Fibroblast growth factor 2 facilitates the differentiation of transplanted bone marrow cells into hepatocytes
We have developed an in vivo mouse model, the green fluorescent protein (GFP)/carbon tetrachloride (CCl(4)) model, and have previously reported that transplanted GFP-positive bone marrow cells (BMCs) differentiate into hepatocytes via hepatoblast intermediates. Here, we have investigated the growth...
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| Veröffentlicht in: | Cell and tissue research 2006-02, Vol.323 (2), p.221-231 |
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| creator | Ishikawa, Tsuyoshi Terai, Shuji Urata, Yohei Marumoto, Yoshio Aoyama, Koji Sakaida, Isao Murata, Tomoaki Nishina, Hiroshi Shinoda, Koh Uchimura, Shunji Hamamoto, Yoshihiko Okita, Kiwamu |
| description | We have developed an in vivo mouse model, the green fluorescent protein (GFP)/carbon tetrachloride (CCl(4)) model, and have previously reported that transplanted GFP-positive bone marrow cells (BMCs) differentiate into hepatocytes via hepatoblast intermediates. Here, we have investigated the growth factors that are closely related to the differentiation of transplanted BMCs into hepatocytes, and the way that a specific growth factor affects the differentiation process in the GFP/CCl(4) model. We performed immunohistochemical analysis to identify an important growth factor in our model, viz., fibroblast growth factor (FGF). In liver samples, the expression of FGF1 and FGF2 and of FGF receptors (FGFRs; FGFR1, FGFR2) was significantly elevated with time after bone marrow transplantation (BMT) compared with other factors, and co-expression of GFP and FGFs or FGFRs could be detected. We then analyzed the effect and molecular mechanism of FGF signaling on the enhancement of BMC differentiation into hepatocytes by immunohistochemistry, immunoblotting, and microarray analysis. Treatment with recombinant FGF (rFGF), especially rFGF2, elevated the repopulation rate of GFP-positive cells in the liver and significantly increased the expression of both Liv2 (hepatoblast marker) and albumin (hepatocyte marker). Administration of rFGF2 at BMT also raised serum albumin levels and improved the survival rate. Transplantation of BMCs with rFGF2 specifically activated tumor necrosis factor-alpha (TNF-alpha) signaling. Thus, FGF2 facilitates the differentiation of transplanted BMCs into albumin-producing hepatocytes via Liv2-positive hepatoblast intermediates through the activation of TNF-alpha signaling. Administration of FGF2 in combination with BMT improves the liver function and prognosis of mice with CCl(4)-induced liver damage. |
| doi_str_mv | 10.1007/s00441-005-0077-0 |
| format | Article |
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Here, we have investigated the growth factors that are closely related to the differentiation of transplanted BMCs into hepatocytes, and the way that a specific growth factor affects the differentiation process in the GFP/CCl(4) model. We performed immunohistochemical analysis to identify an important growth factor in our model, viz., fibroblast growth factor (FGF). In liver samples, the expression of FGF1 and FGF2 and of FGF receptors (FGFRs; FGFR1, FGFR2) was significantly elevated with time after bone marrow transplantation (BMT) compared with other factors, and co-expression of GFP and FGFs or FGFRs could be detected. We then analyzed the effect and molecular mechanism of FGF signaling on the enhancement of BMC differentiation into hepatocytes by immunohistochemistry, immunoblotting, and microarray analysis. Treatment with recombinant FGF (rFGF), especially rFGF2, elevated the repopulation rate of GFP-positive cells in the liver and significantly increased the expression of both Liv2 (hepatoblast marker) and albumin (hepatocyte marker). Administration of rFGF2 at BMT also raised serum albumin levels and improved the survival rate. Transplantation of BMCs with rFGF2 specifically activated tumor necrosis factor-alpha (TNF-alpha) signaling. Thus, FGF2 facilitates the differentiation of transplanted BMCs into albumin-producing hepatocytes via Liv2-positive hepatoblast intermediates through the activation of TNF-alpha signaling. Administration of FGF2 in combination with BMT improves the liver function and prognosis of mice with CCl(4)-induced liver damage.