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4. Cardiac fibroblasts regulate the development of heart failure via Htra3-TGF-β-IGFBP7 axis

Author

Ko, Toshiyuki, Nomura, Seitaro, Yamada, Shintaro, Fujita, Kanna, Fujita, Takanori, Satoh, Masahiro, Oka, Chio, Katoh, Manami, Ito, Masamichi, Katagiri, Mikako, Sassa, Tatsuro, Zhang, Bo, Hatsuse, Satoshi, Yamada, Takanobu, Harada, Mutsuo, Toko, Haruhiro, Amiya, Eisuke, Hatano, Masaru, Kinoshita, Osamu, Nawata, Kan, Abe, Hiroyuki, Ushiku, Tetsuo, Ono, Minoru, Ikeuchi, Masashi, Morita, Hiroyuki, Aburatani, Hiroyuki, and Komuro, Issei

Published
2022
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10. rs3753394 Complement Factor H (CFH) Gene Polymorphism in Patients with Age-Related Macular Degeneration (AMD) in Indonesian Population

Author

Supanji Supanji, Perdamaian Ayudha Bahana Ilham, Anindita Dinda Ajeng, Widayanti Tri Wahyu, Wardhana Firman Setya, Sasongko Muhammad Bayu, Prayogo Mohammad Eko, Agni Angela Nurini, and Oka Chio

Subjects
Microbiology, QR1-502, Physiology, QP1-981, Zoology, QL1-991
Abstract

Neovascular Age-related Macular Degeneration (nAMD) is one of the major factors for blindness and impaired visual acuity in elderly people. The aim of this study was CFH gene screening in Age-Related Macular Degeneration patients in Indonesia. This study was performed in 106 AMD patients and 104 controls for genomic markers in the Complement Factor H (CFH). The diagnosis of AMD was carried out by retinal specialists based on color fundus photography and optical coherence tomography. Informed consent was given to patients then proceed to blood sampling and recording of body parameters (BMI, smoking, other systemic diseases). CFH polymorphisms were then analyzed by PCR-restriction fragment length polymorphism (PCR-RFLP). There was no association between genetics polymorphism with nAMD. From the research can be inferred that association between genetics polymorphism with nAMD was insignificant.

Published
2021
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12. Kadar Plasma 25-Hydroxyvitamin-D (25-OHD) pada Pasien Age-related Macular Degeneration (AMD) Stadium Akhir di Yogyakarta: Studi Korelasi

Author

Supanji, Supanji, Romdhoniyyah, Dewi Fathin, Perdamaian, Ayudha Bahana Ilham, Dianratri, Anindita, Sasongko, Muhammad Bayu, Agni, Angela Nurini, Widayanti, Tri Wahyu, Wardhana, Firman Setya, Sulistyaningrum, Dian Caturini, Prayogo, Mohammad Eko, Kawaichi, Masashi, and Oka, Chio

