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4. Transcriptomics and proteomics analyses of the PACAP38 influenced ischemic brain in permanent middle cerebral artery occlusion model mice

Author

Hori Motohide, Nakamachi Tomoya, Rakwal Randeep, Shibato Junko, Ogawa Tetsuo, Aiuchi Toshihiro, Tsuruyama Tatsuaki, Tamaki Keiji, and Shioda Seiji

Subjects
CRMP2, Crtam, DNA microarray, Gabra6, Ischemia, Il6, Neuroprotection, PACAP, Neurology. Diseases of the nervous system, RC346-429
Abstract

Abstract Introduction The neuropeptide pituitary adenylate cyclase-activating polypeptide (PACAP) is considered to be a potential therapeutic agent for prevention of cerebral ischemia. Ischemia is a most common cause of death after heart attack and cancer causing major negative social and economic consequences. This study was designed to investigate the effect of PACAP38 injection intracerebroventrically in a mouse model of permanent middle cerebral artery occlusion (PMCAO) along with corresponding SHAM control that used 0.9% saline injection. Methods Ischemic and non-ischemic brain tissues were sampled at 6 and 24 hours post-treatment. Following behavioral analyses to confirm whether the ischemia has occurred, we investigated the genome-wide changes in gene and protein expression using DNA microarray chip (4x44K, Agilent) and two-dimensional gel electrophoresis (2-DGE) coupled with matrix assisted laser desorption/ionization-time of flight-mass spectrometry (MALDI-TOF-MS), respectively. Western blotting and immunofluorescent staining were also used to further examine the identified protein factor. Results Our results revealed numerous changes in the transcriptome of ischemic hemisphere (ipsilateral) treated with PACAP38 compared to the saline-injected SHAM control hemisphere (contralateral). Previously known (such as the interleukin family) and novel (Gabra6, Crtam) genes were identified under PACAP influence. In parallel, 2-DGE analysis revealed a highly expressed protein spot in the ischemic hemisphere that was identified as dihydropyrimidinase-related protein 2 (DPYL2). The DPYL2, also known as Crmp2, is a marker for the axonal growth and nerve development. Interestingly, PACAP treatment slightly increased its abundance (by 2-DGE and immunostaining) at 6 h but not at 24 h in the ischemic hemisphere, suggesting PACAP activates neuronal defense mechanism early on. Conclusions This study provides a detailed inventory of PACAP influenced gene expressions and protein targets in mice ischemic brain, and suggests new targets for thereaupetic interventions.

Published
2012
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5. Gp91phox (NOX2) in classically activated microglia exacerbates traumatic brain injury

Author

Tsunawaki Shohko, Song Dandan, Miyamoto Kazuyuki, Satoh Kazue, Yofu Sachiko, Nakamachi Tomoya, Ohtaki Hirokazu, Dohi Kenji, Shioda Seiji, and Aruga Tohru

Subjects
Neurology. Diseases of the nervous system, RC346-429
Abstract

Abstract Background We hypothesized that gp91phox (NOX2), a subunit of NADPH oxidase, generates superoxide anion (O2-) and has a major causative role in traumatic brain injury (TBI). To evaluate the functional role of gp91phox and reactive oxygen species (ROS) on TBI, we carried out controlled cortical impact in gp91phox knockout mice (gp91phox-/-). We also used a microglial cell line to determine the activated cell phenotype that contributes to gp91phox generation. Methods Unilateral TBI was induced in gp91phox-/- and wild-type (Wt) mice (C57/B6J) (25-30 g). The expression and roles of gp91phox after TBI were investigated using immunoblotting and staining techniques. Levels of O2- and peroxynitrite were determined in situ in the mouse brain. The activated phenotype in microglia that expressed gp91phox was determined in a microglial cell line, BV-2, in the presence of IFNγ or IL-4. Results Gp91phox expression increased mainly in amoeboid-shaped microglial cells of the ipsilateral hemisphere of Wt mice after TBI. The contusion area, number of TUNEL-positive cells, and amount of O2- and peroxynitrite metabolites produced were less in gp91phox-/- mice than in Wt. In the presence of IFNγ, BV-2 cells had increased inducible nitric oxide synthase and nitric oxide levels, consistent with a classical activated phenotype, and drastically increased expression of gp91phox. Conclusions Classical activated microglia promote ROS formation through gp91phox and have an important role in brain damage following TBI. Modulating gp91phox and gp91phox -derived ROS may provide a new therapeutic strategy in combating post-traumatic brain injury.

