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1. Involvement of Matricellular Proteins in Cellular Senescence: Potential Therapeutic Targets for Age-Related Diseases.

Author

Fujita, Motomichi, Sasada, Manabu, Iyoda, Takuya, and Fukai, Fumio

Subjects
CELLULAR aging, CELL adhesion, CELL receptors, DRUG target, INTERVERTEBRAL disk, EXTRACELLULAR matrix, PROTEINS, INTEGRINS
Abstract

Senescence is a physiological and pathological cellular program triggered by various types of cellular stress. Senescent cells exhibit multiple characteristic changes. Among them, the characteristic flattened and enlarged morphology exhibited in senescent cells is observed regardless of the stimuli causing the senescence. Several studies have provided important insights into pro-adhesive properties of cellular senescence, suggesting that cell adhesion to the extracellular matrix (ECM), which is involved in characteristic morphological changes, may play pivotal roles in cellular senescence. Matricellular proteins, a group of structurally unrelated ECM molecules that are secreted into the extracellular environment, have the unique ability to control cell adhesion to the ECM by binding to cell adhesion receptors, including integrins. Recent reports have certified that matricellular proteins are closely involved in cellular senescence. Through this biological function, matricellular proteins are thought to play important roles in the pathogenesis of age-related diseases, including fibrosis, osteoarthritis, intervertebral disc degeneration, atherosclerosis, and cancer. This review outlines recent studies on the role of matricellular proteins in inducing cellular senescence. We highlight the role of integrin-mediated signaling in inducing cellular senescence and provide new therapeutic options for age-related diseases targeting matricellular proteins and integrins. [ABSTRACT FROM AUTHOR]

Published
2024
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2. Bioactive TNIIIA2 Sequence in Tenascin-C Is Responsible for Macrophage Foam Cell Transformation; Potential of FNIII14 Peptide Derived from Fibronectin in Suppression of Atherosclerotic Plaque Formation

Author

Iyoda, Takuya, primary, Ohishi, Asayo, additional, Wang, Yunong, additional, Yokoyama, Miyabi-Shara, additional, Kazama, Mika, additional, Okita, Naoyuki, additional, Inouye, Sachiye, additional, Nakagawa, Yoshimi, additional, Shimano, Hitoshi, additional, and Fukai, Fumio, additional

Published
2024
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4. Supplementary Materials and Methods from Aggressive Progression in Glioblastoma Cells through Potentiated Activation of Integrin α5β1 by the Tenascin-C–Derived Peptide TNIIIA2

Author

Fujita, Motomichi, primary, Yamamoto, Tetsuya, primary, Iyoda, Takuya, primary, Fujisawa, Tatsuya, primary, Sasada, Manabu, primary, Nagai, Reo, primary, Kudo, Chikako, primary, Otsuka, Kazuki, primary, Kamiya, Sadahiro, primary, Kodama, Hiroaki, primary, and Fukai, Fumio, primary

Published
2023
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5. Supplementary Movie S1 from Aggressive Progression in Glioblastoma Cells through Potentiated Activation of Integrin α5β1 by the Tenascin-C–Derived Peptide TNIIIA2

Author

Fujita, Motomichi, primary, Yamamoto, Tetsuya, primary, Iyoda, Takuya, primary, Fujisawa, Tatsuya, primary, Sasada, Manabu, primary, Nagai, Reo, primary, Kudo, Chikako, primary, Otsuka, Kazuki, primary, Kamiya, Sadahiro, primary, Kodama, Hiroaki, primary, and Fukai, Fumio, primary

Published
2023
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6. Supplementary table S1 from Aggressive Progression in Glioblastoma Cells through Potentiated Activation of Integrin α5β1 by the Tenascin-C–Derived Peptide TNIIIA2

Author

Fujita, Motomichi, primary, Yamamoto, Tetsuya, primary, Iyoda, Takuya, primary, Fujisawa, Tatsuya, primary, Sasada, Manabu, primary, Nagai, Reo, primary, Kudo, Chikako, primary, Otsuka, Kazuki, primary, Kamiya, Sadahiro, primary, Kodama, Hiroaki, primary, and Fukai, Fumio, primary

Published
2023
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7. Supplementary Figure and Figure legend from Aggressive Progression in Glioblastoma Cells through Potentiated Activation of Integrin α5β1 by the Tenascin-C–Derived Peptide TNIIIA2