Abstract

Background: Age-related Macular Degeneration (AMD) is a degenerative disease caused by multiple factors, including inflammation. This condition may lead to irreversible macular damage. Vitamin D has anti-inflammatory and immune-modulating qualities, therefore, is expected to protect against the development of AMD.Objective: This study aimed to evaluate the correlation between plasma 25-hydroxyvitamin D (plasma 25-OHD) levels and neovascular Age-Related Macular Degeneration (nAMD).Methods: This was a case-control study involving AMD and control subjects. All subjects underwent a standardized eye examination to check for eligibility by a retinal specialist. Blood samples were drawn for analysis using a DRG Elisa Kit to determine the plasma 25-OHD (Total). Plasma 25-OHD levels were categorized into deficiency (50 ng/mL).Results: Total subjects were 39, which consisted of 20 AMD subjects and 19 controls. There were 17 male subjects (43.6%) and 22 female subjects (56.4%). The mean age for the case and control group was 69.35±7.04 and 68.26±6.83, respectively (p=0.612). Those in their 70s dominated the age distribution with a percentage of 56.41% of all participants. The mean plasma 25-OHD in the case group was 32.30±17.10 ng/mL, while the control group was 50.63±11.95 ng/mL (p=0.066). There was no significant association between AMD and plasma 25-OHD levels in all groups (p>0.05).Conclusion: Plasma 25-OHD levels did not correlate positively with nAMD in our study population., Latar Belakang: Age-related Macular Degeneration (AMD) adalah kondisi degeneratif yang menyebabkan kerusakan makula secara ireversibel. AMD disebabkan oleh banyak faktor, termasuk inflamasi. Vitamin D memiliki kemampuan sebagai anti-inflamasi dan pengaktifan sistem imun, sehingga diharapkan dapat membantu mencegah perjalanan penyakit AMD. Tujuan: Penelitian ini bertujuan untuk mengevaluasi hubungan antara kadar plasma 25-hydroxyvitamin-D (plasma 25-OHD) dengan neovaskular Age-related Macular Degeneration (nAMD) di populasi Yogyakarta. Metode: Penelitian ini merupakan studi kasus kontrol yang melibatkan subjek kontrol dan AMD. Seluruh subjek melalui pemeriksaan mata yang terstandar untuk memastikan eligibilitas yang dilakukan oleh spesialis retina. Sampel darah diambil untuk analisis. DRG Elisa Kit digunakan untuk menentukan kadar total 25-OHD pada plasma sampel. Kadar 25-OHD pada plasma dikelompokkan menjadi defisiensi (50 ng/mL). Hasil: Jumlah subjek yaitu sebanyak 39, terdiri dari 20 subjek AMD dan 19 kontrol. Terdapat 17 subjek laki-laki (43.6%) dan 22 subjek perempuan (56.4%). Usia rata-rata untuk kelompok kasus dan kontrol yaitu 69.35±7.04 dan 68.26±6.83 secara berurutan (p=0.612). Subjek dengan usia sekitar 70 tahun mendominasi distribusi usia dengan persentase 56.41% dari seluruh partisipan. Rata-rata kadar 25-OHD pada kelompok kasus adalah. 32.30±17.10 ng/mL, sementara pada kelompok kontrol sebesar 50.63±11.95 ng/mL (p=0.066). Tidak ada hubungan yang signifikan antara AMD dan kadar 25-OHD plasma pada semua kelompok (p>0.05). Kesimpulan: Kadar 25-OHD pada plasma tidak berkorelasi secara positif dengan nAMD di populasi Yogyakarta. Kata kunci: 25-hydroxyvitamin-D; nAMD; Vitamin D; Yogyakarta

Published
2022

13. HtrA1 serine protease expression levels on age-related macular degeneration (AMD) patients in Yogyakarta

Author

Supanji Supanji, Bahana Ilham Perdamaian Ayudha, Dianratri Anindita, Syifarahmah Anditta, Wahyu Widayanti Tri, Setya Wardhana Firman, Bayu Sasongko Muhammad, Eko Prayogo Mohammad, Nurini Agni Angela, and Oka Chio

Subjects
Microbiology, QR1-502, Physiology, QP1-981, Zoology, QL1-991
Abstract

This research aims to investigate the HtrA1 serine protease circulating level of Age-related Macular Degeneration (AMD) patients in Yogyakarta, Indonesia. This study was conducted from January to August 2019 which included 38 AMD patients and 16 Non-AMD patients/controls (two groups). Baseline data and blood sample were collected. ELISA assay was used to measure the HtrA1 serine protease circulating level on both groups. SNP genotyping of rs10490924 was using restriction enzyme digestion. This study used The IBM SPSS® version 24 (Chicago, The USA) to determine the relationship between HtrA1 expression level and AMD incidence. AMD patients had higher HtrA1 serine protease level (35.31) than controls (30.08). However, there is no association found between HtrA1 serine protease level and AMD incidence (p-value>0.05, CI 95 %). However, HtrA1 serine protease did not associate positively to AMD incidence in Yogyakarta samples. Further analysis by grouping AMD patient based on the rs10490924 genotype show no statistical correlation between HTRA1 to the incidence of AMD. This result might be due to the lack of samples in the study groups. Future studies with larger number of samples are advised to better see the association between Htra1 serine protease level and AMD incidence.

Published
2020
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14. rs10737680 polymorphism in complement factor H and neovascular age-related macular degeneration in Yogyakarta, Indonesia

Author

Sigalingging, Talenta, primary, Perdamaian, Ayudha Bahana Ilham, additional, Romdhoniyyah, Dewi Fathin, additional, Prayogo, Muhammad Eko, additional, Wardhana, Firman Setya, additional, Widayanti, Tri Wahyu, additional, Sasongko, Muhammad Bayu, additional, Agni, Angela Nurini, additional, Oka, Chio, additional, and Supanji, Supanji, additional

Published
2022
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16. The capsaicinoid nonivamide suppresses the inflammatory response and attenuates the progression of steatosis in a NAFLD‐rat model.

