IGF-I regulates tight-junction protein claudin-1 during differentiation of osteoblast-like MC3T3-E1 cells via a MAP-kinase pathway

Naoko Hatakeyama, Takashi Kojima, Kousuke Iba, Masaki Murata, Mia M. Thi, David C. Spray, Makoto Osanai, Hideki Chiba, Sumio Ishiai, Toshihiko Yamashita, Norimasa Sawada

Research output: Contribution to journalArticle

24 Citations (Scopus)

Abstract

Insulin-like growth factor I (IGF-I) is expressed in many tissues, including bone, and acts on the proliferation and differentiation of osteoblasts as an autocrine/paracrine regulator. Tight-junction proteins have been detected in osteoblasts, and direct cell-to-cell interactions may modulate osteoblast function with respect, for example, to gap junctions. In order to investigate the regulation of expression of tight-junction molecules and of function during bone differentiation, osteoblast-like MC3T3-E1 cells and osteocyte-like MLO-Y4 cells were treated with IGF-I. In both MC3T3-E1 cells and MLO-Y4 cells, the tight-junction molecules occludin, claudin-1, -2, and -6, and the gap-junction molecule connexin 43 (Cx43) were detected by reverse transcription with polymerase chain reaction. In MC3T3-E1 cells but not MLO-Y4 cells, mRNAs of claudin-1, -2, and -6, Cx43, and type I collagen, and proteins of claudin-1 and Cx43 were increased after treatment with IGF-I. Such treatment significantly decreased paracellular permeability in MC3T3-E1 cells. The expression of claudin-1 in MC3T3-E1 cells after IGF-I treatment was mainly upregulated via a mitogen-activated protein (MAP)-kinase pathway and, in part, modulated by a PI3-kinase pathway, whereas Cx43 expression and the mediated gap-junctional intercellular communication protein did not contribute to the upregulation. Furthermore, in MC3T3-E1 cells during wound healing, upregulation of claudin-1 was observed together with an increase of IGF-I and type I collagen. These findings suggest that the induction of tight-junction protein claudin-1 and paracellular permeability during the differentiation of osteoblast-like MC3T3-E1 cells after treatment with IGF-I is regulated via a MAP-kinase pathway, but not with respect to gap junctions.

Original languageEnglish (US)
Pages (from-to)243-254
Number of pages12
JournalCell and Tissue Research
Volume334
Issue number2
DOIs
StatePublished - Nov 2008

Fingerprint

Zonula Occludens-1 Protein
Claudin-1
Mitogen-Activated Protein Kinases
Osteoblasts
Insulin-Like Growth Factor I
Connexin 43
Gap Junctions
Claudin-2
Tight Junctions
Collagen Type I
Permeability
Up-Regulation
Occludin
Tight Junction Proteins
Bone and Bones
Osteocytes
Intercellular Junctions
Phosphatidylinositol 3-Kinases
Cell Communication
Wound Healing

Keywords

  • Cell culture (murine)
  • Claudin-1
  • IGF-I
  • MAP-kinase
  • Osteoblast
  • Tight junction

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Cell Biology
  • Histology

Cite this

IGF-I regulates tight-junction protein claudin-1 during differentiation of osteoblast-like MC3T3-E1 cells via a MAP-kinase pathway. / Hatakeyama, Naoko; Kojima, Takashi; Iba, Kousuke; Murata, Masaki; Thi, Mia M.; Spray, David C.; Osanai, Makoto; Chiba, Hideki; Ishiai, Sumio; Yamashita, Toshihiko; Sawada, Norimasa.

In: Cell and Tissue Research, Vol. 334, No. 2, 11.2008, p. 243-254.

Research output: Contribution to journalArticle

Hatakeyama, N, Kojima, T, Iba, K, Murata, M, Thi, MM, Spray, DC, Osanai, M, Chiba, H, Ishiai, S, Yamashita, T & Sawada, N 2008, 'IGF-I regulates tight-junction protein claudin-1 during differentiation of osteoblast-like MC3T3-E1 cells via a MAP-kinase pathway', Cell and Tissue Research, vol. 334, no. 2, pp. 243-254. https://doi.org/10.1007/s00441-008-0690-9
Hatakeyama, Naoko ; Kojima, Takashi ; Iba, Kousuke ; Murata, Masaki ; Thi, Mia M. ; Spray, David C. ; Osanai, Makoto ; Chiba, Hideki ; Ishiai, Sumio ; Yamashita, Toshihiko ; Sawada, Norimasa. / IGF-I regulates tight-junction protein claudin-1 during differentiation of osteoblast-like MC3T3-E1 cells via a MAP-kinase pathway. In: Cell and Tissue Research. 2008 ; Vol. 334, No. 2. pp. 243-254.
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AU - Osanai, Makoto

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