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Lysophosphatidic acid stimulates cell proliferation in rat chondrocytes.

Authors: Kim, MK  Lee, HY  Park, KS  Shin, EH  Jo, SH  Yun, J  Lee, SW  Yoo, YH  Lee, YS  Baek, SH  Bae, YS 
Citation: Kim MK, etal., Biochem Pharmacol. 2005 Dec 5;70(12):1764-71. Epub 2005 Oct 20.
Pubmed: (View Article at PubMed) PMID:16242672
DOI: Full-text: DOI:10.1016/j.bcp.2005.09.015

Rat primary chondrocytes express the lysophosphatidic acid (LPA) receptor, LPA1, LPA3, but not LPA2. When chondrocytes were stimulated with LPA, phospholipase C-mediated cytosolic calcium increase was dramatically induced. LPA also stimulated two kinds of mitogen-activated protein kinase, extracellular signal-regulated kinase (ERK) and p38 kinase in chondrocytes. In terms of the LPA-mediated functional modulation of chondrocytes, LPA stimulated cellular proliferation. We examined the signaling pathways involved in LPA-mediated cellular proliferation. LPA-induced chondrocyte proliferation was almost completely blocked by 2'-amino-3'-methoxyflavone (PD98059) but not by 4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)1H-imidazole (SB203580), suggesting that ERK activity is essentially required for the process. Pertussis toxin almost completely inhibited the LPA-induced cellular proliferation and ERK activation, indicating the role of G(i/o) protein(s) in the processes. This study demonstrates the physiological role of LPA on the modulation of rat primary chondrocyte proliferation, and the crucial role played by ERK in the process.


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RGD Object Information
RGD ID: 1626474
Created: 2007-08-09
Species: All species
Last Modified: 2007-08-09
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.