.pdf: 7589285 bytes, checksum: 184010db30b2902501966017dc56d8da (MD5) Previous issue date: 1994","Item marked as restricted to the 'UIUC Users [automated]' Group (id=2) by Howard Ding (hding2@illinois.edu) on 2011-05-07T14:37:59Z Item is restricted indefinitely.","Restriction data tranferred 2014-07-01T11:15:42-05:00 Original Data Group with Access UIUC Users [automated] Release Date: none Reason: ETDs are only available to UIUC Users without author permission","ETDs are only available to UIUC Users without author permission","U of I Only"],"dc:identifier":["AAI9416393","(UMI)AAI9416393","http://hdl.handle.net/2142/19576"],"dc:language":["eng"],"dc:rights":["Copyright 1994 Li, Yongming"],"dc:subject":["Biology, Molecular","Biology, Animal Physiology","Health Sciences, Immunology"],"dc:title":["Molecular interactions among insulin-like growth factor, its receptor and binding proteins on myeloid cells"],"dc:type":["text"],"thesis:degree_discipline":["Animal Sciences"],"thesis:degree_level":["Dissertation"],"thesis:degree_name":["Ph.D."],"thesis:institution_name":["University of Illinois at Urbana-Champaign"]},"updated_at":"2026-07-22T22:25:14Z"}