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139 results on '"Chun, Tae-Hwa"'

7. A Scalable Engineered Extracellular Matrix Platform to Expand Tumor Cells

Author

Moon, Seongjun, primary, Neale, Dylan B., additional, Kim, Do Hoon, additional, Mukherji, Malini, additional, Hughes, Elliot, additional, Deng, Yuxuan, additional, Kerneis, Fabienne, additional, Luo, Xiuquan, additional, Tharp, Darron, additional, Bognar, Ernest, additional, Stanbery, Laura, additional, Nemunaitis, John, additional, Chun, Tae-Hwa, additional, and Lahann, Joerg, additional

Published
2023
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9. Safety and effectiveness of metabolic surgery in older Japanese patients

Author

Takemoto, Minoru, primary, Hayashi, Aiko, additional, Inaba, Yosuke, additional, Tanaka, Tomohiro, additional, Chun, Tae‐Hwa, additional, Hayashi, Hideki, additional, Kasama, Kazunori, additional, Saiki, Atsuhito, additional, Sasaki, Akira, additional, Okazumi, Shinichi, additional, Matsubara, Hisahiro, additional, and Tatsuno, Ichiro, additional

Published
2023
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14. Cellular and Molecular Aspects of C-Type Natriuretic Peptide (CNP)

Author

Itoh, Hiroshi, Suga, Shinichi, Ogawa, Yoshihiro, Komatsu, Yasato, Tamura, Naohisa, Igaki, Toshio, Yamashita, Jun, Doi, Kentaro, Chun, Tae-Hwa, Inoue, Mayumi, Masatsugu, Ken, Ikeda, Tadashi, Shirakami, Gotaro, Matsuda, Katsuhiko, Katsuura, Goro, Ueda, Makiko, Ban, Toshihiko, Nakao, Kazuwa, Conn, P. Michael, editor, Samson, Willis K., editor, and Levin, Ellis R., editor

Published
1997
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17. A Pericellular Collagenase Directs the 3-Dimensional Development of White Adipose Tissue

Author

Chun, Tae-Hwa, Hotary, Kevin B., Sabeh, Farideh, Saltiel, Alan R., Allen, Edward D., and Weiss, Stephen J.

Subjects
Proteolysis, Collagen, Proteases, Adipose tissues, Biological sciences
Abstract

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.cell.2006.02.050 Byline: Tae-Hwa Chun (1), Kevin B. Hotary (1), Farideh Sabeh (1), Alan R. Saltiel (1)(2), Edward D. Allen (1), Stephen J. Weiss (1)(2) Abstract: White adipose tissue (WAT) serves as the primary energy depot in the body by storing fat. During development, fat cell precursors (i.e., preadipocytes) undergo a hypertrophic response as they mature into lipid-laden adipocytes. However, the mechanisms that regulate adipocyte size and mass remain undefined. Herein, we demonstrate that the membrane-anchored metalloproteinase, MT1-MMP, coordinates adipocyte differentiation in vivo. In the absence of the protease, WAT development is aborted, leaving tissues populated by mini-adipocytes which render null mice lipodystrophic. While MT1-MMP preadipocytes display a cell autonomous defect in vivo, null progenitors retain the ability to differentiate into functional adipocytes during 2-dimensional (2-D) culture. By contrast, within the context of the 3-dimensional (3-D) ECM, normal adipocyte maturation requires a burst in MT1-MMP-mediated proteolysis that modulates pericellular collagen rigidity in a fashion that controls adipogenesis. Hence, MT1-MMP acts as a 3-D-specific adipogenic factor that directs the dynamic adipocyte-ECM interactions critical to WAT development. Author Affiliation: (1) Division of Molecular Medicine and Genetics, Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA (2) Life Sciences Institute, University of Michigan, Ann Arbor, MI 48109, USA Article History: Received 21 July 2005; Revised 15 December 2005; Accepted 2 February 2006 Article Note: (miscellaneous) Published: May 4, 2006

Published
2006

27. Immunomagnetic Separation of Fat Depot-Specific Sca1high Adipose-Derived Stem Cells (Ascs)

Author

Barnes, Richard H and Chun, Tae-Hwa

Subjects
Adipogenesis, Adipose Tissue, Immunomagnetic Separation, Stem Cells, Adipocytes, Animals, Cell Differentiation, Article
Abstract

