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23. Effects of Early-Life Adversity on Tooth Enamel Formation

Author

Shaffer, Ida C, Nakano, Yukiko, Pham, Aidan, Short, Annabel, Nanci, Antonio, Zhang, Yan, Shemirani, Rozana, and Besten, Pamela K Den

Subjects
Biomedical and Clinical Sciences, Dentistry, Genetics, Social Determinants of Health, Dental/Oral and Craniofacial Disease, Pediatric, 2.1 Biological and endogenous factors, enamel, early life adversity, mineralization, ameloblasts, RNAseq, limited bedding and nesting
Abstract

In a systemic effort to survive environmental stress, organ systems fluctuate and adapt to overcome external pressures. The evolutionary drive back toward homeostasis makes it difficult to determine if an organism experienced a toxic exposure to stress, especially in early prenatal and neonatal periods of development. Previous studies indicate that primary human teeth may provide historical records of experiences related to stressors during that early time window. To assess the molecular effects of early life adversity on enamel formation, we used a limited bedding and nesting (LBN) mouse model of early life adversity (ELA) to assess changes in the enamel organ gene expression and enamel matrix mineralization. On average, postnatal day 12 (P12) ELA mice weighed significantly less than the controls. When adjusted for animal weight, ELA molar enamel volume was reduced as compared with the controls, and the relative mineral density of molar enamel was significantly increased. There were no obvious changes in enamel matrix crystal morphology or structure in ELA as compared with the control mouse enamel. RNAseq showed extracellular matrix organization to be the most significantly affected GO and reactome pathways, whereas butanote metabolism was the most significantly altered KEGG pathway. Transcripts expressing the enamel matrix proteins amelogenin (Amelx) and enamelin (Enam) were among the top 4 most differentially expressed genes. When evaluating molecular mechanisms for the changes in gene expression in ELA enamel organs, we found significantly increased expression of Dlx3, while transcripts for clock genes Per1 and Nrd1 were downregulated. These findings support the possibility that the developing enamel organ is sensitive to the pressures of early life adversity and produces molecular and structural biomarkers reflecting these challenges.

Published
2022

24. WDR72 regulates vesicle trafficking in ameloblasts

Author

Katsura, Kaitlin, Nakano, Yukiko, Zhang, Yan, Shemirani, Rozana, Li, Wu, and Den Besten, Pamela

Subjects
Biochemistry and Cell Biology, Biomedical and Clinical Sciences, Dentistry, Biological Sciences, Dental/Oral and Craniofacial Disease, Rare Diseases, 1.1 Normal biological development and functioning, Underpinning research, Aetiology, 2.1 Biological and endogenous factors, Generic health relevance, Ameloblasts, Amelogenesis Imperfecta, Brain, Calcification, Physiologic, Cell Differentiation, Dental Enamel, Endocytosis, Humans, Kidney, Liver, Microtubules, Myocardium, Tooth
Abstract

As the hardest tissue in the human body, tooth enamel formation is a highly regulated process involving several stages of differentiation and key regulatory genes. One such gene, tryptophan-aspartate repeat domain 72 (WDR72), has been found to cause a tooth enamel defect when deleted or mutated, resulting in a condition called amelogenesis imperfecta. Unlike the canonical genes regulating tooth development, WDR72 remains intracellularly and is not secreted to the enamel matrix space to regulate mineralization, and is found in other major organs of the body, namely the kidney, brain, liver, and heart. To date, a link between intracellular vesicle transport and enamel mineralization has been suggested, however identification of the mechanistic regulators has yet to be elucidated, in part due to the limitations associated with studying highly differentiated ameloblast cells. Here we show compelling evidence that WDR72 regulates endocytosis of proteins, both in vivo and in a novel in vitro ameloblast cell line. We elucidate WDR72's function to be independent of intracellular vesicle acidification while still leading to defective enamel matrix pH extracellularly. We identify a vesicle function associated with microtubule assembly and propose that WDR72 directs microtubule assembly necessary for membrane mobilization and subsequent vesicle transport. Understanding WDR72 function provides a mechanistic basis for determining physiologic and pathologic tissue mineralization.

Published
2022

26. Style Transfer for Co-Speech Gesture Animation: A Multi-Speaker Conditional-Mixture Approach

Author

Ahuja, Chaitanya, Lee, Dong Won, Nakano, Yukiko I., and Morency, Louis-Philippe

Subjects
Computer Science - Computer Vision and Pattern Recognition, Computer Science - Robotics
Abstract