Author

Wikan, Naruemon, Tocharus, Jiraporn, Oka, Chio, Sivasinprasasn, Sivanan, Chaichompoo, Waraluck, Suksamrarn, Apichart, and Tocharus, Chainarong

Subjects
NF-kappa B, HEPATOCYTE nuclear factors, INFLAMMATION, NON-alcoholic fatty liver disease, PYRIN (Protein), FATTY liver
Abstract

Nonalcoholic fatty liver disease (NAFLD) is relatively associated with comorbidities in obesity and metabolic inflammation. Low‐grade inflammation following the high‐fat diet (HFD)‐induced NAFLD can promote the development of nonalcoholic steatohepatitis (NASH) through particularly liver‐resident immune cell recruitment and hepatic nuclear factor kappa B (NF‐κB) pathway. Therefore, inflammatory intervention may contribute to NASH reduction. Pelargonic acid vanillylamide (PAVA) or nonivamide is one of the pungent capsaicinoids of Capsicum species and has been found in chili peppers. Our previous study demonstrated that PAVA improved hepatic function, decreased oxidative stress and reduced apoptotic cell death but the insight role of PAVA on NAFLD is still unclear. Thus, this study aimed to investigate the underlying anti‐inflammatory mechanism of PAVA in an NAFLD‐rat model. Male Sprague Dawley rats were fed with normal diet or HFD for 16 weeks. Then high‐fat rats were given vehicle or PAVA (1 mg/kg/day) for another 4 weeks. We found that PAVA alleviated hepatic inflammation associated with the reducing toll‐like receptor 4/NF‐κB pathway, showing significantly lower recruitment of cluster of differentiation 44. PAVA also maintained activity of insulin signaling pathway, and attenuated NOD‐, LRR‐ and pyrin domain‐containing protein 3 (NLRP3) inflammasome formation. NAFLD progresses to NASH through transforming growth factor (TGF‐β1), and also recovery to simple stage followed by PAVA suppresses pro‐inflammatory cytokines such as tumor necrosis factor‐α, interleukin‐1β, interleukin‐6, and Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) pathway. Therefore, our findings suggest that PAVA provides a novel therapeutic approach for NAFLD and slows the progression to NASH. [ABSTRACT FROM AUTHOR]

Published
2023
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19. Association of the HtrA1 rs11200638 Polymorphism with Neovascular Age-Related Macular Degeneration in Indonesia

Author

Supanji, Supanji, primary, Perdamaian, Ayudha Bahana Ilham, additional, Romdhoniyyah, Dewi Fathin, additional, Sasongko, Muhammad Bayu, additional, Agni, Angela Nurini, additional, Wardhana, Firman Setya, additional, Widayanti, Tri Wahyu, additional, Prayogo, Muhammad Eko, additional, Oka, Chio, additional, and Kawaichi, Masashi, additional

Published
2021
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23. Associations of ARMS2 and CFH Gene Polymorphisms with Neovascular Age-Related Macular Degeneration

Author

Supanji, Supanji, primary, Romdhoniyyah, Dewi Fathin, additional, Sasongko, Muhammad Bayu, additional, Agni, Angela Nurini, additional, Wardhana, Firman Setya, additional, Widayanti, Tri Wahyu, additional, Prayogo, Muhammad Eko, additional, Perdamaian, Ayudha Bahana Ilham, additional, Dianratri, Aninditta, additional, Kawaichi, Masashi, additional, and Oka, Chio, additional

Published
2021
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32. Epigenetic silencing of serine protease HTRA1 drives polyploidy

Author

Schmidt, Nina, primary, Irle, Inga, additional, Ripkens, Kamilla, additional, Lux, Vanda, additional, Nelles, Jasmin, additional, Johannes, Christian, additional, Parry, Lee, additional, Greenow, Kirsty, additional, Amir, Sarah, additional, Campioni, Mara, additional, Baldi, Alfonso, additional, Oka, Chio, additional, Kawaichi, Masashi, additional, Clarke, Alan R., additional, and Ehrmann, Michael, additional

Published
2016
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33. Synthesis, Photophysical Properties, and Biological Evaluation of trans-Bisthioglycosylated Tetrakis(fluorophenyl)chlorin for Photodynamic Therapy

Author

Hirohara, Shiho, primary, Oka, Chio, additional, Totani, Masayasu, additional, Obata, Makoto, additional, Yuasa, Junpei, additional, Ito, Hiromu, additional, Tamura, Masato, additional, Matsui, Hirofumi, additional, Kakiuchi, Kiyomi, additional, Kawai, Tsuyoshi, additional, Kawaichi, Masashi, additional, and Tanihara, Masao, additional

Published
2015
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36. HTRA1 (High Temperature Requirement A Serine Peptidase 1) Gene Is Transcriptionally Regulated by Insertion/Deletion Nucleotides Located at the 3′ End of the ARMS2 (Age-related Maculopathy Susceptibility 2) Gene in Patients with Age-related Macular Degeneration