Author

Fujita, Motomichi, primary, Yamamoto, Tetsuya, primary, Iyoda, Takuya, primary, Fujisawa, Tatsuya, primary, Sasada, Manabu, primary, Nagai, Reo, primary, Kudo, Chikako, primary, Otsuka, Kazuki, primary, Kamiya, Sadahiro, primary, Kodama, Hiroaki, primary, and Fukai, Fumio, primary

Published
2023
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9. Supplementary Movie legend from Aggressive Progression in Glioblastoma Cells through Potentiated Activation of Integrin α5β1 by the Tenascin-C–Derived Peptide TNIIIA2

Author

Fujita, Motomichi, primary, Yamamoto, Tetsuya, primary, Iyoda, Takuya, primary, Fujisawa, Tatsuya, primary, Sasada, Manabu, primary, Nagai, Reo, primary, Kudo, Chikako, primary, Otsuka, Kazuki, primary, Kamiya, Sadahiro, primary, Kodama, Hiroaki, primary, and Fukai, Fumio, primary

Published
2023
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12. How to prevent contamination with Candida albicans during the fabrication of transplantable oral mucosal epithelial cell sheets

Author

Takagi, Ryo, Kobayashi, Shinichiro, Yamato, Masayuki, Owaki, Toshiyuki, Kasai, Yoshiyuki, Hosoi, Takahiro, Sakai, Yusuke, Kanetaka, Kengo, Minamizato, Tokutaro, Minematsu, Asuka, Kondo, Makoto, Kanai, Nobuo, Yamaguchi, Naoyuki, Nagai, Kazuhiro, Miyazaki, Yasushi, Takeda, Naoya, Fukai, Fumio, Asahina, Izumi, Miyazaki, Taiga, Kohno, Shigeru, Yamamoto, Masakazu, Nakao, Kazuhiko, Eguchi, Susumu, and Okano, Teruo

Published
2015
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18. Potentiated activation of VLA-4 and VLA-5 accelerates proplatelet-like formation

Author

Matsunaga, Takuya, Fukai, Fumio, Kameda, Takuro, Shide, Kotaro, Shimoda, Haruko, Torii, Eri, Kamiunten, Ayako, Sekine, Masaaki, Yamamoto, Shojirou, Hidaka, Tomonori, Kubuki, Yoko, Yokokura, Shigeyuki, Uemura, Makiko, Matsuoka, Akihito, Waki, Fusako, Matsumoto, Kensuke, Kanaji, Nobuhiro, Ishii, Tomoya, Imataki, Osamu, Dobashi, Hiroaki, Bandoh, Shuji, and Shimoda, Kazuya

Published
2012
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24. Fibronectin peptides derived from two distinct regions stimulate adipocyte differentiation by preventing fibronectin matrix assembly

Author

Kamiya, Sadahiro, Kato, Rina, Wakabayashi, Masayoshi, Tohyama, Takehiro, Enami, Isao, Ueki, Masaaki, Yajima, Hirofumi, Ishii, Tadahiro, Nakamura, Hiroshi, Katayama, Takashi, Takagi, Junichi, and Fukai, Fumio

Subjects
Cell adhesion -- Molecular aspects, Fat cells -- Physiological aspects, Fibronectins -- Physiological aspects, Fibrinogen -- Physiological aspects, Biological sciences, Chemistry
Abstract

Results suggest that the 24k Fib 1 and FNIII14 fibronectin fragments-mediated fibronectin fibrillogenesis inhibition leads to adipocyte differentiation of ST-13 cells. Data indicate that the Fib 1 is directly incorporated into the the fibronectin matrix, whereas FNIII14 negatively regulates the fibronectin receptor alpha5beta1 activity.

Published
2002

28. Interaction with heparin and matrix metalloproteinase 2 cleavage expose a cryptic anti-adhesive site fibronectin

Author

Watanabe, Kazuo, Takahashi, Hiroshi, Habu, Yoshiko, Kamiya-Kubushiro, Naoko, Kamiya, Sadahiro, Nakamura, Hiroshi, Yajima, Hirofumi, Ishii, Tadahiro, Katayama, Takashi, Miyazaki, Kaoru, and Fukai, Fumio

Subjects
Biochemistry -- Research, Heparin -- Research, Metalloenzymes -- Research, Fibronectins -- Research, Biological sciences, Chemistry
Abstract

Research has been conducted on fibronectin. Results indicate that the cryptic anti-adhesive activity of fibronectin can be changed after conformational change of the heparin-binding domain 2.