How can we teach robots or virtual assistants to gesture naturally? Can we go further and adapt the gesturing style to follow a specific speaker? Gestures that are naturally timed with corresponding speech during human communication are called co-speech gestures. A key challenge, called gesture style transfer, is to learn a model that generates these gestures for a speaking agent 'A' in the gesturing style of a target speaker 'B'. A secondary goal is to simultaneously learn to generate co-speech gestures for multiple speakers while remembering what is unique about each speaker. We call this challenge style preservation. In this paper, we propose a new model, named Mix-StAGE, which trains a single model for multiple speakers while learning unique style embeddings for each speaker's gestures in an end-to-end manner. A novelty of Mix-StAGE is to learn a mixture of generative models which allows for conditioning on the unique gesture style of each speaker. As Mix-StAGE disentangles style and content of gestures, gesturing styles for the same input speech can be altered by simply switching the style embeddings. Mix-StAGE also allows for style preservation when learning simultaneously from multiple speakers. We also introduce a new dataset, Pose-Audio-Transcript-Style (PATS), designed to study gesture generation and style transfer. Our proposed Mix-StAGE model significantly outperforms the previous state-of-the-art approach for gesture generation and provides a path towards performing gesture style transfer across multiple speakers. Link to code, data, and videos: http://chahuja.com/mix-stage, Comment: 24 pages, 12 figures

Published
2020

34. SATB1 establishes ameloblast cell polarity and regulates directional amelogenin secretion for enamel formation.

Author

Zhang, Yan, Zheng, Liwei, Le, Michael, Nakano, Yukiko, Chan, Barry, Huang, Yulei, Torbaty, Parisa Moravedje, Kohwi, Yoshinori, Marcucio, Ralph, Habelitz, Stefan, Den Besten, Pamela K, and Kohwi-Shigematsu, Terumi

Subjects
Ameloblasts, Dental Enamel, Animals, Humans, Mice, Matrix Attachment Region Binding Proteins, Cell Differentiation, Cell Polarity, Amelogenesis, Ameloblast, Amelogenin, Claudin 1, EPS8, Enamel, Epithelial polarity, Filamentous actin assembly, Membrane trafficking, Special AT-rich sequence-binding protein-1, Tight junction, Dental/Oral and Craniofacial Disease, 1.1 Normal biological development and functioning, Generic health relevance, Developmental Biology, Biological Sciences
Abstract

BACKGROUND:Polarity is necessary for epithelial cells to perform distinct functions at their apical and basal surfaces. Oral epithelial cell-derived ameloblasts at secretory stage (SABs) synthesize large amounts of enamel matrix proteins (EMPs), largely amelogenins. EMPs are unidirectionally secreted into the enamel space through their apical cytoplasmic protrusions, or Tomes' processes (TPs), to guide the enamel formation. Little is known about the transcriptional regulation underlying the establishment of cell polarity and unidirectional secretion of SABs. RESULTS:The higher-order chromatin architecture of eukaryotic genome plays important roles in cell- and stage-specific transcriptional programming. A genome organizer, special AT-rich sequence-binding protein 1 (SATB1), was discovered to be significantly upregulated in ameloblasts compared to oral epithelial cells using a whole-transcript microarray analysis. The Satb1-/- mice possessed deformed ameloblasts and a thin layer of hypomineralized and non-prismatic enamel. Remarkably, Satb1-/- ameloblasts at the secretory stage lost many morphological characteristics found at the apical surface of wild-type (wt) SABs, including the loss of Tomes' processes, defective inter-ameloblastic adhesion, and filamentous actin architecture. As expected, the secretory function of Satb1-/- SABs was compromised as amelogenins were largely retained in cells. We found the expression of epidermal growth factor receptor pathway substrate 8 (Eps8), a known regulator for actin filament assembly and small intestinal epithelial cytoplasmic protrusion formation, to be SATB1 dependent. In contrast to wt SABs, EPS8 could not be detected at the apical surface of Satb1-/- SABs. Eps8 expression was greatly reduced in small intestinal epithelial cells in Satb1-/- mice as well, displaying defective intestinal microvilli. CONCLUSIONS:Our data show that SATB1 is essential for establishing secretory ameloblast cell polarity and for EMP secretion. In line with the deformed apical architecture, amelogenin transport to the apical secretory front and secretion into enamel space were impeded in Satb1-/- SABs resulting in a massive cytoplasmic accumulation of amelogenins and a thin layer of hypomineralized enamel. Our studies strongly suggest that SATB1-dependent Eps8 expression plays a critical role in cytoplasmic protrusion formation in both SABs and in small intestines. This study demonstrates the role of SATB1 in the regulation of amelogenesis and the potential application of SATB1 in ameloblast/enamel regeneration.

Published
2019

43. Modifiers of the Risk of Diabetes for Long-Term Outcomes After Coronary Revascularization: CREDO-Kyoto PCI/CABG Registry

