Coexpression of Notch3 and Rgs5 in the pericyte-vascular smooth muscle cell axis in response to pulp injury.
Recent studies have shown that the pulp of human teeth contains a population of cells with stem cell properties and it has been suggested that these cells originate from pericytes. Molecules of the Notch signaling pathway regulate stem cell fate specification, while Rgs5 represents an excellent marker for pericytes. Pathological conditions such as dental trauma and carious lesion stimulate pulp stem cells to elaborate reparative dentin. Previous studies have shown that genes involved in the Notch pathway are activated in response to pulp injury in rodent and humans. To demonstrate the importance of pericytes as a source of stem cells during dental repair, we have studied Rgs5 and Notch3 mRNA expression by in situ hybridization in developing, adult intact and injured rodent teeth. Furthermore, we have examined the distribution of Notch3 protein in carious and injured human teeth using immunohistochemistry. Overlapping expression patterns of Rgs5 and Notch3 were observed during rodent tooth development as well as immediately after injury. Both genes were expressed in vascular structures during development and in perivascular and single capillary cells of injured teeth. However, the expression patterns of Rgs5 and Notch3 were different during tooth repair, with relatively extensive Rgs5 expression along the pericyte-vascular smooth muscle cell axis in central pulp arterioles. These results show co-expression of Rgs5 and Notch3 in pericytes of developing and injured teeth and furthermore indicate the importance of vascular-derived stem cells during pulp healing.
Lovschall
Henrik
H
Department of Dental Pathology, Operative Dentistry and Endodontics, Royal Dental College, Faculty of Health Sciences, University of Aarhus, DK-8000 Aarhus C, Denmark. loev@odont.au.dk
Mitsiadis
Thimios A
TA
Poulsen
Knud
K
Jensen
Kristina H
KH
Kjeldsen
Annette L
AL
D000818:Animals; D003782:Dental Pulp / Q000378:metabolism; D005786:Gene Expression Regulation; D006801:Humans; D008297:Male; D051379:Mice; D009131:Muscle, Smooth, Vascular / Q000378:metabolism; D009693:Nucleic Acid Hybridization; D020286:Pericytes / Q000378:metabolism*; D020710:RGS Proteins / Q000096:biosynthesis*; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D000071656:Receptor, Notch3; D051880:Receptors, Notch / Q000096:biosynthesis* / Q000378:metabolism; D015398:Signal Transduction; D014070:Tooth / Q000196:embryology / Q000378:metabolism*; D014945:Wound Healing
C499374:NOTCH3 protein, human; D020710:RGS Proteins; C491349:RGS5 protein, human; D012333:RNA, Messenger; D000071656:Receptor, Notch3; D051880:Receptors, Notch