Apoptosis of Dental Pulp Cells and Their Elimination by Macrophages and MHC Class II-expressing Dendritic Cells

Nishikawa, Sumio; Sasaki, Fumio

doi:10.1177/002215549904700304

Cited by 26 publications

(38 citation statements)

References 21 publications

(28 reference statements)

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“…The sections were further labeled with 1 g/ml Hoechst 33342 (Molecular Probes; Eugene, OR) to detect the transition zone (Nishikawa and Sasaki 1999a) or rhodamine-phalloidin (Molecular Probes) diluted 1:20 with PBS to detect ruffle-ended (RA) or smoothended ameloblasts (SA) (Nishikawa and Josephsen 1987). Procedures for pre-embedding immunoelectron microscopy were described elsewhere (Nishikawa and Sasaki 1999b). Briefly, thick cryosections fixed with paraformaldehyde and decalcified with EDTA were labeled with c-jun/ AP-1(Ab-1) diluted 1:10 at 4C overnight, followed by HRPconjugated anti-rabbit IgG at 4C overnight.…”

Section: Methodsmentioning

confidence: 99%

Localization of Transcription Factor AP-1 Family Proteins in Ameloblast Nuclei of the Rat Incisor

Nishikawa

2000

J Histochem Cytochem.

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We examined by immunocytochemistry the localization of the AP-1 family proteins c-Jun, JunB, JunD, c-Fos, FosB, Fra-1, and Fra-2 in rat incisor ameloblasts. Most of the antibodies against AP-1 family proteins, except for c-Fos-specific antibody, labeled ameloblast nuclei. The labeling intensity of the c-Jun, JunD, and Fra-2 antibodies was stronger than that of JunB, FosB, and Fra-1. Antibody reactivities of c-Jun, JunD, and Fra-2 were greatly enhanced during or after the transition zone. Furthermore, c-Jun antibodies labeled maturation ameloblasts in a cyclic pattern, which was correlated with ameloblast modulation. Disruption of ameloblast modulation by colchicine injection resulted in greatly decreased reactivity of the c-Jun antibody in the ameloblast nuclei of the maturation zone. Phospho-specific antibodies to c-Jun labeled ameloblast nuclei only weakly throughout the secretion, transition, and maturation zones. These results suggest that the stage-specific localization of AP-1 in ameloblasts is closely related to tooth enamel formation.

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Section: Methodsmentioning

confidence: 99%

Localization of Transcription Factor AP-1 Family Proteins in Ameloblast Nuclei of the Rat Incisor

Nishikawa

2000

J Histochem Cytochem.

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“…Odontoblasts line the periphery of the pulp, to elaborate dentin matrices [8,26]. Immune competent cells, such as macrophages and dendritic cells, have also been reported to be abundant in the dental pulp [9,14,16,17]. It is thought that these cells function in immunological defense [9,17], clearance of apoptotic fragments [14] and elimination of degenerated odontoblasts from the incisal pulp [16].…”

Section: Introductionmentioning

confidence: 99%

“…Immune competent cells, such as macrophages and dendritic cells, have also been reported to be abundant in the dental pulp [9,14,16,17]. It is thought that these cells function in immunological defense [9,17], clearance of apoptotic fragments [14] and elimination of degenerated odontoblasts from the incisal pulp [16]. In rat tissues, the distribution of MHC Class II antigen and CD68-like antigen, both found in dentritic cells and macrophages, can be determined using OX6 and ED1 antibodies, respectively, while the distribution of an antigen specific for macrophages can be determined using ED2 [4,5,11].…”

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

“…In the middle pulp region, these macrophages or dendritic cells are greater in number and often contain ingested apoptotic nuclei [14]. In the late pulp region where pulp cavity is smaller and the dentin thicker, numerous ED1 + , ED2 + , or OX6 + cells are present [14]. Cystatin C is an endogenous cysteine protease inhibitor and is secreted extracellularly to function with cysteine proteases, such as cathepsins, in proteolytic regulation [3,25].…”

Section: Introductionmentioning

confidence: 99%

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Cystatin C-positive Macrophages and Dendritic Cells in the Rat Incisor Pulp

Nishikawa

2004

Acta Histochem. Cytochem

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Localization of cystatin C, an endogenous cysteine protease inhibitor, was examined in the dental pulp of rat incisors using immunofluorescence microscopy. Based on double labeling with ED1 and anti-cystatin C antibodies, it was determined that anti cystatin C-labeled cells were macrophages and/or dendritic cells. Furthermore, cells in the incisor pulp were characterized by triple labeling with anti-cystatin C antibodies, ED2 antibodies for resident macrophages and OX6 antibodies for MHC class II antigens. Three cysteine proteases, cathepsin B, L and S, were also examined with immunocytochemistry. The results showed, firstly, that cystatin C single-positive cells were localized in early apical pulp, and that these cells were presumably immature macrophages invading newly formed dental pulp. Secondly, about half of OX6 + cells in the middle and incisal pulp were ED2 + , indicating that resident macrophages in addition to dendritic cells contribute to antigen surveillance via MHC Class II presentation. Thirdly, cathepsin S was present in cystatin C + cells, and therefore they may be involved in formation of proteolytic environment in whole dental pulp. In conclusion, cystatin C-positive macrophages and possibly dendritic cells may play a role in regulating the proteolytic environment of the dental pulp as well as in immunological surveillance.

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Histomorphology and innate immunity during the progression of osteoarthritis: Does synovitis affect cartilage degradation?

Wang

Yang

et al. 2017

Journal Cellular Physiology

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Osteoarthritis (OA) is a common chronic degenerative disease that affects all joints. At present, the pathological processes and mechanisms of OA are still unclear. Innate immunity, a key player in damage to the structure of the joint and the mechanism by which the host attempts to repair OA, affects all pathological stages of the disease. In the present study, our aim was to assess changes in innate immunity during the pathological processes of OA in articular cartilage (AC) and the synovial membrane (SM), which are the major structures in joints, and to systematically examine the histological changes in AC and SM in mild, moderate and severe cases of OA, in order to further speculate about the manner in which the interactions of AC and SM are facilitated by innate immunity. Histological methods (including HE and Safranin O-fast green staining), immunofluorescent double staining, TUNEL stain, and Western blots were used to assess the morphological changes within AC and SM tissues in healthy and mild, moderate, or severe OA rats. Our results showed that the damage to AC and SM within the joints progressively worsened in different degrees during the course of the disease, and that the innate immune system was closely involved in the AC and SM during each stage of OA. These findings also confirmed that SM may affect the pathological changes in AC through the innate immune system, and therefore affect the progress of OA.

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Apoptosis of Dental Pulp Cells and Their Elimination by Macrophages and MHC Class II-expressing Dendritic Cells

Cited by 26 publications

References 21 publications

Localization of Transcription Factor AP-1 Family Proteins in Ameloblast Nuclei of the Rat Incisor

Localization of Transcription Factor AP-1 Family Proteins in Ameloblast Nuclei of the Rat Incisor

Cystatin C-positive Macrophages and Dendritic Cells in the Rat Incisor Pulp

Histomorphology and innate immunity during the progression of osteoarthritis: Does synovitis affect cartilage degradation?

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