The isolation of adipose-derived stem cells (ASCs) is an important method in the field of adipose tissue biology, adipogenesis, and extracellular matrix (ECM) remodeling. In vivo, ECM-rich environment consisting of fibrillar collagens provides a structural support to adipose tissues during the progression and regression of obesity. Physiological ECM remodeling mediated by matrix metalloproteinases (MMPs) plays a major role in regulating adipose tissue size and function(1,2). The loss of physiological collagenolytic ECM remodeling may lead to excessive collagen accumulation (tissue fibrosis), macrophage infiltration, and ultimately, a loss of metabolic homeostasis including insulin resistance(3,4). When a phenotypic change of the adipose tissue is observed in gene-targeted mouse models, isolating primary ASCs from fat depots for in vitro studies is an effective approach to define the role of the specific gene in regulating the function of ASCs. In the following, we define an immunomagnetic separation of Sca1(high) ASCs.

Published
2016

29. Fibro-Adipogenic Remodeling of the Diaphragm in Obesity-Associated Respiratory Dysfunction.

Author

Buras, Eric D., Converso-Baran, Kimber, Davis, Carol S., Takeshi Akama, Fumihito Hikage, Michele, Daniel E., Brooks, Susan V., Tae-Hwa Chun, Akama, Takeshi, Hikage, Fumihito, and Chun, Tae-Hwa

Subjects
OBESITY, RESPIRATORY diseases, DIAPHRAGM (Anatomy), HIGH-fat diet, HYPERCAPNIA, THROMBOSPONDIN-1, CELL proliferation, ADIPOSE tissue physiology, ADIPOSE tissues, ANIMAL experimentation, CELL culture, CELL physiology, COLLAGEN, COMPARATIVE studies, FAT cells, IMMUNOHISTOCHEMISTRY, RESEARCH methodology, MEDICAL cooperation, MICE, RESEARCH, RESEARCH funding, ULTRASONIC imaging, WESTERN immunoblotting, EVALUATION research, METABOLISM
Abstract

Respiratory dysfunction is a common complication of obesity, conferring cardiovascular morbidity and increased mortality and often necessitating mechanical ventilatory support. While impaired lung expansion in the setting of increased adipose mass and reduced central response to hypercapnia have been implicated as pathophysiological drivers, the impact of obesity on respiratory muscles-in particular, the diaphragm-has not been investigated in detail. Here, we demonstrate that chronic high-fat diet (HFD) feeding impairs diaphragm muscle function, as assessed in vivo by ultrasonography and ex vivo by measurement of contractile force. During an HFD time course, progressive adipose tissue expansion and collagen deposition within the diaphragm parallel contractile deficits. Moreover, intradiaphragmatic fibro-adipogenic progenitors (FAPs) proliferate with long-term HFD feeding while giving rise to adipocytes and type I collagen-depositing fibroblasts. Thrombospondin 1 (THBS1), a circulating adipokine, increases with obesity and induces FAP proliferation. These findings suggest a novel role for FAP-mediated fibro-adipogenic diaphragm remodeling in obesity-associated respiratory dysfunction. [ABSTRACT FROM AUTHOR]

Published
2019
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30. Coordinate regulation of endothelin and adrenomedullin secretion by oxidative stress in endothelial cells

Author

SAITO, TAKATOSHI, ITOH, HIROSHI, CHUN, TAE-HWA, FUKUNAGA, YASUTOMO, YAMASHITA, JUN, DOI, KENTARO, TANAKA, TOKUJI, INOUE, MAYUMI, MASATSUGU, KEN, SAWADA, NAOKI, SAKAGUCHI, SATSUKI, ARAI, HIROSHI, MUKOYAMA, MASASHI, TOJO, KATSUYOSHI, HOSOYA, TATSUO, and NAKAO, KAZUWA

Subjects
Hydrogen peroxide -- Physiological aspects, Nitric oxide -- Physiological aspects, Oxidation, Physiological -- Research, Peripheral vascular diseases -- Prevention, Biological sciences
Abstract