</description><identifier>ISSN: 0302-766X</identifier><identifier>EISSN: 1432-0878</identifier><identifier>DOI: 10.1007/s00441-005-0077-0</identifier><identifier>PMID: 16228231</identifier><language>eng</language><publisher>Germany: Springer Nature B.V</publisher><subject>Animals ; Bone Marrow Cells - drug effects ; Bone Marrow Cells - metabolism ; Bone Marrow Transplantation ; Carbon Tetrachloride - toxicity ; Cell Differentiation - drug effects ; Cell Differentiation - physiology ; Disease Models, Animal ; Female ; Fibroblast Growth Factor 2 - physiology ; Green Fluorescent Proteins - metabolism ; Hepatocytes - cytology ; Hepatocytes - drug effects ; Hepatocytes - metabolism ; Immunohistochemistry ; Liver Cirrhosis, Experimental - chemically induced ; Mice ; Mice, Inbred C57BL ; Oligonucleotide Array Sequence Analysis ; Recombinant Proteins ; RNA, Messenger - metabolism ; Signal Transduction</subject><ispartof>Cell and tissue research, 2006-02, Vol.323 (2), p.221-231</ispartof><rights>Springer-Verlag 2006</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c326t-cb8621b8a60573e8c4ad8af1f3c078642aec0eb4415990f717c84d0520ede1a23</citedby><cites>FETCH-LOGICAL-c326t-cb8621b8a60573e8c4ad8af1f3c078642aec0eb4415990f717c84d0520ede1a23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,27905,27906</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16228231$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ishikawa, Tsuyoshi</creatorcontrib><creatorcontrib>Terai, Shuji</creatorcontrib><creatorcontrib>Urata, Yohei</creatorcontrib><creatorcontrib>Marumoto, Yoshio</creatorcontrib><creatorcontrib>Aoyama, Koji</creatorcontrib><creatorcontrib>Sakaida, Isao</creatorcontrib><creatorcontrib>Murata, Tomoaki</creatorcontrib><creatorcontrib>Nishina, Hiroshi</creatorcontrib><creatorcontrib>Shinoda, Koh</creatorcontrib><creatorcontrib>Uchimura, Shunji</creatorcontrib><creatorcontrib>Hamamoto, Yoshihiko</creatorcontrib><creatorcontrib>Okita, Kiwamu</creatorcontrib><title>Fibroblast growth factor 2 facilitates the differentiation of transplanted bone marrow cells into hepatocytes</title><title>Cell and tissue research</title><addtitle>Cell Tissue Res</addtitle><description>We have developed an in vivo mouse model, the green fluorescent protein (GFP)/carbon tetrachloride (CCl(4)) model, and have previously reported that transplanted GFP-positive bone marrow cells (BMCs) differentiate into hepatocytes via hepatoblast intermediates. Here, we have investigated the growth factors that are closely related to the differentiation of transplanted BMCs into hepatocytes, and the way that a specific growth factor affects the differentiation process in the GFP/CCl(4) model. We performed immunohistochemical analysis to identify an important growth factor in our model, viz., fibroblast growth factor (FGF). In liver samples, the expression of FGF1 and FGF2 and of FGF receptors (FGFRs; FGFR1, FGFR2) was significantly elevated with time after bone marrow transplantation (BMT) compared with other factors, and co-expression of GFP and FGFs or FGFRs could be detected. We then analyzed the effect and molecular mechanism of FGF signaling on the enhancement of BMC differentiation into hepatocytes by immunohistochemistry, immunoblotting, and microarray analysis. Treatment with recombinant FGF (rFGF), especially rFGF2, elevated the repopulation rate of GFP-positive cells in the liver and significantly increased the expression of both Liv2 (hepatoblast marker) and albumin (hepatocyte marker). Administration of rFGF2 at BMT also raised serum albumin levels and improved the survival rate. Transplantation of BMCs with rFGF2 specifically activated tumor necrosis factor-alpha (TNF-alpha) signaling. Thus, FGF2 facilitates the differentiation of transplanted BMCs into albumin-producing hepatocytes via Liv2-positive hepatoblast intermediates through the activation of TNF-alpha signaling. Administration of FGF2 in combination with BMT improves the liver function and prognosis of mice with CCl(4)-induced liver damage.</description><subject>Animals</subject><subject>Bone Marrow Cells - drug effects</subject><subject>Bone Marrow Cells - metabolism</subject><subject>Bone Marrow Transplantation</subject><subject>Carbon Tetrachloride - toxicity</subject><subject>Cell Differentiation - drug effects</subject><subject>Cell Differentiation - physiology</subject><subject>Disease Models, Animal</subject><subject>Female</subject><subject>Fibroblast Growth Factor 2 - physiology</subject><subject>Green Fluorescent Proteins - metabolism</subject><subject>Hepatocytes - cytology</subject><subject>Hepatocytes - drug effects</subject><subject>Hepatocytes - metabolism</subject><subject>Immunohistochemistry</subject><subject>Liver Cirrhosis, Experimental - chemically induced</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Oligonucleotide Array Sequence 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growth factor 2 facilitates the differentiation of transplanted bone marrow cells into hepatocytes</title><author>Ishikawa, Tsuyoshi ; Terai, Shuji ; Urata, Yohei ; Marumoto, Yoshio ; Aoyama, Koji ; Sakaida, Isao ; Murata, Tomoaki ; Nishina, Hiroshi ; Shinoda, Koh ; Uchimura, Shunji ; Hamamoto, Yoshihiko ; Okita, Kiwamu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c326t-cb8621b8a60573e8c4ad8af1f3c078642aec0eb4415990f717c84d0520ede1a23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Animals</topic><topic>Bone Marrow Cells - drug