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3. Regulation of Brain Primary Cilia Length by MCH Signaling: Evidence from Pharmacological, Genetic, Optogenetic, and Chemogenic Manipulations

Author

Alhassen, Wedad, Kobayashi, Yuki, Su, Jessica, Robbins, Brianna, Nguyen, Henry, Myint, Thant, Yu, Micah, Nauli, Surya M, Saito, Yumiko, and Alachkar, Amal

Subjects
Pharmacology and Pharmaceutical Sciences, Biomedical and Clinical Sciences, Behavioral and Social Science, Neurosciences, Basic Behavioral and Social Science, Underpinning research, 1.1 Normal biological development and functioning, Neurological, Animals, Caudate Nucleus, Cilia, Hypothalamic Hormones, Melanins, Mice, Mice, Knockout, Neurons, Optogenetics, Pituitary Hormones, Prefrontal Cortex, Pyrimidinones, Rats, Rats, Wistar, Receptors, Somatostatin, Thiophenes, Melanin-concentrating hormone, Signaling, Brain, Activation, Inactivation, Psychology, Cognitive Sciences, Neurology & Neurosurgery, Biochemistry and cell biology
Abstract

The melanin-concentrating hormone (MCH) system is involved in numerous functions, including energy homeostasis, food intake, sleep, stress, mood, aggression, reward, maternal behavior, social behavior, and cognition. In rodents, MCH acts on MCHR1, a G protein-coupled receptor, which is widely expressed in the brain and abundantly localized to neuronal primary cilia. Cilia act as cells' antennas and play crucial roles in cell signaling to detect and transduce external stimuli to regulate cell differentiation and migration. Cilia are highly dynamic in terms of their length and morphology; however, it is not known if cilia length is causally regulated by MCH system activation in vivo. In the current work, we examined the effects of activation and inactivation of MCH system on cilia lengths by using different experimental models and methodologies, including organotypic brain slice cultures from rat prefrontal cortex (PFC) and caudate-putamen (CPu), in vivo pharmacological (MCHR1 agonist and antagonist GW803430), germline and conditional genetic deletion of MCHR1 and MCH, optogenetic, and chemogenetic (designer receptors exclusively activated by designer drugs (DREADD)) approaches. We found that stimulation of MCH system either directly through MCHR1 activation or indirectly through optogenetic and chemogenetic-mediated excitation of MCH-neuron, caused cilia shortening, detected by the quantification of the presence of ADCY3 protein, a known primary cilia marker. In contrast, inactivation of MCH signaling through pharmacological MCHR1 blockade or through genetic manipulations - germline deletion of MCHR1 and conditional ablation of MCH neurons - induced cilia lengthening. Our study is the first to uncover the causal effects of the MCH system in the regulation of the length of brain neuronal primary cilia. These findings place MCH system at a unique position in the ciliary signaling in physiological and pathological conditions and implicate MCHR1 present at primary cilia as a potential therapeutic target for the treatment of pathological conditions characterized by impaired primary cilia function associated with the modification of its length.

Published
2022

6. Patterns of cilia gene dysregulations in major psychiatric disorders

Author

Alhassen, Wedad, Chen, Siwei, Vawter, Marquis, Robbins, Brianna Kay, Nguyen, Henry, Myint, Thant Nyi, Saito, Yumiko, Schulmann, Anton, Nauli, Surya M, Civelli, Olivier, Baldi, Pierre, and Alachkar, Amal

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Genetics, Depression, Mental Health, Bipolar Disorder, Schizophrenia, Mental Illness, Autism, Brain Disorders, Major Depressive Disorder, Serious Mental Illness, Intellectual and Developmental Disabilities (IDD), Neurosciences, 2.1 Biological and endogenous factors, 1.1 Normal biological development and functioning, Neurological, Mental health, Brain, Cilia, Databases, Genetic, Gene Expression Profiling, Gene Expression Regulation, Humans, Mental Disorders, Compartments, Bipolar disorder, DEGs, Medical and Health Sciences, Clinical Sciences, Psychology and Cognitive Sciences, Psychiatry, Biochemistry and cell biology, Clinical sciences
Abstract

