Adiponectin, a new member of the family of soluble defense collagens, negatively regulates the growth of myelomonocytic progenitors and the functions of macrophages

T. Yokota, K. Oritani, I. Takahashi, J. Ishikawa, Akifumi Matsuyama, N. Ouchi, S. Kihara, T. Funahashi, A. J. Tenner, Y. Tomiyama, Y. Matsuzawa

Research output: Contribution to journalArticle

1042 Citations (Scopus)

Abstract

We investigated the functions of adiponectin, an adipocyte-specific secretory protein and a new member of the family of soluble defense collagens, in hematopoiesis and immune responses. Adiponectin suppressed colony formation from colony-forming units (CFU)-granulocyte-macrophage, CFU-macrophage, and CFU-granulocyte, whereas it had no effect on that of burst-forming unitserythroid or mixed erythroid-myeloid CFU. In addition, adiponectin inhibited proliferation of 4 of 9 myeloid cell lines but did not suppress proliferation of erythroid or lymphoid cell lines except for one cell line. These results suggest that adiponectin predominantly inhibits proliferation of myelomonocytic lineage cells. At least one mechanism of the growth inhibition is induction of apoptosis because treatment of acute myelomonocytic leukemia lines with adiponectin induced the appearance of subdiploid peaks and oligonucleosomal DNA fragmentation. Aside from inhibiting growth of myelomonocytic progenitors, adiponectin suppressed mature macrophage functions. Treatment of cultured macrophages with adiponectin significantly inhibited their phagocytic activity and their lipopolysaccharide-induced production of tumor necrosis factor α. Suppression of phagocytosis by adiponectin is mediated by one of the complement C1q receptors, C1qRp, because this function was completely abrogated by the addition of an anti-C1qRp monoclonal antibody. These observations suggest that adiponectin is an important negative regulator in hematopoiesis and immune systems and raise the possibility that it may be involved in ending inflammatory responses through its inhibitory functions. (C) 2000 by The American Society of Hematology.

Original languageEnglish
Pages (from-to)1723-1732
Number of pages10
JournalBlood
Volume96
Issue number5
Publication statusPublished - 01-09-2000

Fingerprint

Macrophages
Adiponectin
Collagen
Growth
Granulocyte-Macrophage Progenitor Cells
Cells
Hematopoiesis
Cell Line
Complement C1q
Leukemia, Myelomonocytic, Acute
Complement Receptors
Erythroid Precursor Cells
Erythroid Cells
Immune system
DNA Fragmentation
Myeloid Cells
Phagocytosis
Adipocytes
Lipopolysaccharides
Immune System

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Immunology
  • Hematology
  • Cell Biology

Cite this

Yokota, T. ; Oritani, K. ; Takahashi, I. ; Ishikawa, J. ; Matsuyama, Akifumi ; Ouchi, N. ; Kihara, S. ; Funahashi, T. ; Tenner, A. J. ; Tomiyama, Y. ; Matsuzawa, Y. / Adiponectin, a new member of the family of soluble defense collagens, negatively regulates the growth of myelomonocytic progenitors and the functions of macrophages. In: Blood. 2000 ; Vol. 96, No. 5. pp. 1723-1732.
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abstract = "We investigated the functions of adiponectin, an adipocyte-specific secretory protein and a new member of the family of soluble defense collagens, in hematopoiesis and immune responses. Adiponectin suppressed colony formation from colony-forming units (CFU)-granulocyte-macrophage, CFU-macrophage, and CFU-granulocyte, whereas it had no effect on that of burst-forming unitserythroid or mixed erythroid-myeloid CFU. In addition, adiponectin inhibited proliferation of 4 of 9 myeloid cell lines but did not suppress proliferation of erythroid or lymphoid cell lines except for one cell line. These results suggest that adiponectin predominantly inhibits proliferation of myelomonocytic lineage cells. At least one mechanism of the growth inhibition is induction of apoptosis because treatment of acute myelomonocytic leukemia lines with adiponectin induced the appearance of subdiploid peaks and oligonucleosomal DNA fragmentation. Aside from inhibiting growth of myelomonocytic progenitors, adiponectin suppressed mature macrophage functions. Treatment of cultured macrophages with adiponectin significantly inhibited their phagocytic activity and their lipopolysaccharide-induced production of tumor necrosis factor α. Suppression of phagocytosis by adiponectin is mediated by one of the complement C1q receptors, C1qRp, because this function was completely abrogated by the addition of an anti-C1qRp monoclonal antibody. These observations suggest that adiponectin is an important negative regulator in hematopoiesis and immune systems and raise the possibility that it may be involved in ending inflammatory responses through its inhibitory functions. (C) 2000 by The American Society of Hematology.",
author = "T. Yokota and K. Oritani and I. Takahashi and J. Ishikawa and Akifumi Matsuyama and N. Ouchi and S. Kihara and T. Funahashi and Tenner, {A. J.} and Y. Tomiyama and Y. Matsuzawa",
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Yokota, T, Oritani, K, Takahashi, I, Ishikawa, J, Matsuyama, A, Ouchi, N, Kihara, S, Funahashi, T, Tenner, AJ, Tomiyama, Y & Matsuzawa, Y 2000, 'Adiponectin, a new member of the family of soluble defense collagens, negatively regulates the growth of myelomonocytic progenitors and the functions of macrophages', Blood, vol. 96, no. 5, pp. 1723-1732.