Published
2000

29. TAp63 represses transcription of MYCN/NCYM gene and its high levels of expression are associated with favorable outcome in neuroblastoma

Author

Suenaga, Yusuke, primary, Yamamoto, Mami, additional, Sakuma, Tetsushi, additional, Sasada, Manabu, additional, Fukai, Fumio, additional, Ohira, Miki, additional, Yamaguchi, Yohko, additional, Yamamoto, Takashi, additional, Ando, Kiyohiro, additional, Ozaki, Toshinori, additional, and Nakagawara, Akira, additional

Published
2019
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30. Aggressive Progression in Glioblastoma Cells through Potentiated Activation of Integrin α5β1 by the Tenascin-C–Derived Peptide TNIIIA2

Author

Fujita, Motomichi, primary, Yamamoto, Tetsuya, additional, Iyoda, Takuya, additional, Fujisawa, Tatsuya, additional, Sasada, Manabu, additional, Nagai, Reo, additional, Kudo, Chikako, additional, Otsuka, Kazuki, additional, Kamiya, Sadahiro, additional, Kodama, Hiroaki, additional, and Fukai, Fumio, additional

Published
2019
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32. Combining peptide TNIIIA2 with all-trans retinoic acid accelerates N-Myc protein degradation and neuronal differentiation in MYCN-amplified neuroblastoma cells

Author

Otsuka, Kazuki, Sasada, Manabu, Iyoda, Takuya, Nohara, Yusuke, Sakai, Shunsuke, Asayama, Tatsufumi, Suenaga, Yusuke, Yokoi, Sana, Higami, Yoshikazu, Kodama, Hiroaki, and Fukai, Fumio

Subjects
Original Article, neoplasms
Abstract

Neuroblastoma is one of the common solid tumors of childhood. Nearly half of neuroblastoma patients are classified into the high-risk group, and their 5-year event-free survival (EFS) rates remain unsatisfactory in the range of 30-40%. High-risk neuroblastoma is characterized by amplification of the MYCN gene and excessive expression of its protein product, N-Myc. Because N-Myc is a transcription factor for various pro-proliferative proteins, the excessive expression causes aberrant or blocked neuronal differentiation during development of sympathetic nervous system, which is a central aspect of neuroblastoma genesis. The current main treatment for high-risk neuroblastoma is intensive chemotherapy using anti-cancer drugs that induce apoptosis in tumor cells, but intensive chemotherapy has another serious risk of long-lasting side effects, so-called “late effects”, that occur many years after chemotherapy has ended. As a solution for such situation, differentiation therapy has been expected as a mild chemotherapy with a low risk of late effects, and an application of retinoic acid (RA) and its derivatives as treatment for high-risk neuroblastoma has long been attempted. However, the clinical outcome has not been sufficient with the use of retinoids, including all-trans retinoic acid (ATRA), mainly because of the inhibition of differentiation caused by N-Myc. In the present study, we succeeded in synergistically accelerating the ATRA-induced neuronal differentiation of MYCN-amplified neuroblastoma cells by combining a peptide derived from tenascin-C, termed TNIIIA2, which has a potent ability to activate β1-integrins. Accelerated differentiation was caused by a decrease in N-Myc protein level in neuroblastoma cells after the combined treatment of TNIIIA2 with ATRA. That is, combination treatment using ATRA with TNIIIA2 induced proteasomal degradation in the N-Myc oncoprotein of neuroblastoma cells with MYCN gene amplification, and this caused acceleration of neuronal differentiation and attenuation of malignant properties. Furthermore, an in vivo experiment using a xenograft mouse model showed a therapeutic potential of the combination administration of ATRA and TNIIIA2 for high-risk neuroblastoma. These results provide a new insight into differentiation therapy for high-risk neuroblastoma based on N-Myc protein degradation.