Primary cilia function as cells' antennas to detect and transduce external stimuli and play crucial roles in cell signaling and communication. The vast majority of cilia genes that are causally linked with ciliopathies are also associated with neurological deficits, such as cognitive impairments. Yet, the roles of cilia dysfunctions in the pathogenesis of psychiatric disorders have not been studied. Our aim is to identify patterns of cilia gene dysregulation in the four major psychiatric disorders: schizophrenia (SCZ), autism spectrum disorder (ASD), bipolar disorder (BP), and major depressive disorder (MDD). For this purpose, we acquired differentially expressed genes (DEGs) from the largest and most recent publicly available databases. We found that 42%, 24%, 17%, and 15% of brain-expressed cilia genes were significantly differentially expressed in SCZ, ASD, BP, and MDD, respectively. Several genes exhibited cross-disorder overlap, suggesting that typical cilia signaling pathways' dysfunctions determine susceptibility to more than one psychiatric disorder or may partially underlie their pathophysiology. Our study revealed that genes encoding proteins of almost all sub-cilia structural and functional compartments were dysregulated in the four psychiatric disorders. Strikingly, the genes of 75% of cilia GPCRs and 50% of the transition zone proteins were differentially expressed in SCZ. The present study is the first to draw associations between cilia and major psychiatric disorders, and is the first step toward understanding the role that cilia components play in their pathophysiological processes, which may lead to novel therapeutic targets for these disorders.

Published
2021

9. Ciliary length variations impact cilia-mediated signaling and biological responses.

Author

Kobayashi, Yuki, Hamamoto, Akie, and Saito, Yumiko

Subjects
G protein coupled receptors, CILIA & ciliary motion, CELL anatomy, COBALT chloride, CELL communication, CELL receptors
Abstract

Primary cilia are thin hair-like organelles that protrude from the surface of most mammalian cells. They act as specialized cell antennas that can vary widely in response to specific stimuli. However, the effect of changes in cilia length on cellular signaling and behavior remains unclear. Therefore, we aimed to characterize the elongated primary cilia induced by different chemical agents, lithium chloride (LiCl), cobalt chloride (CoCl2) and rotenone, using human retinal pigmented epithelial 1 (hRPE1) cells expressing ciliary G protein-coupled receptor (GPCR), melanin-concentrating hormone (MCH) receptor 1 (MCHR1). MCH induces cilia shortening mainly via MCHR1-mediated Akt phosphorylation. Therefore, we verified the proper functioning of the MCH-MCHR1 axis in elongated cilia. Although MCH shortened cilia that were elongated by LiCl and rotenone, it did not shorten CoCl2-induced elongated cilia, which exhibited lesser Akt phosphorylation. Furthermore, serum readdition was found to delay cilia shortening in CoCl2-induced elongated cilia. In contrast, rotenone-induced elongated cilia rapidly shortened via a chopping mechanism at the tip of the cilia. Conclusively, we found that each chemical exerted different effects on ciliary GPCR signaling and serum-mediated ciliary structure dynamics in cells with elongated cilia. These results provide a basis for understanding the functional consequences of changes in ciliary length. [ABSTRACT FROM AUTHOR]

Published
2024
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16. Contributors