Author

Kimura, Takeshi, Shiomi, Hiroki, Matsuda, Mitsuo, Takeuchi, Yuzo, Mitsuoka, Hirokazu, Uegaito, Takashi, Nakagawa, Yoshihisa, Tamura, Toshihiro, Konishi, Takashi, Ootani, Seiji, Fujiwara, Hisayoshi, Takatsu, Yoshiki, Sato, Yukihito, Taniguchi, Ryoji, Kataoka, Kazuaki, Inoko, Moriaki, Nohara, Ryuji, Nakano, Kimisato, Miyamoto, Syoichi, Kunihiko, Nagai, Murakami, Tomoyuki, Takeda, Teruki, Ishida, Katsuya, Nobuyoshi, Masakiyo, Yamaji, Kyohei, Yasumoto, Hitoshi, Iwabuchi, Masashi, Ando, Kenji, Domei, Takenori, Kato, Masayuki, Tatami, Ryozo, Shirotani, Manabu, Hattori, Ryuichi, Kita, Toru, Furukawa, Yutaka, Ehara, Natsuhiko, Kihara, Yasuki, Eizawa, Hiroshi, Kato, Hiroshi, Ishii, Katsuhisa, Aoyama, Takeshi, Sakurai, Takahiro, Kawanami, Masaki, Suyama, Tamaki, Tada, Eiji, Tanaka, Masaru, Inada, Tsukasa, Uzui, Hiroyasu, Nakano, Akira, Lee, Jong-Dae, Onodera, Tomoya, Takizawa, Akinori, Ryuzo, Nawada, Shinoda, Eiji, Takahashi, Masaaki, Yamada, Miho, Horie, Minoru, Yamamoto, Takashi, Takashima, Hiroyuki, Sakai, Hiroshi, Tamura, Takashi, Toyofuku, Mamoru, Kotoura, Hajime, Miura, Akira, Takahashi, Mamoru, Matoba, Yoshiki, Takumi, Takuro, Tei, Chuwa, Hamasaki, Shuichi, Doi, Osamu, Kambara, Hirofumi, Kaburagi, Satoshi, Sakamoto, Hiroki, Tada, Tomohisa, Mitsudo, Kazuaki, Kadota, Kazushige, Tada, Takeshi, Miki, Shinji, Mizoguchi, Tetsu, Akira, Yoshida, Kaneda, Kazuhisa, Ogawa, Hisao, Sugamura, Koichi, Sugiyama, Seigo, Doyama, Kiyoshi, Araki, Makoto, Suwa, Satoru, Sakata, Ryuzo, Ikeda, Tadashi, Marui, Akira, Minatoya, Kenji, Yamazaki, Kazuhiro, Onoe, Masahiko, Ogawa, Tatsuya, Yamanaka, Kazuo, Iwakura, Atsushi, Ohno, Nobuhisa, Fujiwara, Keiichi, Hanyu, Michiya, Soga, Kinji, Matsushita, Tsutomu, Nishiwaki, Noboru, Yoshida, Yuichi, Tamura, Nobushige, Okada, Yukikatsu, Nasu, Michihiro, Koyama, Tadaaki, Nakayama, Shogo, Tanaka, Kuniyoshi, Koshiji, Takaaki, Morioka, Koichi, Shimamoto, Mitsuomi, Yamazaki, Fumio, Terai, Yasuhiko, Nishizawa, Junichiro, Aota, Masaki, Kanemitsu, Naoki, Hara, Hiroyuki, Tabata, Takafumi, Imoto, Yutaka, Yamamoto, Hiroyuki, Matsuda, Katsuhiko, Nara, Masafumi, Tsuneyoshi, Hiroshi, Komiya, Tatsuhiko, Nakajima, Hiroyuki, Esaki, Jiro, Kawasuji, Michio, Moriyama, Syuji, Tambara, Keiichi, Arimura, Sakiko, Fujino, Yumika, Hanazawa, Miya, Hibi, Chikako, Kato, Risa, Kinoshita, Yui, Kitagawa, Kumiko, Kitamura, Masayo, Kuwahara, Takahiro, Sachiko, Maeda, Miki, Izumi, Minematsu, Saeko, Nishida, Satoko, Okamoto, Naoko, Saeki, Asuka, Sasae, Hitomi, Sato, Yuki, Takahashi, Asuka, Takinami, Emi, Tezuka, Saori, Tsuda, Marina, Tsumori, Miyuki, Uchida, Yuriko, Yamamoto, Yuko, Yamauchi, Misato, Yamazaki, Itsuki, Yoshimoto, Mai, Abe, Mitsuru, Fuki, Masayuki, Hayano, Mamoru, Kato, Eri, Kato, Yoshihiro, Matsumura-Nakano, Yukiko, Nakajima, Tetsu, Nakatsuma, Kenji, Natsuaki, Masahiro, Takeji, Yasuaki, Tazaki, Junichi, Tokushige, Akihiro, Watanabe, Hiroki, Yaku, Hidenori, Yamamoto, Erika, Yamamoto, Ko, Yamashita, Yugo, Yoshikawa, Yusuke, Morimoto, Takeshi, Kato, Eri T., Imada, Kazuaki, Nishikawa, Ryusuke, Mabuchi, Hiroshi, and Soga, Yoshiharu

Published
2022
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50. Extracellular Matrix Proteins: Nomenclature and Functions in Biomineralization

Author

Goldberg, Michel, DenBesten, Pamela, Nakano, Yukiko, Karamanos, Nikos K., Series Editor, Kletsas, Dimitris, Editorial Board Member, Oh, Eok-Soo, Editorial Board Member, Passi, Alberto, Editorial Board Member, Pihlajaniemi, Taina, Editorial Board Member, Ricard-Blum, Sylvie, Editorial Board Member, Sagi, Irit, Editorial Board Member, Savani, Rashmin, Editorial Board Member, Watanabe, Hideto, Editorial Board Member, Goldberg, Michel, editor, and Den Besten, Pamela, editor

Published
2021
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