Author

Iejima, Daisuke, primary, Itabashi, Takeshi, additional, Kawamura, Yuich, additional, Noda, Toru, additional, Yuasa, Shinsuke, additional, Fukuda, Keiichi, additional, Oka, Chio, additional, and Iwata, Takeshi, additional

Published
2015
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38. trans-Bisglycoconjugation is an Efficient and Robust Architecture for PDT Photosensitizers Based on 5,10,15,20-Tetrakis(pentafluorophenyl)porphyrin Derivatives

Author

Hirohara, Shiho, primary, Sharyo, Kohei, additional, Kawasaki, Yuji, additional, Totani, Masayasu, additional, Tomotsuka, Ayumi, additional, Funasako, Ryota, additional, Yasui, Nobutaka, additional, Hasegawa, Yasuchika, additional, Yuasa, Junpei, additional, Nakashima, Takuya, additional, Kawai, Tsuyoshi, additional, Oka, Chio, additional, Kawaichi, Masashi, additional, Obata, Makoto, additional, and Tanihara, Masao, additional

Published
2013
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40. ▪

Author

Hasan, Md. Zobaer, primary, Oka, Chio, additional, and Kawaichi, Masashi, additional

Published
2013
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42. High Temperature Requirement Factor A1 (HTRA1) Gene Regulates Angiogenesis through Transforming Growth Factor-β Family Member Growth Differentiation Factor 6

Author

Zhang, Li, primary, Lim, Siok Lam, additional, Du, Hongjun, additional, Zhang, Ming, additional, Kozak, Igor, additional, Hannum, Gregory, additional, Wang, Xiaolei, additional, Ouyang, Hong, additional, Hughes, Guy, additional, Zhao, Ling, additional, Zhu, Xuemei, additional, Lee, Clara, additional, Su, Zhiguang, additional, Zhou, Xinrong, additional, Shaw, Robert, additional, Geum, Dongho, additional, Wei, Xinran, additional, Zhu, Jin, additional, Ideker, Trey, additional, Oka, Chio, additional, Wang, Ningli, additional, Yang, Zhenglin, additional, Shaw, Peter X., additional, and Zhang, Kang, additional

Published
2012
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47. HtrA1 serine protease inhibits signaling mediated by Tgfβ family proteins

Author

Oka, Chio, primary, Tsujimoto, Rumi, additional, Kajikawa, Miwa, additional, Koshiba-Takeuchi, Kazuko, additional, Ina, Junko, additional, Yano, Masato, additional, Tsuchiya, Akiho, additional, Ueta, Yoshihumi, additional, Soma, Akinobu, additional, Kanda, Hidenobu, additional, Matsumoto, Michio, additional, and Kawaichi, Masashi, additional

Published
2004
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50. Binding of proteins to the PDZ domain regulates proteolytic activity of HtrA1 serine protease

Author

YANO, Masato, UETA, Yoshifumi, MURASAKI, Ai, KANDA, Hidenobu, OKA, Chio, and KAWAICHI, Masashi

Abstract

HtrA1, a member of the mammalian HtrA (high temperature requirement A) serine protease family, has a highly conserved protease domain followed by a PDZ domain. Accumulating evidence has indicated that PDZ domains regulate protease activity of HtrA proteins. We searched for binding partners of the PDZ domain of mouse HtrA1 by yeast two-hybrid screening, and isolated proteins that were recognized by the HtrA1 PDZ domain through their C-terminal ends with a core consensus Φ-X-Φ-[V/L/F/A]-COOH sequence (where Φ is a hydrophobic/non-polar amino acid). C-propeptides of fibrillar collagens were most frequently isolated. Type III procollagen α1 C-propeptide, which was used as a model protein, was digested by HtrA1. HtrA1 cleavage of the collagen C-propeptide was enhanced by reductive denaturation of the C-propeptide and partly inhibited by removal of the C-terminal four amino acids from the C-propeptide, suggesting that the substrate recognition was facilitated by the binding of the free C-terminal ends of substrates to the PDZ domain of HtrA1. The synthetic oligopeptide (GM130Pep) that fitted the consensus recognition sequence bound to HtrA1 with a high affinity (Kd=6.0 nM). GM130Pep stimulated HtrA1 protease activity 3- to 4-fold, but did not efficiently stimulate the activity of an HtrA1 mutant lacking the PDZ domain, supporting the notion that the PDZ domain enhances protease activity upon ligand binding. The peptide derived from Type III collagen α1 C-propeptide specifically stimulated protease activity of HtrA1, but did not stimulate nor significantly bind to HtrA2, suggesting that the collagen C-propeptide is a specific physiological regulator of HtrA1.

Published
2004
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