scispace - formally typeset
T

Takashi Nishida

Researcher at Okayama University

Publications -  8
Citations -  1042

Takashi Nishida is an academic researcher from Okayama University. The author has contributed to research in topics: Growth factor & CTGF. The author has an hindex of 8, co-authored 8 publications receiving 996 citations. Previous affiliations of Takashi Nishida include Hamamatsu University School of Medicine.

Papers
More filters
Journal ArticleDOI

Effects of CTGF/Hcs24, a product of a hypertrophic chondrocyte-specific gene, on the proliferation and differentiation of chondrocytes in culture.

TL;DR: Investigating CTGF/Hcs24 function in the chondrocytic cell line HCS-2/8 and rabbit growth cartilage (RGC) cells found that it proliferated more rapidly and expressed more mRNA of aggrecan and type X collagen than the control cells.
Journal ArticleDOI

Effects of CTGF/Hcs24, a hypertrophic chondrocyte-specific gene product, on the proliferation and differentiation of osteoblastic cells in vitro.

TL;DR: Nakanishi et al. as discussed by the authors investigated the effects of CTGF/Hcs24 on the proliferation and differentiation of osteoblastic cell lines in vitro and revealed that CTGF is a novel, potent stimulator for the proliferation in addition to chondrocytes and endothelial cells.
Journal ArticleDOI

Connective tissue growth factor increased by hypoxia may initiate angiogenesis in collaboration with matrix metalloproteinases

TL;DR: The findings suggest that hypoxia stimulates MDA231 cells to release CTGF as an angiogenic modulator, which initiates the invasive angiogenesis cascade by modulating the balance of extracellular matrix synthesis and degradation via MMPs secreted by endothelial cells in response to CTGF.
Journal ArticleDOI

CTGF/Hcs24 induces chondrocyte differentiation through a p38 mitogen‐activated protein kinase (p38MAPK), and proliferation through a p44/42 MAPK/extracellular‐signal regulated kinase (ERK)

TL;DR: It is suggested that ERK mediates the CTGF/Hcs24-induced proliferation of chondrocytes, and that p38 MAPK mediating the CT GF/HCS24- induced differentiation of chondocytes.
Journal ArticleDOI

CTGF/Hcs24, a hypertrophic chondrocyte-specific gene product, stimulates proliferation and differentiation, but not hypertrophy of cultured articular chondrocytes

TL;DR: The results indicate that CTGF/Hcs24 promotes the proliferation and differentiation of articular chondrocytes, but does not promote their hypertrophy or calcification, and suggest that it may be useful for the repair ofArticular cartilage.