Published
2019

34. Release of biological activities from quiescent fibronectin by a conformational change and limited proteolysis by matrix metalloproteinases

Author

Fukai, Fumio, Ohtaki, Mitsuru, Fujii, Nozomi, Yajima, Hirofumi, Ishii, Tadahiro, Nishizawa, Yoshinori, Miyazaki, Kaoru, and Katayama, Takashi

Subjects
Fibronectins -- Research, Metalloenzymes -- Physiological aspects, Biological sciences, Chemistry
Abstract

The activity of the central cell-binding domain (Cell domain) of fibronectin (Fn), a glycoprotein, is induced by structural changes, while that of the amino-terminal fibrin-binding domain (Fib 1 domain) and the carboxyl-terminal fibrin-binding domain (Fib 2 domain) are induced by fragmentation of fibronectin. Inactive Fn shows Cell domain activity on exposure to urea or surface adsorption. Fn shows Fib 1 and Fib 2 domain activity on exposure to matrix metalloproteinases such as collagenase and gelatinase A. The activity of all the domains is more if they are not linked to surrounding domains.

Published
1995

35. An amino-terminal fibronectin fragment stimulates the differentiation of ST-13 preadipocytes

Author

Fukai, Fumio, Iso, Takako, Sekiguchi, Kiyotoshi, Miyatake, Norifumi, Tsugita, Akira, and Katayama, Takashi

Subjects
Fat cells -- Research, Fibronectins -- Research, Cell differentiation -- Research, Biological sciences, Chemistry
Abstract

A cloned preadipocyte cell line, ST-13, was used to study the effects of fibronectin (FN) and FN fragments on adipocyte differentiation. Fibronectin, an element of the extracellular matrix, has been known to regulate cell differentiation including adipocyte conversion. Results showed that FN in solution and as matrices inhibit differentiation of ST-13 preadipocytes, which can be reversed with GRGDPS cell recognition peptide or anti-alpha5beta1. FN fragments, on the other hand, stimulate preadipocyte differentiation.

Published
1993

36. TNIIIA2, The Peptide of Tenascin-C, as a Candidate for Preventing Articular Cartilage Degeneration

Author

Hattori, Tetsuya, Hasegawa, Masahiro, Unno, Hironori, Iino, Takahiro, Fukai, Fumio, Yoshida, Toshimichi, and Sudo, Akihiro

Abstract

Objective TNIIIA2 is a peptide of the extracellular matrix glycoprotein tenascin-C. We evaluated whether intra-articular injection of TNIIIA2 could prevent articular cartilage degeneration without inducing synovitis in an osteoarthritis mice model.Design Ten micrograms per milliliter of TNIIIA2 were injected into the knee joint of mice (group II) to evaluate the induction of synovitis. The control group received an injection of phosphate buffered saline (group I). Synovitis was evaluated using synovitis score 2 and 4 weeks after injection. The ligaments of knee joints of mice were transected to make the osteoarthritis model. After transection, 10 µg/mL of TNIIIA2 was injected into the knee joint (group IV). The control group received an injection of phosphate buffered saline after transection (group III). Histologic examinations were made using hematoxylin and eosin and safranin-O staining at 2, 4, 8, and 12 weeks postoperatively. An in vitrostudy was also performed to determine the mechanism by which TNIIIA2 prevents cartilage degeneration. Human chondrocytes were isolated, cultured, and treated with TNIIIA2. The expressions of various mRNAs, including inflammatory cytokines, and anabolic and catabolic factors for cartilage were compared using real-time polymerase chain reaction.Results There were no differences between groups in the study of intra-articular injection of mice (group I vs. group II). In the osteoarthritis model, we found development of osteoarthritis was suppressed in group IV at 4 and 8 weeks. TNIIIA2 upregulated the expressions of tumor necrosis factor-α, matrix metalloproteinase 3, and basic fibroblast growth factor.Conclusion We demonstrated that TNIIIA2 could prevent cartilage degeneration without synovitis.

Published
2021
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49. Coadministration of the FNIII14 Peptide Synergistically Augments the Anti-Cancer Activity of Chemotherapeutic Drugs by Activating Pro-Apoptotic Bim

Author

Iyoda, Takuya, primary, Nagamine, Yumi, additional, Nakane, Yoshitomi, additional, Tokita, Yuya, additional, Akari, Shougo, additional, Otsuka, Kazuki, additional, Fujita, Motomichi, additional, Itagaki, Keisuke, additional, Takizawa, You-ichi, additional, Orita, Hiroaki, additional, Owaki, Toshiyuki, additional, Taira, Jyunichi, additional, Hayashi, Ryo, additional, Kodama, Hiroaki, additional, and Fukai, Fumio, additional

Published
2016
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