Localization of Core Planar Cell Polarity Proteins, PRICKLEs, in Ameloblasts of Rat Incisors: Possible Regulation of Enamel Rod Decussation

Abstract

To confirm the possible involvement of planar cell polarity proteins in odontogenesis, one group of core proteins, PRICKLE1, PRICKLE2, PRICKLE3, and PRICKLE4, was examined in enamel epithelial cells and ameloblasts by immunofluorescence microscopy. PRICKLE1 and PRICKLE2 showed similar localization in the proliferation and secretory zones of the incisor. Immunoreactive dots and short rods in ameloblasts and stratum intermedium cells were evident in the proliferation to differentiation zone, but in the secretion zone, cytoplasmic dots decreased and the distal terminal web was positive for PRICKLE1 and PRICKLE2. PRICKLE3 and PRICKLE4 showed cytoplasmic labeling in ameloblasts and other enamel epithelial cells. Double labeling of PRICKLE2 with VANGL1, which is another planar cell polarity protein, showed partial co-localization. To examine the transport route of PRICKLE proteins, PRICKLE1 localization was examined after injection of a microtubule-disrupting reagent, colchicine, and was compared with CX43, which is a membrane protein transported as vesicles via microtubules. The results confirmed the retention of immunoreactive dots for PRICKLE1 in the cytoplasm of secretory ameloblasts of colchicine-injected animals, but fewer dots were observed in control animals. These results suggest that PRICKLE1 and PRICKLE2 are transported as vesicles to the junctional area, and are involved in pattern formation of distal junctional complexes and terminal webs of ameloblasts, further implying a role in the formed enamel rod arrangement.

C-Jun N-terminal kinase (JNK) pathway activation is essential for dental papilla cells polarization

“…In this study, Prickle3, a planar cell polarity protein, RhoA, prototypical Rho GTPases have shown to have an integral role in cytoskeletal arrangement, membrane-trafficking pathways, and ECM interactions, which are all crucial steps for cell polarization [ 31 ]. Interestingly, the expression of RhoA in our study showed the same trend as Prickle3, which has shown to be positively expressed in papillary layer cells and some singular cells adjacent to the dentin [ 6 ] In our previous study, we examined the role of RhoA on the migration of human dental papilla cells using RhoA mutant adenoviruses and found that RhoA activity could active JNK signaling [ 14 ]. In the present study, JNK inhibitor treatment down-regulated the expression of RhoA mRNA and inhibited RhoA activity.…”

“…MAP1B [ 5 ], PRICKLEs [ 6 ], and Celsr1 [ 7 ] have been considered as essential polarity proteins localized in the odontoblastic layer C-Jun N-terminal kinase (JNK) kinase, which affects the spine morphology [ 8 ], regulates the expression of polarity complex genes Celsr2, Numb, Prkcz, Llgl2 in bone marrow hematopoietic progenitor cells [ 9 ]. Furthermore, previous studies have shown that JNK signaling participates in cell proliferation, differentiation, apoptosis, and cytoskeleton reorganization [ 10 – 12 ], and regulates plane cell polarity (PCP) [ 13 ].…”

Multivariate GWAS of Structural Dental Anomalies and Dental Caries in a Multi-Ethnic Cohort

“…In addition, this variant is also ∼300 kb upstream of PRICKLE2, a planar cell polarity protein involved in amelogenesis. In rats, Prickle2 in rats is expressed in the differentiating inner enamel epithelial cells and early inner enamel-secretory ameloblasts (29).…”

Growth and Transcription Factors in Tooth Development

“…Amelogenesis: Similar to dentinogenesis, in amelogenesis many different factors have also effects on enamel secretion and/or mineralization, thus we design again a Table where the factors are classified according to its role in secretion and/or mineralization (Table 4) [50,52,67,77,83,98,100,103,119,126,[128][129][130][131][132][133][134].…”