Biomol Ther.  2017 Jul;25(4):354-361. 10.4062/biomolther.2016.263.

Role of TAZ in Lysophosphatidic Acid-Induced Migration and Proliferation of Human Adipose-Derived Mesenchymal Stem Cells

Affiliations
  • 1Department of Physiology, Pusan National University School of Medicine, Yangsan 50612, Republic of Korea. jhkimst@pusan.ac.kr
  • 2Department of Oral Biochemistry and Molecular Biology, Pusan National University School of Dentistry, Yangsan 50612, Republic of Korea.
  • 3BK21 PLUS Project, Pusan National University School of Dentistry, Yangsan 50612, Republic of Korea.
  • 4Research Institute of Convergence Biomedical Science and Technology, Pusan National University Yangsan Hospital, Yangsan 50612, Republic of Korea.

Abstract

Transcriptional co-activator with a PDZ-binding motif (TAZ) is an important factor in lysophosphatidic acid (LPA)-induced promotion of migration and proliferation of human mesenchymal stem cells (MSCs). The expression of TAZ significantly increased at 6 h after LPA treatment, and TAZ knockdown inhibited the LPA-induced migration and proliferation of MSCs. In addition, embryonic fibroblasts from TAZ knockout mice exhibited the reduction in LPA-induced migration and proliferation. The LPA1 receptor inhibitor Ki16425 blocked LPA responses in MSCs. Although TAZ knockdown or knockout did not reduce LPA-induced phosphorylation of ERK and AKT, the MEK inhibitor U0126 or the ROCK inhibitor Y27632 blocked LPA-induced TAZ expression along with the reduction in the proliferation and migration of MSCs. Our data suggest that TAZ is an important mediator of LPA signaling in MSCs in the downstream of MEK and ROCK signaling.

Keyword

LPA; TAZ; Mesenchymal stem cells; MEK; ROCK

MeSH Terms

Animals
Fibroblasts
Humans*
Mesenchymal Stromal Cells*
Mice
Mice, Knockout
Phosphorylation
Receptors, Lysophosphatidic Acid
Receptors, Lysophosphatidic Acid
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