To elucidate the significance of oxidative stress in the modulation of endothelial functions, we examined the effects of [H.sub.2][O.sub.2] on the expression of two endothelium-derived vasoactive peptides, endothelin (ET) and adrenomedullin (Am), and their interaction. [H.sub.2][O.sub.2] dose dependently suppressed ET secretion and ET-1 mRNA expression in bovine carotid endothelial cells (ECs). Menadion sodium bisulfate, a redox cycling drug, also decreased ET secretion in a dose-dependent manner. Catalase, a [H.sub.2][O.sub.2] reductase, and dl-[Alpha]-tocopherol (vitamin E) significantly inhibited [H.sub.2][O.sub.2]-induced suppression of ET secretion. Downregulation of ET-1 mRNA under oxidative stress was regulated at the transcriptional level. In contrast, [H.sub.2][O.sub.2] increased Am secretion (and its mRNA expression) accompanied by the augmentation of cAMP production. Am, as well as 8-bromo-cAMP and forskolin decreased ET secretion in a dose-dependent fashion. Furthermore, an anti-Am monoclonal antibody that we developed abolished [H.sub.2][O.sub.2]-induced suppression of ET secretion at 6-24 h after the addition of [H.sub.2][O.sub.2]. [H.sub.2][O.sub.2] increased the intracellular [Ca.sup.2+] concentration ([[[Ca.sup.2+]].sub.i]). Moreover, treatment with ionomycin, a [Ca.sup.2+] ionophore, and thapsigargin, an inhibitor of endoplasmic reticulum ATPase, decreased ET secretion dose dependently for 3 h. These results suggest that the production of ET was decreased via activation of the Am-cAMP pathway and by the elevation of [[[Ca.sup.2+]].sub.i] under oxidative stress. These findings elucidate the coordinate expression of two local vascular hormones, ET and Am, under oxidative stress, which may protect against vascular diseases. intracellular [Ca.sup.2+]; hydrogen peroxide; cAMP; nitric oxide; C-type natriuretic peptide

Published
2001

33. HIF2A-LOX Pathway Promotes Fibrotic Tissue Remodeling in Thyroid-Associated Orbitopathy.

Author

Hikage, Fumihito, Atkins, Stephen, Kahana, Alon, Smith, Terry J, and Chun, Tae-Hwa

Abstract

Thyroid-associated orbitopathy (TAO) is a disfiguring periocular connective tissue disease associated with autoimmune thyroid disorders. It is a potentially blinding condition, for which no effective pharmacological treatment has been established. Despite a suggested role played by autoimmune thyrotropin receptor activation in the pathogenesis of TAO, the cellular and molecular events contributing to the fibrotic and inflammatory disease process of TAO are not fully defined. By developing a three-dimensional organoid culture of human orbital fibroblasts (OFs), we sought to determine the molecular mechanism underlying the fibrotic disease process of TAO. In this ex vivo model, we have demonstrated that hypoxia-inducible factor (HIF) 2α (HIF2A), but not its paralog HIF1A, accelerates extracellular matrix (ECM) deposition by inducing a collagen-cross-linking enzyme, lysyl oxidase (LOX). Inhibiting HIF2A and LOX with short hairpin RNA or small molecular antagonists effectively ameliorated fibrotic disease process within TAO organoids. Conversely, the overexpression of a constitutively active HIF2A in mouse OFs was sufficient to initiate LOX-dependent fibrotic tissue remodeling in OF organoids. Consistent with these findings, HIF2A and LOX were highly expressed in human TAO tissues paralleling excess ECM deposition. We propose that the HIF2A-LOX pathway can be a potential therapeutic target for the prevention and treatment of TAO.

Published
2019
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38. MT1-matrix metalloproteinase directs arterial wall invasion and neointima formation by vascular smooth muscle cells

Author

Filippov, Sergey, Koenig, Gerald C, Chun, Tae-Hwa, Hotary, Kevin B, Ota, Ichiro, Bugge, Thomas H, Roberts, Joseph D, Fay, William P, Birkedal-Hansen, Henning, Holmbeck, Kenn, Sabeh, Farideh, Allen, Edward D, Weiss, Stephen J, Filippov, Sergey, Koenig, Gerald C, Chun, Tae-Hwa, Hotary, Kevin B, Ota, Ichiro, Bugge, Thomas H, Roberts, Joseph D, Fay, William P, Birkedal-Hansen, Henning, Holmbeck, Kenn, Sabeh, Farideh, Allen, Edward D, and Weiss, Stephen J