Author

Amano, Masafumi, primary, Ando, Hironori, additional, Andoh, Tadashi, additional, Baker, Michael E., additional, Cameron, Melissa S., additional, Daubnerová, Ivana, additional, Donald, John A., additional, Fukumura, Keisuke, additional, Funaba, Masayuki, additional, Haraguchi, Shogo, additional, Hayakawa, Yoichi, additional, Hirako, Satoshi, additional, Hyodo, Susumu, additional, Iguchi, Taisen, additional, Inui, Akio, additional, Kaiya, Hiroyuki, additional, Kakizawa, Sho, additional, Kamiyama, Takumi, additional, Kanamori, Yohei, additional, Kanda, Shinji, additional, Katayama, Hidekazu, additional, Kato, Takashi, additional, Katsu, Yoshinao, additional, Katsuura, Goro, additional, Kawada, Tsuyoshi, additional, Kimura, Atsushi P., additional, Kitamura, Keiichiro, additional, Kobayashi, Yuki, additional, Kodani, Yu, additional, Konno, Norifumi, additional, Kuraku, Shigehiro, additional, Minakata, Hiroyuki, additional, Mita, Masatoshi, additional, Miyagawa, Shinichi, additional, Miyazato, Mikiya, additional, Mizusawa, Kanta, additional, Mori, Kenji, additional, Morishita, Fumihiro, additional, Moriyama, Shunsuke, additional, Nagasaki, Hiroshi, additional, Nagata, Shinji, additional, Nakamachi, Tomoya, additional, Niwa, Ryusuke, additional, Ogino, Yukiko, additional, Ogoshi, Maho, additional, Ohira, Tsuyoshi, additional, Ohki-Hamazaki, Hiroko, additional, Ohtaki, Hirokazu, additional, Ohyama, Yoshihiko, additional, Oka, Yoshitaka, additional, Okamoto, Naoki, additional, Onizawa, Moe, additional, Osugi, Tomohiro, additional, Saito, Yumiko, additional, Sakai, Takafumi, additional, Sakamoto, Hirotaka, additional, Sakamoto, Tatsuya, additional, Sakata, Ichiro, additional, Satake, Honoo, additional, Sato, Seiichi, additional, Sato, Tomomi, additional, Seike, Hitomi, additional, Sekiguchi, Toshio, additional, Shimizu, Munetaka, additional, Shinki, Toshimasa, additional, Shinoda, Tetsuro, additional, Shiomi, Kunihiro, additional, Suzuki, Nobuo, additional, Tachibana, Tetsuya, additional, Takahashi, Akiyoshi, additional, Takahashi, Toshio, additional, Takaoka, Akinori, additional, Takei, Yoshio, additional, Takenoya, Fumiko, additional, Takeuchi, Sakae, additional, Tanaka, Yoshiaki, additional, Toshinai, Koji, additional, Tsukada, Takehiro, additional, Tsutsui, Kazuyoshi, additional, Tsutsui, Naoaki, additional, Ubuka, Takayoshi, additional, Ukena, Kazuyoshi, additional, Wada, Nobuhiro, additional, Watanabe, Jun, additional, Wong, Marty Kwok-Shing, additional, Yamada, Taisho, additional, Yamaguchi, Yoko, additional, Yamanaka, Naoki, additional, Yamauchi, Kiyoshi, additional, Yuge, Shinya, additional, Zhou, Yijun, additional, and Žitňan, Dušan, additional

Published
2021
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36. Augmentative and Alternative Communication Practice in the Pursuit of Family Quality of Life: A Review of the Literature

Author

Saito, Yumiko and Turnbull, Ann

Abstract

Augmentative and Alternative Communication (AAC) practice may have both positive and negative impacts on quality of life (QOL) of children with AAC as well as their entire family. Thirteen studies were reviewed to analyze family outcomes and perspectives on AAC practice by using a family quality of life (FQOL) framework comprised of five empirically derived domains in order to identify issues that families perceive as important to their lives. The impact of current AAC practices encompasses all five domains: family interaction, parenting, physical/material well-being, disability-related support, and emotional well-being. Implications are drawn for practitioners and researchers for AAC practices that impact positive FQOL outcomes. (Contains 3 tables and 1 figure.)

Published
2007

37. Self-Determination: What Do We Know? Where Do We Go?

Author

Chambers, Cynthia R., Wehmeyer, Michael L., and Saito, Yumiko

Abstract

Promoting self-determination has become an important aspect of the educational programs of students with disabilities. There is now a sufficient literature base to support some syntheses that enable researchers to judge their progress in this area to date and to provide direction for future research and practice. For this study, we conducted a literature review of studies that measured or examined global self-determination.

Published
2007
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38. Multidisciplinary Approach for Adult Patients With Childhood-Onset Chronic Disease Focusing on Promoting Pediatric to Adult Healthcare Transition Interventions: An Updated Systematic Review

Author

WAKIMIZU, Rie, Sasaki, Keita, Yoshimoto, Mitsuki, Miyazaki, Akari, and Saito, Yumiko