Adiponectin, a new member of the family of soluble defense collagens, negatively regulates the growth of myelomonocytic progenitors and the functions of macrophages. / Yokota, T.; Oritani, K.; Takahashi, I.; Ishikawa, J.; Matsuyama, Akifumi; Ouchi, N.; Kihara, S.; Funahashi, T.; Tenner, A. J.; Tomiyama, Y.; Matsuzawa, Y.

In: Blood, Vol. 96, No. 5, 01.09.2000, p. 1723-1732.

Research output: Contribution to journalArticle

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T1 - Adiponectin, a new member of the family of soluble defense collagens, negatively regulates the growth of myelomonocytic progenitors and the functions of macrophages

AU - Yokota, T.

AU - Oritani, K.

AU - Takahashi, I.

AU - Ishikawa, J.

AU - Matsuyama, Akifumi

AU - Ouchi, N.

AU - Kihara, S.

AU - Funahashi, T.

AU - Tenner, A. J.

AU - Tomiyama, Y.

AU - Matsuzawa, Y.

PY - 2000/9/1

Y1 - 2000/9/1

N2 - We investigated the functions of adiponectin, an adipocyte-specific secretory protein and a new member of the family of soluble defense collagens, in hematopoiesis and immune responses. Adiponectin suppressed colony formation from colony-forming units (CFU)-granulocyte-macrophage, CFU-macrophage, and CFU-granulocyte, whereas it had no effect on that of burst-forming unitserythroid or mixed erythroid-myeloid CFU. In addition, adiponectin inhibited proliferation of 4 of 9 myeloid cell lines but did not suppress proliferation of erythroid or lymphoid cell lines except for one cell line. These results suggest that adiponectin predominantly inhibits proliferation of myelomonocytic lineage cells. At least one mechanism of the growth inhibition is induction of apoptosis because treatment of acute myelomonocytic leukemia lines with adiponectin induced the appearance of subdiploid peaks and oligonucleosomal DNA fragmentation. Aside from inhibiting growth of myelomonocytic progenitors, adiponectin suppressed mature macrophage functions. Treatment of cultured macrophages with adiponectin significantly inhibited their phagocytic activity and their lipopolysaccharide-induced production of tumor necrosis factor α. Suppression of phagocytosis by adiponectin is mediated by one of the complement C1q receptors, C1qRp, because this function was completely abrogated by the addition of an anti-C1qRp monoclonal antibody. These observations suggest that adiponectin is an important negative regulator in hematopoiesis and immune systems and raise the possibility that it may be involved in ending inflammatory responses through its inhibitory functions. (C) 2000 by The American Society of Hematology.

AB - We investigated the functions of adiponectin, an adipocyte-specific secretory protein and a new member of the family of soluble defense collagens, in hematopoiesis and immune responses. Adiponectin suppressed colony formation from colony-forming units (CFU)-granulocyte-macrophage, CFU-macrophage, and CFU-granulocyte, whereas it had no effect on that of burst-forming unitserythroid or mixed erythroid-myeloid CFU. In addition, adiponectin inhibited proliferation of 4 of 9 myeloid cell lines but did not suppress proliferation of erythroid or lymphoid cell lines except for one cell line. These results suggest that adiponectin predominantly inhibits proliferation of myelomonocytic lineage cells. At least one mechanism of the growth inhibition is induction of apoptosis because treatment of acute myelomonocytic leukemia lines with adiponectin induced the appearance of subdiploid peaks and oligonucleosomal DNA fragmentation. Aside from inhibiting growth of myelomonocytic progenitors, adiponectin suppressed mature macrophage functions. Treatment of cultured macrophages with adiponectin significantly inhibited their phagocytic activity and their lipopolysaccharide-induced production of tumor necrosis factor α. Suppression of phagocytosis by adiponectin is mediated by one of the complement C1q receptors, C1qRp, because this function was completely abrogated by the addition of an anti-C1qRp monoclonal antibody. These observations suggest that adiponectin is an important negative regulator in hematopoiesis and immune systems and raise the possibility that it may be involved in ending inflammatory responses through its inhibitory functions. (C) 2000 by The American Society of Hematology.

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