Abstract

During pathologic vessel remodeling, vascular smooth muscle cells (VSMCs) embedded within the collagen-rich matrix of the artery wall mobilize uncharacterized proteolytic systems to infiltrate the subendothelial space and generate neointimal lesions. Although the VSMC-derived serine proteinases, plasminogen activator and plasminogen, the cysteine proteinases, cathepsins L, S, and K, and the matrix metalloproteinases MMP-2 and MMP-9 have each been linked to pathologic matrix-remodeling states in vitro and in vivo, the role that these or other proteinases play in allowing VSMCs to negotiate the three-dimensional (3-D) cross-linked extracellular matrix of the arterial wall remains undefined. Herein, we demonstrate that VSMCs proteolytically remodel and invade collagenous barriers independently of plasmin, cathepsins L, S, or K, MMP-2, or MMP-9. Instead, we identify the membrane-anchored matrix metalloproteinase, MT1-MMP, as the key pericellular collagenolysin that controls the ability of VSMCs to degrade and infiltrate 3-D barriers of interstitial collagen, including the arterial wall. Furthermore, genetic deletion of the proteinase affords mice with a protected status against neointimal hyperplasia and lumen narrowing in vivo. These studies suggest that therapeutic interventions designed to target MT1-MMP could prove beneficial in a range of human vascular disease states associated with the destructive remodeling of the vessel wall extracellular matrix.

Published
2005

39. An MT1-MMP-PDGF receptor-beta axis regulates mural cell investment of the microvasculature

Author

Lehti, Kaisa, Allen, Edward, Birkedal-Hansen, Henning, Holmbeck, Kenn, Miyake, Yasuhiro, Chun, Tae-Hwa, Weiss, Stephen J, Lehti, Kaisa, Allen, Edward, Birkedal-Hansen, Henning, Holmbeck, Kenn, Miyake, Yasuhiro, Chun, Tae-Hwa, and Weiss, Stephen J

Abstract

Platelet-derived growth factor (PDGF)/PDGFRbeta-dependent investment of the vascular endothelium by mural cells (i.e., pericytes and vascular smooth muscle cells; VSMCs) is critical for normal vessel wall structure and function. In the developing vasculature, mural cell recruitment is associated with the functionally undefined expression of the type I transmembrane proteinase, membrane-type 1 matrix metalloproteinase (MT1-MMP). In this paper, using VSMCs and tissues isolated from gene-targeted mice, we identify MT1-MMP as a PDGF-B-selective regulator of PDGFRbeta-dependent signal transduction and mural cell function. In VSMCs, catalytically active MT1-MMP associates with PDGFRbeta in membrane complexes that support the efficient induction of mitogenic signaling by PDGF-B in a matrix metalloproteinase inhibitor-sensitive fashion. In contrast, MT1-MMP-deficient VSMCs display PDGF-B-selective defects in chemotaxis and proliferation as well as ERK1/2 and Akt activation that can be rescued in tandem fashion following retroviral transduction with the wild-type protease. Consistent with these in vitro findings, MT1-MMP-deficient brain tissues display a marked reduction in mural cell density as well as abnormal vessel wall morphology similar to that reported in mice expressing PDGF-B or PDGFRbeta hypomorphic alleles. Together, these data identify MT1-MMP as a novel proteolytic modifier of PDGF-B/PDGFRbeta signal transduction that cooperatively regulates vessel wall architecture in vivo.

Published
2005

40. MT1-matrix metalloproteinase directs arterial wall invasion and neointima formation by vascular smooth muscle cells

Author

Filippov, Sergey, primary, Koenig, Gerald C., additional, Chun, Tae-Hwa, additional, Hotary, Kevin B., additional, Ota, Ichiro, additional, Bugge, Thomas H., additional, Roberts, Joseph D., additional, Fay, William P., additional, Birkedal-Hansen, Henning, additional, Holmbeck, Kenn, additional, Sabeh, Farideh, additional, Allen, Edward D., additional, and Weiss, Stephen J., additional

Published
2005
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41. Angiotensin II suppresses growth arrest specific homeobox (Gax) expression via redox-sensitive mitogen-activated protein kinase (MAPK)

Author

Saito, Takatoshi, primary, Itoh, Hiroshi, additional, Yamashita, Jun, additional, Doi, Kentaro, additional, Chun, Tae-Hwa, additional, Tanaka, Tokuji, additional, Inoue, Mayumi, additional, Masatsugu, Ken, additional, Fukunaga, Yasutomo, additional, Sawada, Naoki, additional, Sakaguchi, Satsuki, additional, Arai, Hiroshi, additional, Tojo, Katsuyoshi, additional, Tajima, Naoko, additional, Hosoya, Tatsuo, additional, and Nakao, Kazuwa, additional