Subjects
Pediatrics, Perinatology and Child Health
Abstract

IntroductionOwing to improved prognosis, the number of adult patients with childhood-onset chronic disease (APCCD) has increased. In this systematic review, we evaluated a multidisciplinary approach toward APCCD, focusing on promoting pediatric to adult healthcare transition interventions and their effects.MethodsWe reviewed literature comparing the effects of pediatric to adult healthcare transition interventions in children and adolescents with childhood-onset chronic disease, using PubMed, MEDLINE, and CINAHL, from 2010 to 2021 (keywords: “transition,” “children,” “intervention,” “healthcare,” etc.). The inclusion criteria were as follows: (i) original studies, (ii) studies on pediatric to adult healthcare transition interventions in children with chronic disease, (iii) patients including “adolescents” aged 12 and older receiving intervention, and (iv) studies that included the four elements of the PICO model: Patient/ Problem, Intervention, Comparison and Outcome model.ResultsAfter evaluating 678 studies, 16 were selected, comprising topics such as “individual education programs” (n = 6), “group meetings” (n = 6), “active learning using information and communications technology” (n = 2), and “transition clinics” (n = 2). The effects obtained varied, depending on the contents and methods of the intervention. Additionally, there was no evidence of adverse outcomes from these interventions.ConclusionsPediatric to adult healthcare transition interventions provide systematic support for the transition, patient independence, and social participation; thus, they should be adopted based on their expected effects.

Published
2022
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45. List of Contributors

Author

Amano, Masafumi, primary, Ando, Hironori, additional, Andoh, Tadashi, additional, Daubnerova, Ivana, additional, Donald, John A., additional, Forgan, Leonard G., additional, Haraguchi, Shogo, additional, Hayakawa, Yoichi, additional, Hirako, Satoshi, additional, Hyodo, Susumu, additional, Iguchi, Taisen, additional, Inui, Akio, additional, Kageyama, Haruaki, additional, Kaiya, Hiroyuki, additional, Kakizawa, Sho, additional, Kanda, Shinji, additional, Kaneko, Hiroyuki, additional, Kataoka, Hiroshi, additional, Katayama, Hidekazu, additional, Kato, Takashi, additional, Katsu, Yoshinao, additional, Katsuura, Goro, additional, Kawada, Tsuyoshi, additional, Kimura, Atsushi P., additional, Kobayashi, Yuki, additional, Konno, Norifumi, additional, Konogami, Tadafumi, additional, Minakata, Hiroyuki, additional, Mita, Masatoshi, additional, Miyagawa, Shinichi, additional, Miyazato, Mikiya, additional, Mizoguchi, Akira, additional, Mizusawa, Kanta, additional, Mori, Kenji, additional, Morishita, Fumihiro, additional, Moriyama, Shunsuke, additional, Nagasaki, Hiroshi, additional, Nagata, Shinji, additional, Nakagawa, Yoshiaki, additional, Nakamachi, Tomoya, additional, Niimi, Teruyuki, additional, Ogino, Yukiko, additional, Ogoshi, Maho, additional, Ohira, Tsuyoshi, additional, Ohki-Hamazaki, Hiroko, additional, Ohtaki, Hirokazu, additional, Ohyama, Yoshihiko, additional, Oka, Yoshitaka, additional, Okamoto, Naoki, additional, Osugi, Tomohiro, additional, Park, Min Kyun, additional, Saito, Kazuki, additional, Saito, Yumiko, additional, Sakai, Takafumi, additional, Sakamoto, Hirotaka, additional, Sakamoto, Tatsuya, additional, Satake, Honoo, additional, Sato, Tomomi, additional, Sekiguchi, Toshio, additional, Shimizu, Munetaka, additional, Shinki, Toshimasa, additional, Shinoda, Tetsuro, additional, Sonobe, Haruyuki, additional, Suzuki, Koichi, additional, Suzuki, Nobuo, additional, Tachibana, Tetsuya, additional, Takahashi, Akiyoshi, additional, Takahashi, Toshio, additional, Takei, Yoshio, additional, Takenoya, Fumiko, additional, Takeuchi, Sakae, additional, Tanaka, Yoshiaki, additional, Tanizaki, Yuta, additional, Tsukada, Takehiro, additional, Tsukamoto, Yusuke, additional, Tsutsui, Kazuyoshi, additional, Tsutsui, Naoaki, additional, Ubuka, Takayoshi, additional, Ukena, Kazuyoshi, additional, Wada, Nobuhiro, additional, Watanabe, Jun, additional, Wong, Marty K.S., additional, Xu, Zhifang, additional, Yaginuma, Toshinobu, additional, Yamauchi, Kiyoshi, additional, Yuge, Shinya, additional, and Zitnan, Dusan, additional

Published
2016
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