Published
2010
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8. Intraperitoneal administration of α‐melanocyte stimulating hormone (α‐MSH) suppresses food intake and induces anxiety‐like behavior via the brain MC4 receptor‐signaling pathway in goldfish.

Author

Watanabe, Keisuke, Konno, Norifumi, Nakamachi, Tomoya, and Matsuda, Kouhei

Subjects
PEPTIDE hormones, MELANOCORTIN receptors, FOOD consumption, ALIMENTARY canal, DIENCEPHALON
Abstract

α‐Melanocyte stimulating hormone (α‐MSH) is a peptide hormone released from the intermediate lobe of the pituitary which regulates body pigmentation. In addition to the pituitary, α‐MSH is also produced in the midbrain, and exerts both anorexigenic and an anxiogenic actions. Acyl ghrelin and cholecystokinin are peripheral hormones derived from the digestive tract which affect the brain to control food intake and feeding behavior in vertebrates. In the present study, hypothesizing that plasma α‐MSH may also stimulate the brain and exert central effects, we examined whether peripherally administered α‐MSH affects food intake and psychomotor activity using a goldfish model. Intraperitoneal (IP) administration of α‐MSH at 100 pmol g−1 body weight (BW) reduced food consumption and enhanced thigmotaxis. These α‐MSH‐induced actions were blocked by intracerebroventricular administration of HS024, an antagonist of the melanocortin 4 receptor (MC4R), at 50 pmol g−1 BW, whereas these actions were not attenuated by pretreatment with an IP‐injected excess amount of capsaicin, a neurotoxin that destroys primary sensory (vagal and splanchnic) afferents, at 160 nmol g−1 BW. Transcripts for the MC4R showed higher expression in the diencephalon in other regions of the brain. These results suggest that, in goldfish, IP administered α‐MSH is taken up by the brain, and also acts as anorexigenic and anxiogenic factor via the MC4R signaling pathway. [ABSTRACT FROM AUTHOR]

Published
2024
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18. 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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28. Endogenous Pituitary Adenylate Cyclase Activating Polypeptide Is Involved in Suppression of Edema in the Ischemic Brain

Author

Nakamachi, Tomoya, Ohtaki, Hirokazu, Yofu, Sachiko, Dohi, Kenji, Watanabe, Jun, Mori, Hiroyoshi, Sato, Atsushi, Hashimoto, Hitoshi, Shintani, Norihito, Baba, Akemichi, Shioda, Seiji, Czernicki, Zbigniew, editor, Baethmann, Alexander, editor, Ito, Umeo, editor, Katayama, Yoichi, editor, Kuroiwa, Toshihiko, editor, and Mendelow, David, editor

Published
2010
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46. 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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47. PACAP Attenuates NMDA-Induced Retinal Damage in Association with Modulation of the Microglia/Macrophage Status into an Acquired Deactivation Subtype

Author

Wada, Yoshihiro, Nakamachi, Tomoya, Endo, Kimi, Seki, Tamotsu, Ohtaki, Hirokazu, Tsuchikawa, Daisuke, Hori, Motohide, Tsuchida, Masashi, Yoshikawa, Akira, Matkovits, Attila, Kagami, Nobuyuki, Imai, Nori, Fujisaka, Shiho, Usui, Isao, Tobe, Kazuyuki, Koide, Ryohei, Takahashi, Haruo, and Shioda, Seiji

Published
2013
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