Journal of Nippon Medical School: Vol.67 No.4 page.235

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ArticleTitle Matrix Metalloproteinase and Tissue Inhibitor of Metalloproteinase in Human Bone Marrow Tissues -An Immunohistochemical Study-

AuthorList Maki Ogawa^{1, 2}, Masashi Kawamoto² and Nobuaki Yamanaka²

Affiliation ¹Division of Pathology, Tokyo Metropolitan Police Hospital ²Department of Pathology (I), Nippon Medical School

Language EN

Volume 67

Issue 4

Year 2000

Page 235-241

Received March 3, 2000

Accepted April 18, 2000

Keywords human bone marrow, myelofibrosis, MMP-2, MMP-9, TIMP-2

Abstract Unlike other tissues, bone marrow (BM) seldom displays fibrosis after injury, suggesting a possible suppressive mechanism against secondary myelofibrosis in BM tissues. We investigated if fibrosis-related factors, such as matrix metalloproteinase (MMP) and tissue inhibitor of metalloproteinase (TIMP), were expressed in BM tissues in vivo. We attempted immunohistochemical studies on specimens of 16 BM aspiration materials with normal hematological findings and 21 BM tissues from autopsy cases who had succumbed to acute heart failure or cerebrovascular diseases without any BM injuries. Identification of immunohistochemically reactive MMP-2, MMP-9 and TIMP-2 in BM tissue samples revealed for the first time that MMP-2 was localized in the myeloid cells, erythroblasts and megakaryocytes, MMP-9 in the myeloid cells and megakaryocytes. In addition, expression of TIMP-2 in the megakaryocytes as well as in the histiocytes within the stroma was verified. In the non-pathological condition, MMP/TIMP expressions were not encountered in BM stromal cells, such as fibroblasts, vascular endothelial cells, reticulum cells on adipocytes, except for TIMP-2 identification in stromal histiocytes. It is highly possible that these MMP and TIMP expressions in the BM hematopoietic cells and stromal histiocytes are significantly associated with suppression or induction of myelofibrosis.

Correspondence to Maki Ogawa, Division of Pathology, Tokyo Metropolitan Police Hospital, 2-10-41 Fujimi, Chiyoda-ku, Tokyo 102-8161, Japan

ArticleTitle	Matrix Metalloproteinase and Tissue Inhibitor of Metalloproteinase in Human Bone Marrow Tissues -An Immunohistochemical Study-
AuthorList	Maki Ogawa^{1, 2}, Masashi Kawamoto² and Nobuaki Yamanaka²
Affiliation	¹Division of Pathology, Tokyo Metropolitan Police Hospital ²Department of Pathology (I), Nippon Medical School
Language	EN
Volume	67
Issue	4
Year	2000
Page	235-241
Received	March 3, 2000
Accepted	April 18, 2000
Keywords	human bone marrow, myelofibrosis, MMP-2, MMP-9, TIMP-2
Abstract	Unlike other tissues, bone marrow (BM) seldom displays fibrosis after injury, suggesting a possible suppressive mechanism against secondary myelofibrosis in BM tissues. We investigated if fibrosis-related factors, such as matrix metalloproteinase (MMP) and tissue inhibitor of metalloproteinase (TIMP), were expressed in BM tissues in vivo. We attempted immunohistochemical studies on specimens of 16 BM aspiration materials with normal hematological findings and 21 BM tissues from autopsy cases who had succumbed to acute heart failure or cerebrovascular diseases without any BM injuries. Identification of immunohistochemically reactive MMP-2, MMP-9 and TIMP-2 in BM tissue samples revealed for the first time that MMP-2 was localized in the myeloid cells, erythroblasts and megakaryocytes, MMP-9 in the myeloid cells and megakaryocytes. In addition, expression of TIMP-2 in the megakaryocytes as well as in the histiocytes within the stroma was verified. In the non-pathological condition, MMP/TIMP expressions were not encountered in BM stromal cells, such as fibroblasts, vascular endothelial cells, reticulum cells on adipocytes, except for TIMP-2 identification in stromal histiocytes. It is highly possible that these MMP and TIMP expressions in the BM hematopoietic cells and stromal histiocytes are significantly associated with suppression or induction of myelofibrosis.
Correspondence to	Maki Ogawa, Division of Pathology, Tokyo Metropolitan Police Hospital, 2-10-41 Fujimi, Chiyoda-ku, Tokyo 102-8161, Japan