effects</topic><topic>Bone Marrow Cells - metabolism</topic><topic>Bone Marrow Transplantation</topic><topic>Carbon Tetrachloride - toxicity</topic><topic>Cell Differentiation - drug effects</topic><topic>Cell Differentiation - physiology</topic><topic>Disease Models, Animal</topic><topic>Female</topic><topic>Fibroblast Growth Factor 2 - physiology</topic><topic>Green Fluorescent Proteins - metabolism</topic><topic>Hepatocytes - cytology</topic><topic>Hepatocytes - drug effects</topic><topic>Hepatocytes - metabolism</topic><topic>Immunohistochemistry</topic><topic>Liver Cirrhosis, Experimental - chemically induced</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Oligonucleotide Array Sequence Analysis</topic><topic>Recombinant Proteins</topic><topic>RNA, Messenger - metabolism</topic><topic>Signal Transduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ishikawa, Tsuyoshi</creatorcontrib><creatorcontrib>Terai, Shuji</creatorcontrib><creatorcontrib>Urata, Yohei</creatorcontrib><creatorcontrib>Marumoto, Yoshio</creatorcontrib><creatorcontrib>Aoyama, Koji</creatorcontrib><creatorcontrib>Sakaida, Isao</creatorcontrib><creatorcontrib>Murata, Tomoaki</creatorcontrib><creatorcontrib>Nishina, Hiroshi</creatorcontrib><creatorcontrib>Shinoda, 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Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ishikawa, Tsuyoshi</au><au>Terai, Shuji</au><au>Urata, Yohei</au><au>Marumoto, Yoshio</au><au>Aoyama, Koji</au><au>Sakaida, Isao</au><au>Murata, Tomoaki</au><au>Nishina, Hiroshi</au><au>Shinoda, Koh</au><au>Uchimura, Shunji</au><au>Hamamoto, Yoshihiko</au><au>Okita, Kiwamu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Fibroblast growth factor 2 facilitates the differentiation of transplanted bone marrow cells into hepatocytes</atitle><jtitle>Cell and tissue research</jtitle><addtitle>Cell Tissue Res</addtitle><date>2006-02</date><risdate>2006</risdate><volume>323</volume><issue>2</issue><spage>221</spage><epage>231</epage><pages>221-231</pages><issn>0302-766X</issn><eissn>1432-0878</eissn><abstract>We have developed an in vivo mouse model, the green fluorescent protein (GFP)/carbon tetrachloride (CCl(4)) model, and have previously reported that transplanted GFP-positive bone marrow cells (BMCs) differentiate into hepatocytes via hepatoblast intermediates. Here, we have investigated the growth factors that are closely related to the differentiation of transplanted BMCs into hepatocytes, and the way that a specific growth factor affects the differentiation process in the GFP/CCl(4) model. We performed immunohistochemical analysis to identify an important growth factor in our model, viz., fibroblast growth factor (FGF). In liver samples, the expression of FGF1 and FGF2 and of FGF receptors (FGFRs; FGFR1, FGFR2) was significantly elevated with time after bone marrow transplantation (BMT) compared with other factors, and co-expression of GFP and FGFs or FGFRs could be detected. We then analyzed the effect and molecular mechanism of FGF signaling on the enhancement of BMC differentiation into hepatocytes by immunohistochemistry, immunoblotting, and microarray analysis. Treatment with recombinant FGF (rFGF), especially rFGF2, elevated the repopulation rate of GFP-positive cells in the liver and significantly increased the expression of both Liv2 (hepatoblast marker) and albumin (hepatocyte marker). Administration of rFGF2 at BMT also raised serum albumin levels and improved the survival rate. Transplantation of BMCs with rFGF2 specifically activated tumor necrosis factor-alpha (TNF-alpha) signaling. Thus, FGF2 facilitates the differentiation of transplanted BMCs into albumin-producing hepatocytes via Liv2-positive hepatoblast intermediates through the activation of TNF-alpha signaling. Administration of FGF2 in combination with BMT improves the liver function and prognosis of mice with CCl(4)-induced liver damage.</abstract><cop>Germany</cop><pub>Springer Nature B.V</pub><pmid>16228231</pmid><doi>10.1007/s00441-005-0077-0</doi><tpages>11</tpages></addata></record> |
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| subjects | Animals Bone Marrow Cells - drug effects Bone Marrow Cells - metabolism Bone Marrow Transplantation Carbon Tetrachloride - toxicity Cell Differentiation - drug effects Cell Differentiation - physiology Disease Models, Animal Female Fibroblast Growth Factor 2 - physiology Green Fluorescent Proteins - metabolism Hepatocytes - cytology Hepatocytes - drug effects Hepatocytes - metabolism Immunohistochemistry Liver Cirrhosis, Experimental - chemically induced Mice Mice, Inbred C57BL Oligonucleotide Array Sequence Analysis Recombinant Proteins RNA, Messenger - metabolism Signal Transduction |
| title | Fibroblast growth factor 2 facilitates the differentiation of transplanted bone marrow cells into hepatocytes |
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