Midkine is present in the early stage of cerebral infarct

Yoshida, Yasuhiko; Goto, Masamichi; Tsutsui, Jun-ichiro; Ozawa, Masayuki; Satô, Eiichi; Osame, Mitsuhiro; Muramatsu, Takashi

doi:10.1016/0165-3806(94)00183-z

Cited by 93 publications

(87 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This profile resembles that of the migration induced by PDGF-BB alone, but not that in the case of MK alone. DISCUSSION MK has been reported to be induced in areas of a variety of types of tissue injury, such as cerebral and heart infarction, bone fractures, skin burns, and arterial endothelial injury (12,13,14,36,37). In the case of arterial endothelial injury, we found not only the induction of MK expression in wild-type mice, but also dramatically suppressed neointima formation in MK-deficient mice (14).…”

Section: Mk Induces Haptotactic Migration Of Osteoblast-type Cells-mentioning

confidence: 57%

“…MK and pleiotrophin (PTN, also called HB-GAM for heparin-binding growth-associated molecule) comprise a family of heparinbinding growth/differentiation factors and are not related to other heparin-binding growth factors such as fibroblast growth factor or hepatocyte growth factor (5,6,7). MK has been reported to promote neuronal survival and neurite outgrowth (8,9) and to play roles in carcinogenesis (10,11) and tissue remodeling (12,13).…”

mentioning

confidence: 99%

See 1 more Smart Citation

Haptotactic Migration Induced by Midkine

Ikematsu²,

Maeda

et al. 2001

Journal of Biological Chemistry

Self Cite

142

View full text Add to dashboard Cite

Midkine, a heparin-binding growth factor, plays a critical role in cell migration causing suppression of neointima formation in midkine-deficient mice. Here we have determined the molecules essential for midkineinduced migration. Midkine induced haptotaxis of osteoblast-like cells, which was abrogated by the soluble form of midkine or pleiotrophin, a midkine-homologous protein. Chondroitin sulfate B, E, chondroitinase ABC, B, and orthovanadate, an inhibitor of protein-tyrosine phosphatase, suppressed the migration. Supporting these data, the cells examined expressed PTP, a receptor-type protein-tyrosine phosphatase that exhibits high affinity to both midkine and pleiotrophin and harbors chondroitin sulfate chains. Furthermore, strong synergism between midkine and platelet-derived growth factor in migration was detected. The use of specific inhibitors demonstrated that mitogen-activated protein (MAP) kinase and protein-tyrosine phosphatase were involved in midkine-induced haptotaxis but not PDGF-induced chemotaxis, whereas phosphatidylinositol 3 (PI3)-kinase and protein kinase C were involved in both functions. Midkine activated both PI3-kinase and MAP kinases, the latter activation was blocked by a PI3-kinase inhibitor. Midkine further recruited PTP and PI3-kinase. These results indicate that PTP and concerted signaling involving PI3-kinase and MAP kinase are required for midkine-induced migration and demonstrate for the first time the synergism between midkine and platelet-derived growth factor in cell migration.

show abstract

Section: Mk Induces Haptotactic Migration Of Osteoblast-type Cells-mentioning

confidence: 57%

mentioning

confidence: 99%

Haptotactic Migration Induced by Midkine

Ikematsu²,

Maeda

et al. 2001

Journal of Biological Chemistry

Self Cite

142

View full text Add to dashboard Cite

show abstract

“…Midkine (MK), originally isolated as a product of a retinoic acid-responsive gene in an embryonal carcinoma cell differentiation system, is a heparin-binding growth factor (Kadomatsu et al, 1988;Tomomura et al, 1990 a,b) implicated in neuronal survival and differentiation (Muramatsu and Muramatsu, 1991;Michikawa et al, 1993;Unoki et al, 1994), carcinogenesis (Tsutsui et al, 1993;Nakagawara et al, 1995), fibrinolysis (Kojima et al, 1995), wound healing (Yoshida et al, 1995) and development (Kadomatsu et al, 1990;Mitsiadis et al, 1995a, b). MK belongs to a novel growth factor family whose only members so far are MK and pleiotrophin (PTN)/HB-GAM (Muramatsu, 1993(Muramatsu, , 1994.…”

mentioning

confidence: 99%

Midkine induces the transformation of NIH3T3 cells

Kadomatsu

Hagihara²,

Akhter³

et al. 1997

Br J Cancer

138

111

View full text Add to dashboard Cite

Summary Midkine (MK) is a heparin-binding growth factor and is frequently expressed at high levels in many human carcinomas. To investigate further the roles of MK in the regulation of cell growth, we introduced MK expression in NIH3T3 cells. A mixture of transfectants of an MK expression vector, but not a control vector, formed colonies in soft agar, showed an elevated cell number at confluence, and formed tumours in nude mice. An interesting characteristic of the transformed cells was that they became spontaneously detached from the culture dish substratum. In the transformed cells, MK was not only secreted, but also localized, in the perinuclear region as spots. The present data indicate that MK has the potential to transform NIH3T3 cells and suggest that overexpression of the MK gene may promote unregulated cell growth in vivo.

show abstract

“…Furthermore, midkine accumulation is noted in senile plaques in the brains of Alzheimer's disease patients [16] . Midkine is expressed around the damaged neuronal site after cerebral infarction [17] , suggesting a role for midkine in tissue repair.…”

Section: Introductionmentioning

confidence: 99%

Midkine secretion protects Hep3B cells from cadmium induced cellular damage

Yazıhan¹,

Ataoglu²,

Akçıl³

et al. 2008

WJG

View full text Add to dashboard Cite

AIM:To evaluate role of midkine secretion during Cadmium (Cd) exposure in the human hepatocyte cell line Hep3B cells. METHODS:Different dosages of Cd (0.5-1-5-10 μg/mL) were applied to Hep3B cells and their effects to apoptosis, lactate dehydrogenase (LDH) leakage and midkine secretion were evaluated as time dependent m a n n e r. S a m e e x p e r i m e n t s w e re re p e a t e d w i t h exogenously applied midkine (250-5000 pg/mL) and/or 5 μg/mL Cd.

show abstract

Midkine is present in the early stage of cerebral infarct

Cited by 93 publications

References 25 publications

Haptotactic Migration Induced by Midkine

Haptotactic Migration Induced by Midkine

Midkine induces the transformation of NIH3T3 cells

Midkine secretion protects Hep3B cells from cadmium induced cellular damage

Contact Info

Product

Resources

About