Published
2005
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44. C-Type Natriuretic Peptide Induces Redifferentiation of Vascular Smooth Muscle Cells With Accelerated Reendothelialization

Author

Doi, Kentaro, primary, Ikeda, Tadashi, additional, Itoh, Hiroshi, additional, Ueyama, Koji, additional, Hosoda, Kiminori, additional, Ogawa, Yoshihiro, additional, Yamashita, Jun, additional, Chun, Tae-Hwa, additional, Inoue, Mayumi, additional, Masatsugu, Ken, additional, Sawada, Naoki, additional, Fukunaga, Yasutomo, additional, Saito, Takatoshi, additional, Sone, Masakatsu, additional, Yamahara, Kenichi, additional, Kook, Hyun, additional, Komeda, Masashi, additional, Ueda, Makiko, additional, and Nakao, Kazuwa, additional

Published
2001
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45. Oxidized LDL Regulates Vascular Endothelial Growth Factor Expression in Human Macrophages and Endothelial Cells Through Activation of Peroxisome Proliferator–Activated Receptor-γ

Author

Inoue, Mayumi, primary, Itoh, Hiroshi, additional, Tanaka, Tokuji, additional, Chun, Tae-Hwa, additional, Doi, Kentaro, additional, Fukunaga, Yasutomo, additional, Sawada, Naoki, additional, Yamshita, Jun, additional, Masatsugu, Ken, additional, Saito, Takatoshi, additional, Sakaguchi, Satsuki, additional, Sone, Masakatsu, additional, Yamahara, Ken-ichi, additional, Yurugi, Takami, additional, and Nakao, Kazuwa, additional

Published
2001
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46. Altered gene expression of uncoupling protein-2 and -3 in stroke-prone spontaneously hypertensive rats

Author

Fukunaga, Yasutomo, primary, Itoh, Hiroshi, additional, Hosoda, Kiminori, additional, Doi, Kentaro, additional, Matsuda, Junichi, additional, Son, Cheol, additional, Yamashita, Jun, additional, Chun, Tae-Hwa, additional, Tanaka, Tokuji, additional, Inoue, Mayumi, additional, Masatsugu, Ken, additional, Saito, Takatoshi, additional, Sawada, Naoki, additional, and Nakao, Kazuwa, additional

Published
2000
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47. Inhibition of Rho-Associated Kinase Results in Suppression of Neointimal Formation of Balloon-Injured Arteries

Author

Sawada, Naoki, primary, Itoh, Hiroshi, additional, Ueyama, Koji, additional, Yamashita, Jun, additional, Doi, Kentaro, additional, Chun, Tae-Hwa, additional, Inoue, Mayumi, additional, Masatsugu, Ken, additional, Saito, Takatoshi, additional, Fukunaga, Yasutomo, additional, Sakaguchi, Satsuki, additional, Arai, Hiroshi, additional, Ohno, Nobuhisa, additional, Komeda, Masashi, additional, and Nakao, Kazuwa, additional

Published
2000
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48. Oxidative stress augments secretion of endothelium-derived relaxing peptides, C-type natriuretic peptide and adrenomedullin

Author

Chun, Tae-Hwa, primary, Itoh, Hiroshi, additional, Saito, Takatoshi, additional, Yamahara, Ken-ichi, additional, Doi, Kentaro, additional, Mori, Yuko, additional, Ogawa, Yoshihiro, additional, Yamashita, Jun, additional, Tanaka, Tokuji, additional, Inoue, Mayumi, additional, Masatsugu, Ken, additional, Sawada, Naoki, additional, Fukunaga, Yasutomo, additional, and Nakao, Kazuwa, additional

Published
2000
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49. Vascular Endothelial Growth Factor (VEGF) Expression in Human Coronary Atherosclerotic Lesions

Author

Inoue, Mayumi, primary, Itoh, Hiroshi, additional, Ueda, Makiko, additional, Naruko, Takahiko, additional, Kojima, Akiko, additional, Komatsu, Ryushi, additional, Doi, Kentaro, additional, Ogawa, Yoshihiro, additional, Tamura, Naohisa, additional, Takaya, Kazuhiko, additional, Igaki, Toshio, additional, Yamashita, Jun, additional, Chun, Tae-Hwa, additional, Masatsugu, Ken, additional, Becker, Anton E., additional, and Nakao, Kazuwa, additional

Published
1998
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